I have seen many elderly folks in the office in the past few weeks, some of them getting around with canes, others with walkers, and then the lucky few who could still rely on their own two feet alone.  Some of them have fallen in the past and are very concerned about doing it again.  My grandmother always says, once you break a hip it's all down hill from there.  While that's not entirely true, many elderly people don't recover completely from fall injuries.  The other day my preceptor was explaining to a patient a few exercises she could do to improve her balance and decrease her risk of falling.  So, I was wondering, what's the evidence behind this?

 
One randomized, controlled study had the intervention group do weight-bearing group exercises and the control group did flexibility and relaxation exercises over a 12 month period.  There were 22% fewer falls in the intervention group.  The weight-bearing group exercise included "aerobic exercises, specific strengthening exercises, and activities for balance, hand-eye and foot-eye coordination, and flexibility".  For more details of the exercises you can link to the full text article if you are on the intranet.  I also looked at a review article, which found that the most effective way to prevent falls was with a multifactorial risk assessment and management program.

This time of year brings countless cases of acute pharyngitis and tonsillitis to family practice physicians and pediatricians alike.  As we all know, the currently accepted course of treatment rests on the determination of whether or not the etiologic agent is viral or bacterial in nature.  In the case of a streptococcal infection or other bacteria, a short course of antibiotics and symptomatic treatment is generally sufficient to clear the ailment while a viral colonization is only treated symptomatically and is usually self-resolving within 10 days.  This, of course, is nothing new.  However, from a primary care standpoint, what is the recommended approach when a child or adult repeatedly suffers from similar cases of tonsillitis far more often than the average individual?

This question was not originally posed by myself but by the mother of a patient that presented with a second case of tonsillitis/pharyngitis within the past year.  "What ever happened to tonsillectomies for the treatment of tonsillitis?," asked the mother.  "Well," I replied, "I'm really not sure."  The mother then went on to describe how she remembers as a kid that if a child came down with a case of tonsillitis, the doctor was practically waiting with the scalpel in hand to cut out the kid's tonsils.  Although I didn't have a definite answer for her, I knew that things had changed and that tonsillectomies must have dropped in occurrence over the past few decades.

To investigate this question, I performed a few literature searches on the topic and to my surprise, the the debate is anything but settled.  In fact, it seems as though the medical industry may be just as far from a definitive answer as it was half a century ago.  One article I found on the internet suggested that the rate of tonsillectomies has decreased by 75% over the past thirty years from approximately 1,000,000 per year to 250,000 per year, so clearly there has been some ideological shift in the belief of their necessity.  According to the same article the shift in thinking is based on recent evidence (in addition to newer antibiotics) indicating little to no improvement in rates of reinfection of children undergoing tonsillectomy when compared to children using a "watchful waiting" approach.  In essence, the benefits of the procedure may not outweigh the risks of surgery.

According to a 2001 Cochrane Systematic Review on the topic of treatment approach to chronic and/or recurrent acute tonsillitis, "There is no evidence from randomized controlled trials to guide the clinician in formulating the indications for surgery in adults or children."  The review identifies a serious lack of true, unbiased randomized control trials with which to evaluate the effectiveness of tonsillectomy as a treatment for recurrent acute tonsillitis, citing significant differences in comparison groups prior to the start of the trials.  Not surprisingly the review calls for additional trials before some consensus can be reached.  The same message was echoed in an evidence-based response published in the Journal of Family Practice in 2002.

Then why are physicians continuing to refer their patients for tonsillectomies at all?  It would seem that their may be some usefulness to the procedure after all--at least in more severe or intractable cases of acute tonsillitis.  Another review article published in Pediatric Clinics of North America urges that more recent data is pointing toward the effectiveness of tonsillectomies in treating "proper patients."  But who are the "proper patients" that should receive tonsillectomies?  Some authors suggest patients with at least 5 episodes of sore throat caused by tonsillitis per year or 3-4 episodes per year for at least three years should be treated with tonsillectomy while others are less certain.

So how should the family physician treat a patient with recurrent episodes of acute tonsillitis/pharyngitis?  Well, aside from the obvious administration of antibiotics and symptomatic treatment as necessary, it seems as though the jury is still out on the subject of surgery and is likely to be for some time.  It would appear that common sense should still prevail and given a case where a patient is suffering from regular chronic, recurrent or severe symptoms, the recommendation should be to send that patient for surgery.  Unfortunately, at this time physicians are unable to rely on good evidence based medicine to help them make a decision.

"Thirty to forty minutes, three to four times a week, something that makes your heart go pitter-patter" and makes you sweat. This is a phrase I've heard in almost every physical and in many other visits over the last few weeks.  Exercise is obviously important, but what are the actual recommendations and the real benefits for patients?

Heart disease is still the leading cause of death in the United States. Major modifiable risk factors for heart disease are smoking, physical inactivity, and overweight. Yet, the U.S. is becoming increasingly more sedentary and two-thirds of the U.S. > 20 years old are overweight or obese.  "Poor diet and physical inactivity lead to 300,000 deaths each year—second only to tobacco use."  These deaths could be significantly reduced through regular physical activity. So then, how much do we need?

The USDA and department of Health and Human Services outline recommendations in "Dietary Guidelines for Americans 2005".  They recommend the following: 1) "To reduce the risk of chronic disease in adulthood: Engage in at least 30 minutes of moderate-intensity physical activity, above usual activity at work or home on most days of the week. 2) To help manage body weight and prevent gradual, unhealthy body weight gain in adulthood: Engage in approximately 60 minutes of moderate- to vigorous-intensity activity on most days of the week while not exceeding caloric intake requirements. 3) To sustain weight loss in adulthood: Participate in at least 60-90 minutes of daily moderate-intensity physical activity while not exceeding caloric intake requirements. Some people may need to consult with a healthcare provider before participating in this level of activity." By understanding the differences in these recommendations we can better tailor our advice and help patients gain realistic expectations with regard to their exercise (i.e. reduce disease risk, maintain weight, or weight loss). It is important to note that benefits from exercise appear to be dose dependent.

The following are some benefits of exercise that may be helpful when encouraging patients to exercise. Exercise:

Reduces the risk of dying prematurely
Reduces the risk of dying from heart disease
Reduces the risk of developing diabetes
Reduces the risk of developing high blood pressure
Helps reduce blood pressure in people who already have high blood pressure
Reduces the risk of developing colon cancer
Reduces feelings of depression and anxiety
Helps control weight
Helps build and maintain healthy bones, muscles, and joints
Helps older adults become stronger and better able to move about without falling
Promotes psychological well-being

Although the USPSTF has determined that there is insufficient data to determine whether or not behavioral counseling to promote physical activity is beneficial in a primary care setting, the risks of physical inactivity seem too great to avoid encouraging patients to exercise when the opportunity presents itself.

We see at least one patient a day in the family practice office regarding toe/nail fungus. Even though the insurance most of the time doesn't cover the cosmetic treatment, my patients are usually presented with the clear decision in mind of receiving treatment. When I give them options these are usually based on my limited knowledge. So I did some research and would like to share with you my findings on this topic.

Treatment of all forms of onychomycosis is the same, i.e. oral vs. topical. Traditional topical therapies are generally ineffective for clearing the primary infection and even oral therapy is associated with a high rate of treatment failure and recurrence. Nevertheless, treatment is often indicated in documented cases because of the morbidity associated with the infection.

Although continuous itraconazole and terbunafine appear to have similar efficacy in short-term studies (up to one year), long-term cure rates may be better with terbinafine. A systematic review found that mycologic cure rates were better with terbinafine than itraconazole, but there was no adequate assessment of clinical cure. A randomized, double-blind trial reported that terbinafine was more effective than itraconazole pulse therapy on measures of long-term clinical outcomes.  Another randomized, double-blind study, for example, treatment with terbinafine (250 mg/day) for 12 weeks was associated with a significantly higher rate of complete clinical cure than treatment with fluconazole (150 mg once weekly) for 24 weeks (67 versus 32 percent, respectively)

All of the azoles can cause hepatotoxicity. Routine monitoring of liver function tests during therapy may not be necessary in patients without underlying liver disease, although many clinicians routinely get pretreatment values and check an additional set midway through treatment for patients taking the medications for longer periods of time.

Patients should be advised that improvement will continue after oral therapy has stopped; it may take months to accurately assess cure. Repeat courses of therapy can be tried if the patient experiences a recurrence.

A topical antifungal nail lacquer, ciclopirox (penlaq), has been approved by the United States Food and Drug Administration for the treatment of mild to moderate onychomycosis without involvement of the lunula. Combined results from two randomized, controlled trials suggest that complete resolution occurs in approximately 7 percent of treated patients compared with 0.4 percent using placebo. Thus, only 1 of 15 patients who use the lacquer will have a favorable outcome, and recurrence is common after stopping therapy. The lacquer is applied once daily to the affected nail, 5 mm of surrounding skin, and to the nail bed, hyponychium, and undersurface of the nail plate if possible. The nail is wiped clean with alcohol once weekly, and the unattached infected part of the nail is removed periodically. A pharmacoeconomic analysis demonstrates that despite its limited efficacy, ciclopirox is safe and relatively inexpensive (approximately $300 for 48 weeks of therapy)

While interviewing a pt who was suffering from gas pains, I was asked about the efficacy of beano.  After having no clue as to what beano was or how it worked, and only being able to recall the "be-no-gas" advertisement, I decided to learn more about beano.

When undigested carbohydrates enter the colon, bacterial fermentation of these carbohydrates produces intestinal gas, which can lead to abdominal pain and flatulence.  Beano is an over-the-counter oral solution of alpha-galactosidase, which is used to prevent flatus and other gastrointestinal symptoms resulting from a high-fiber (=high carb) diet.  In theory, beano is supposed to enhance the breakdown of carbohydrates before they reach the lower intestine.  More broken down carbs = less carbs for intestinal bacterial to ferment = less gas.  But does it work?

Believe it or not, there was actually a small study where 19 subjects were fed chili and monitored for 6 hours.  Two groups were made; one received beano and another received placebo.  One week later, the group treatments were switched and the groups were re-fed.  The study reported that the number of flatulence events per hour was significantly less in a group treated with alpha-galactosidase than a placebo group over the 6-hour follow-up period.  Who knew?

 

Another study evaluated beano and its effect on acarbose treatment (an alpha-glucosidase inhibitor used in the treatment of type 2 diabetes mellitus).  This study found that patients who took Beano with acarbose had  significantly less flatulence than did those who took acarbose alone (0.79 vs 1.09).  Breath hydrogen concentration was lower after administration of acarbose plus Beano than with acarbose alone (31.2 ppm vs 50.5 ppm). However, Beano had variable effects on the ability of acarbose to reduce the postprandial serum glucose concentration.  It was observed that postprandial serum glucose levels were higher in patients who received acarbose plus Beano than in those who received acarbose alone.  However, both treatments (with or without Beano) resulted in postprandial serum glucose levels that were significantly lower than those seen with placebo. The study concluded that while Beano appeared to decrease the activity of acarbose, postprandial serum glucose concentrations were still decreased significantly while the flatulence associated with acarbose treatment was alleviated.  

     We recently saw a young female patient who had been recently been diagnosed with human papillomavirus (HPV) virus and who had come in for her regular PAP smear.  She was quite anxious and upset with her new diagnosis and she mentioned to us that her boyfriend had been tested for STDs and came back negative but then ended up giving her this disease that could cause her to have cervical cancer in the future.  And to top it all off, he never had any symptoms.  We really didn't have much to say to reassure her for now, except to tell her to get her regular PAP smears. 

     However, I found an article that talks about vaccination against HPV.  One vaccine that seems promising targets HPV types 16 and 18, which cause approximately 70% of cervical cancers in the world.   This study was a randomized, double-blind trial to test the safety, efficacy, and immunogenicity of a bivalent HPV 16/18 vaccine containing an L1 virus-like particle.  This vaccine was being tested for its ability to prevent incident and persistent infection with the 2 virus types, cervical cytological abnormalities, and precancerous lesions.  Women ages 15-25 were randomized and given doses of the vaccine or placebo in North America and Brazil and were examined for evidence of infection by cytology and cervicovaginal samples for up to 27 months.  The results were that the vaccine efficacy was 91.6% against incident infection and 100% against persistent infection.  The vaccine was also proven to be safe, immunogenic and well tolerated by most subjects.  The use of this vaccine against HPV could substantially reduce the incidence of cervical cancer.

     Phase III trials are currently underway to confirm these findings.  It seems that if all goes well, this vaccine could be on the market in 2 or 3 years.  More information is available at the NCI's cancer information service (CIS) website and more information on clinical trials is available at cancer.gov on the internet.

Vytorin combines two lipid lowering drugs, Ezetimibe and Simvastatin.  It works through complementary mechanisms to block the sources of cholesterol and improve lipid profiles.  Ezetimibe or better known as Zetia prevents the intestinal absorption of dietary cholesterol while Simvastatin inhibits the biosynthesis of cholesterol in the liver.  In effect, the combo reduces cholesterol derived from both endogenous and exogenous sources.  Although Vytorin is a newer drug, it's really just a combo of older drugs that have already been out on the market.  Above all, this seems to be "hot" new drug that many of our patients are being switched to from Lipitor or Pravachol.  The patients that have been switched usually presents with no change or even elevation in their LDL cholesterol.  In addition, some patients also complain of significant myalgia from the Lipitor and inquire about newer drugs.  My preceptor seems to heavily favor this drug, not as the first-line treatment for dyslipidemia but as an alternative for patients who cannot tolerate or see any improvement with the traditional statins alone.  So far in the clinic setting, our follow up response rate has been promising, as we have seen drops in LDL and less side effects with Vytorin. 

So in terms of the data, there have been recent studies looking at the efficacy and safety of combination therapy compared with statins alone:

*  One study published in the American Journal of Cardiology randomized 788 patients into 3 groups:  (1) 10 mg of atorvastatin as the initial dose, titrated up to 80 mg; (2) co-administration of 10 mg of ezetimibe and 10 mg of simvastatin, titrated up to 10/80 mg; and (3) co-administration of 10/20 mg of ezetimibe + simvastatin, titrated up to10/80 mg.  Baseline LDL and HDL cholesterol levels were comparable between all the treatment groups.  At the end of treatment period 1, the mean decrease of LDL cholesterol was significantly greater for co-administration of 10/10 mg and 10/20 mg of Vytorin than for 10 mg of atorvastatin, alone. At the end of treatment period 4, co-administration of 10/80 mg of Vytorin was superior to 80 mg of atorvastatin in the percent LDL cholesterol decrease (-59.4% vs 52.5%) and HDL cholesterol increase (12.3% vs 6.5%).  

*  Even more interesting, I found another recent study that looked at the effect of Vytorin on high sensitivity C-reactive protein (hs-CRP) in 1089 study subjects.  They found that Ezetimibe coadministered with simvastatin more than doubled the hs-CRP reduction compared to simvastatin monotherapy.   The significant reduction in hs-CRP seen in the combination suggests a possible anti-inflammatory/anti-atherosclerotic action. 
 
*  They even compared the effects of the combination therapy in both genders and found that it was equally efficacious in women and men in reducing blood levels of LDL-C, apolipoprotein B, and triglycerides and raising HDL-C.  

* In looking at patients with familial hypercholesterolemia, an article from the American Journal of Cardiovascular Drugs conducted a double blind randomized controlled multicenter study.  They looked at the mean percentage change in LDL cholesterol in patients with familial hypercholesterolemia and found that Ezetimibe plus statin-40/80 significantly reduced LDL-C levels compared with statin-80 (-20.7% versus -6.7%).

I have noticed that despite the fact that there have been clinical trials to support the early aggressive use of statins, most physicians are inclined to use lower dose statins.  Many review articles describe how physicians fail to appropriately titrate statins therapy to a therapeutic dose.  Perhaps, the use of a combination drug such as Vytorin may be more acceptable to physicians, (rather than continuously increasing doses of statins) while increasing the likelihood of achieving target lipid levels in their patients. 

A male patient in his mid 50's presented with his 2nd fasting blood glucose of around 115.  According to Harrison's, this is considered prediabetes, also known to the medical world as impaired glucose tolerance synonymous with impaired fasting glucose.  My doctor asked me how to treat prediabetes: "Anything you can do besides recommend the good ol' 3 month try at diet and exercise?"

A study done at George Washington showed that in patients with Impaired Glucose Intolerance, treatment with metformin was associated with 31 percent relative reduction in the progression of diabetes.  3,234 patients were assigned to a lifestyle-modification program with the goals of 7 percent weight loss and at least 150 minutes of physical activity per week; to 850 mg metformin bid; or to placebo.  2.8 yrs followup showed that that lifestyle intervention reduced diabetes incidence 58% and metformin by 31% compared to placebo. 

It is interesting to note that metformin was more effective in decreasing incidences of diabetes in younger patients with a higher BMI and higher fasting plasma glucose levels, and was least effective in patients older than 60 years.

There have been additional studies done with Acarbose in preventing diabetes in patients with IGT.  The STOP-NIDDM Trial has shown that acarbose treatment in subjects with IGT is associated with a significant risk reduction in the development of not only diabetes, but also hypertension and cardiovascular complications.

The AAFP declares that although diet and exercise should be recommended first, they realize that lifestyle interventions can be impractical for many of today's prediabetic patients: "Drug therapy can be considered when aggressive lifestyle interventions are unsuccessful."  

Maybe someone out there knows some good stationary activities patients with severe osteoarthritis, osteoporosis,  or fibromyalgia.  For instance, I had a middle aged obese man with both knee pain and full length shin ulcers.  What kind of exercise is appropriate for him?  Walking hurts his knees and no lifeguard would let him into a pool with those kind of debilitating ulcers.

It would also be helpful if there were statistical methods to categorize patients that are more likely to attempt diet and exercise and those that aren't.  Call me crazy, but it seems that there are a certain minority of patients that may do better by prescribing medication than by convincing them to exercise and diet. 

Take home points: 1.) Studies show that the best way to decrease the incidence of diabetes in the prediabetic patient is by educating them about the importance of diet and exercise 2.)  Prescribing a medication (see links above for Metformin and Acarbose) in the prediabetic patient is better than placebo in preventing diabetes.  3.) There are no studies to my knowledge studying prediabetic patients on lifestyle changes AND diabetic medications.  

This past week I encountered a patient who is a poorly controlled type 2 diabetic.  My preceptor said that he has been seeing the patient for a few years now and continues to struggle with him about taking his medications regularly and modifying his behavior in order to better control his diabetes and prevent negative health outcomes in the future.   the patient said he continued to lack the motivation he needed to make the changes to his lifestyle that his doctor continuely tells him will help improve his health and possibly save his life.

I walked out ot the exam room after the encounter convinced that I had just met one of the most stubborn individuals I have ever dealt with and I conveyed this feeling while presenting to my preceptor.  At this point he drew my attention to the patient's med list where I noticed that the patient was taking Zoloft. My preceptor then commented that depression may be the reason he doesnt have the desire to change and that he may need an increase in his dosage of Zoloft.  This encounter caused me to wonder how often depressed patients are dismissed as simply being nonadherent.

Unfortunately for me, my training during my Psych rotation was not enough for me to have been aware of the possiblity of depression as a cause of the patient's presentation.  Looking back on the encounter now, I dont know how I missed the signs.  However, literature shows that such overlooking of symptoms is common. A page dealing with the topic of "Depression among Patients with diabetes" states that 1 in 5 patients with diabetes type 1 or 2 suffers from major depression and that less than a third of these patients are identified and treated.  As can be expected, the relationship of untreated major depression and diabetes leads to poor management and eventually negative sequela of the disease (i.e. cardiovascular disease).  To help, this page also includes a diagnostic checklist that should be kept in mind when dealing with diabetic patients - though this information may also be applied to patients with other diseases and conditions.

A study published in Diabetes Care observed the relationship between depression and diabetes self-care, medical adherence, and preventive care. The study involved the distribution of a questionnaire to close to 5,000 diabetic patients assessing presence of depression, self-care, and diabetic monitoring.  The results showed that major depression was associated with decreased levels of physical activity, unhealthy diet, and lower adherence to prescribed medications.

In conclusion, a link between depression and various medical conditions - especially chronic medical conditions such as diabetes, HIV, hyper and hypothyroidism -  has already been established therefore all patients who repeatedly fail to adhere to treatment should be evaluated for possible depression rather than being quickly labeled as "nonadhrent" or unwilling to be treated and to help treat themselves.

This week I witnessed a very interesting treatment regimen for the eradication of H. Pylori for a patient suffering from dyspepsia with an H. Pylori-induced ulcer.  This patient had been refractory to treatment with PPI's and H2-blockers for several weeks and finally had an endoscopy/biopsy performed that revealed a positive culture of H. Pylori induced peptic ulcer disease.  I figured that my preceptor would prescribe the traditional 7 day triple therapy regimen consisting of metronidazole, Pepto-bismol, and amoxicillin, with or without a PPI.  Instead, he prescribed a one-day regimen to eliminate H. Pylori and handed both the patient and myself a copy of an article that found that one-day treatment is as effective as a 7-day treatment.   

This one day "cocktail" consists of: flagyl (metronidazole) 500mg, two 262-mg tablets of bismuth subsalicylate, and 2g of Amoxicillin (suspension), all taken 4 times that day.  This is taken along with a one-time dose of 60mg of lansoprazole (prevacid).  This study was a randomized, non-blinded controlled trial done in an outpatient setting, comparing 160 adults with dyspepsia and a positive urea breath test.  The patients were randomized to 1, 3, or 7-day treatments and at the end of the study eradication rates were 95% in the 1-day group, and 90% in the 7 day group.  The level of eradication was determined by the urea breath test.  The major benefit from this 1-day treatment would be lower side effects from using various different antibiotics and the prevention of resistance.  However, since the side effects in this study were tallied at the 5-week follow-up rather that immediately after treatment, the side effect profiles may not be totally accurate.  

In order to establish a record of successful eradication with this 1-day regimen, the urea breath test was utilized.  This test has been found to be very simple, affordable, tolerable, and extremely accurate.  When the "grey zone of 13C-UBT was set at a level of 2.5 to 5.0/1000" after eradication therapy, the sensitivity and specificity of 13C-UBT was 100% and 98.4% compared to the gold standard.  As far as the standard therapy
for H. Pylori eradication, 7-day therapy with a PPI, such as rabeprazole, clarithromycin, and amoxicillin has been found to be similar in efficacy to 10-day therapies and had similar efficacy in patients with and without ulcer disease. In the past, complex multi-drug regimens have not been broadly accepted because of the adverse effects and frequent H. Pylori eradication failures.  With respect to how many of which medicines should be used, it was found that with a PPI is combined with a bismuth-based triple therapy - making it a quadruple therapy, eradication rates are significantly increased as compared with triple therapy alone. 

This 1-day treatment for H. Pylori eradication can prove to be quite beneficial for both patient compliance, and fewer adverse effects.  Of course further evaluation is necessary to determine whether this four-drug, one-day treatment is adequate in all patients with recurrent peptic ulcer disease or even those suffering from malignancies from H. Pylori such as MALT-lymphomas. 

In my brief 4 weeks at the clinic, I have met numerous patients who either practice or are interested in alternative/complementary medicine.  Unfortunately, we do not receive much education in this realm of medicine, and in some ways it is even considered taboo.

One form of complementary medicine I recently learned about was the use of D-mannose as a natural treatment for UTI.  UTI is a very common problem seen in the FP setting.  Once diagnosed, we treat this extremely uncomfortable and potentially dangerous condition with our prescription pad, Trimethoprim-sulfamethoxazole/Bactrim DS one tab PO bid x 7-10 days or Nitrofurantoin/Macrobid 100 mg PO bid x 7days.  Although this often relieves the patient's symptoms and cures them of their UTI, antibiotics are not a benign treatment and can lead to numerous side-effects, including diarrhea or consipation caused when the normal GI flora is disrupted, susceptibility to other yeast (particularly Candida albicans causing yeast infection), molds, and bacteria leading to the need for more medication, and allergic reactions in some individuals.  For young sexually active women on oral contraceptives, some antibiotics which increase liver metabolism, may make their birth control less effective.  Finally, last but not least, the overuse of antibiotics has promoted antibiotic resistance.  

D-mannose, a simple sugar and stereoisomer of glucose, is completely benign and has been shown to effectively treat UTI caused by E. coli, which is 90% of cases, within 1 to 2 days without killing a single bacterium and without any of the side-effects found with antibiotics.  As med students, it is only natural for us to want to know why this works?  What is the mechanism of action?  In UTI, E. coli attaches to cells lining the bladder and urinary tract using hair-like projections called fimbria, and at the tip of each fimbrium, there is a glycoprotein that binds to the first molecule of mannose it encounters.  Mannose is produced inside the cells lining the urinary tract and bladder and act like receptors to the fimbria allowing them to bind tightly and cause UTI.  When we consume D-mannose, it is absorbed 8x slower than glucose and is not converted to glycogen or stored in the liver, but instead goes directly to the blood stream from the upper GI tract and is mostly filtered through the kidneys and routed to the bladder.  D-mannose is a naturally occurring sugar similar in structure to but metabolized differently than glucose. Because the body metabolizes only small amounts of D-mannose and excretes the rest in the urine, it does not interfere with blood-sugar regulation and is safe for use in diabetics.  D-mannose molecules bind the fimbria and fill up all of the bacterial anchoring sites, so the bacteria can no longer attach to the bladder wall and are flushed away. Unlike antibiotics, D-mannose does not kill any bacteria simply helps to displace them.  In over 90% of UTI, 1 teaspoon of D-mannose every 2 to 3 hours usually clears the infection in 1 to 3 days.  However, if a UTI treated with D-mannose does not show significant improvement within 24 hours, which is about 10% of cases, it is likely that the causative organism is not E. coli, and treatment with conventional antibiotic may be necessary.

There have been numerous studies that are consistent with and support the clinical treatment of UTI with D-mannose.  In this article, the effect of D-mannose on adherence of 73 E. coli strains to vaginal and buccal epithelial cells from women with recurrent UTI was tested. Urinary, vaginal or anal isolates from women with such infections were used.  Of the strains 66 (90%) demonstrated adherence to epithelial cells.  D-mannose inhibited completely the adherence of 25 strains (42%) that adhered to vaginal cells and inhibited an additional 11 strains (18%) by at least 50%.  Similar results were obtained with buccal cells. The inhibitory effect of D-mannose was similar regardless of the origin of the strains.  The results suggest that mannose-sensitive as well as mannose-resistant adhesins frequently mediate E. coli adherence to vaginal epithelial cells, and may contribute to vaginal colonization and cystitis, hence the effectiveness of D-mannose in treating UTI.

As future physicians in a society that looks everything up on the internet and want alternatives to our "Western medicine," I think it is important to educate ourselves on the things our patients are using as an alternative or in conjunction with the care we offer.  There is a plethora of information available, and I know for me, it was difficult to know where to start this self-learning process.  One book that came highly recommended was Complementary and Alternative Medicine Secrets edited by Wendy Kohatsu.  As in most things in life, we need a good starting point, that will not overwhelm us with the vastness of information and at the same time, keep our interest in the subject at hand. 

As we all remember from lectures in first and second year, there is no patient benefit in suppressing cough in an acute upper respiratory tract infection.  As we know, cough is a very effective means of clearing the lungs of irritants like excess mucus.  However, there may be a benefit for patients who need to be relieved of symptoms to return to school or work or who are being deprived of sleep secondary to their cough.  I'm sure we all want to make them feel better, so we think that we can prescribe some medication or recommend an OTC remedy to reduce their cough and help them feel better.  In my practice, lots of docs all like to give different drugs for symptomatic relief, so I decided to find out what the evidence says is the best.

Most attendings and residents here have told me that codeine is the gold standard of cough suppressants but they don't like to put patients on it because of side effects (constipation, altered mentation, dependence, tolerance, etc.)  I thought this would be a good drug to examine first, so I dug up an RCT on PubMed.  This study was randomized and double-blinded between 50 mg codeine and placebo for patients with acute URI and cough, studied twice, 2-5 days apart.  Objective (sound and sound-pressure recorders) as well as subjective (patient severity scales) measures were taken before and 90 min after drug delivery on both study sessions.  The result was that both placebo and codeine significantly reduced cough but there was no difference between the groups.  In other words, all of the benefit of narcotic therapy was placebo effect, so codeine is not much use in the acute setting (but effective in the chronic cough setting, but that is another blog).

I was surprised to find this about codeine, allegedly the biggest gun in our medical arsenal, so I grew curious about OTC remedies.  Well it just so happens that I am not the first person to be curious about this topic and I found a Cochrane Database review article on PubMed that analyzed multiple studies comparing different drugs in patients with acute URI and cough: 

1. Dextromethorphan is an OTC antitussive (and a new trendy young person's legal drug of choice) that was better than placebo in two studies but no different in a third.

2. Guaifenesin is an OTC expectorant that was subjectively effective vs. placebo in one study but not in another.

3. Antihistamines were found to be no more effective than placebo in 3 of 3 studies examined.

4. Antihistamine-decongestant combinations vs. placebo had mixed results: one study found a benefit while a second did not.

5. In the peds population, one study examined two pediatric cough syrup brands vs. placebo and found that a "satisfactory response" was achieved in 46% and 56% of treatment patients vs. 21% of controls.  (Unfortunately, those brand names were not provided by the review authors nor were the p-values.  Dr. Mayer would be so ashamed.) 

The overall conclusion of the meta-analysis is that there is no good evidence for or against treatment of acute cough with OTC remedies.

My own conclusion after reading these studies is that placebo is better than nothing.  The one consistent finding in all studies illustrated above (and especially the codeine trial) is that controls significantly improved after placebo.  I certainly would recommend against treating acute cough with codeine (a narcotic with potentially significant side effects and abuse potential), but the jury is still out on OTC remedies.  Even if these remedies don't have any benefit over placebo, recommending one that is relatively innocuous (like an antihistamine such as diphenhydramine) may be of little risk and potential benefit to your patients if they believe you when you tell them it will work.  I found no direct evidence to support this supposition but it seems logical. 

P.S. If someone finds better evidence on this subject, please add a comment or post a blogof your own, as I'd really like to hear about it.  Colds suck.

A postmenopausal female patient presented for an annual physical exam. She has a dual diagnosis of hypertension well-controlled by a hydrochlorothiazide and hyperlipidemia with excellent control by Lipitor. Besides these two medications she takes a multivitamin daily and an 81 mg Aspirin on a daily basis. In response to the inquiry of whether she has any questions, concerns or complains today she wonders if what she has heard on TV about Aspirin is actually true. The news claimed that unlike men, aspirin does not protect women from MI, but only from stroke.

 

Daily low-dose aspirin lowers women's risk of stroke but does not prevent heart attacks, according to a new study released this month. Those findings are the opposite of what is known about aspirin's effects on men.

 

Recently announced results of the large, primary-prevention randomized trial among women looks at the effect of aspirin at lowering the risk of death from cardiovascular cause, such as stroke and myocardial infarction. The Women's Health Sudy randomly assigned 39,876 initially healthy women 45 years of age or older to receive 100 mg of aspirin on alternate days or placebo and then monitored them for 10 years for a first major cardiovascular event (i.e., nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes).

 

Researchers reported a 17% reduction in stroke risk and a 24% reduction in ischemic stroke risk in the aspirin group compared with those on placebo group.

 

As compared with placebo, aspirin had no significant effect on the risk of fatal or nonfatal myocardial infarction or death from cardiovascular causes. Subgroup analyses, however, showed that aspirin significantly reduced the risk of major cardiovascular events, ischemic stroke, and myocardial infarction among women 65 years of age or older.

 

By contrast, in studies involving men, aspirin has caused a significant reduction in the risk of myocardial infarction but no significant reduction in strokes, the researchers reported. Researchers do not know why aspirin affects men and women differently, the article said, but experts say it may be related to the size of blood vessels leading to the brain, which are smaller than those leading to the heart.

 

The results, they said, highlight the importance of studying women as well as men in clinical trials, and the need for physicians to consider individual risk profiles when deciding whether to recommend aspirin.

 

 

A postmenopausal female patient presented to the family practice office for an annual physical exam. She has a dual diagnosis of hypertension well-controlled by a hydrochlorothiazide and hyperlipidemia with excellent control by Lipitor. Besides these two medications she takes a multivitamin daily and an 81 mg Aspirin on a daily basis. In response to the inquiry of whether she has any questions, concerns or complains today she wonders if what she has heard on TV about Aspirin is actually true. The news claimed that unlike men, aspirin does not protect women from MI, but only from stroke.

 

 

Daily low-dose aspirin lowers women's risk of stroke but does not prevent heart attacks, according to a new study released this month. Those findings are the opposite of what is known about aspirin's effects on men.

 

 

Recently announced results of the large, primary-prevention randomized trial among women looks at the effect of aspirin at lowering the risk of death from cardiovascular cause, such as stroke and myocardial infarction. The Women's Health Sudy randomly assigned 39,876 initially healthy women 45 years of age or older to receive 100 mg of aspirin on alternate days or placebo and then monitored them for 10 years for a first major cardiovascular event (i.e., nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes).

 

 

Researchers reported a 17% reduction in stroke risk and a 24% reduction in ischemic stroke risk in the aspirin group compared with those on placebo group.

 

 

As compared with placebo, aspirin had no significant effect on the risk of fatal or nonfatal myocardial infarction or death from cardiovascular causes. Subgroup analyses, however, showed that aspirin significantly reduced the risk of major cardiovascular events, ischemic stroke, and myocardial infarction among women 65 years of age or older.

 

 By contrast, in studies involving men, aspirin has caused a significant reduction in the risk of myocardial infarction but no significant reduction in strokes, the researchers reported. Researchers do not know why aspirin affects men and women differently, the article said, but experts say it may be related to the size of blood vessels leading to the brain, which are smaller than those leading to the heart.

 

The results, they said, highlight the importance of studying women as well as men in clinical trials, and the need for physicians to consider individual risk profiles when deciding whether to recommend aspirin.

 

 

 

I see many patients with symptoms of a URI, but it is unclear whether they have a viral or a bacterial condition, and what should be done for them.  Most of my patients would prefer to leave the appointment with some antibiotics, but since viral URIs are most common, they leave without any antibiotics.  I wanted to make sure I was correctly diagnosing and treating these patients, so I went to the computer for a treatment algorithm. 

According to a very thorough review article I found on PubMed, the Gold standard is either needle aspiration of the sinuses, or surgical collection of sputum.  Clearly we cannot perform either of these procedures regularly on patients who very likely have a "cold," as they are invasive and expensive.  So we use the clinical signs/symptoms to distinguish between of bacterial sinusitis and viral rhino-sinusitis.  Those signs/Sx that support bacterial etiology include fever, maxillary tooth ache, purulent nasal secretions, lack of response to decongestants, discolored nasal discharge, and abnormalities in sinus transillumination.  If three of these are present the positive likelihood ratio for bacterial etiology is 2.6, and if four are present the positive likelihood ratio is 6.4.  Another sign suggestive of bacterial origin is a worsening of symptoms after initial improvement.  Any symptoms that persist longer than 10 days should also arouse suspicion of bacterial origin. 

So now what do we do to help the patient. In the case where we suspect their condition is viral in origin, the paper suggests the following; avoid cigarette smoke, drink adequate fluids, inhale steam to loosed mucus, apply warm packs to face 5-10 minutes/day, use saline spray, and take acetaminophen or ibuprofen for pain, and rest plenty.  If the clinical assessment more supports a bacterial origin then we should recommend Amoxicillin 1.5-3.5 g/day BID for 7-10 days, and consider Augmentin if no improvement is seen within 48-72 hours.  Erythromycin, azithromycin, clarthromycin, and trimethoprim-sufa are agents to be used in patients with penicillin allergy.

   During a recent well child visit the mother approached me with a concern over the safety of her child's upcoming vaccinations.  She had heard in the news that vaccinations could "give her child autism."  While I appreciate the mother's concern over foreign drugs/vaccines that are placed in her baby's body, I explained the importance of adhering to the vaccine schedule to protect the child.  I did, however, want to check the literature to see if any validity existed for the mother's concern of vaccine-induced autism.

   The Institute of Medicine has issued a statement that there is epidemiological evidence to reject "a causal relationship between the MMR vaccine...thimerosal-containing vaccines and autism."  This statement is, in part, based on studies (Study 1, Study 2) that point to a lack of evidence showing a relationship between vaccination and autism.

   However, one recent study did conclude that there was evidence showing an increased number of neurodevelopmental disorders in children that received vaccines with Thimerosal in them. Thimerosal is a mercury-containing compound used as a preservative in some vaccines.  According to the FDA thimerosal has been removed from most of the vaccines on the market, with the exception of the inactivated influenza vaccine. A version with only trace thimerosal content is available for infants, children, and pregnant women.  The FDA has a table of vaccinations and thimerosal content to evaluate which vaccinations might be inappropriate to use.

   Another study evaluated whole-cell vs. acellular pertussis vaccines and neurological disorders.  They determined that there is an association between whole-cell pertussis vaccine (with over 3,000 proteins, endotoxin, pertussis toxin, & adenylate cyclase) and serious neurological disorders.  The 2-5 protein acellular pertussis vaccine, DTaP, has been developed and is in common use now without known neurological complications.

   In conclusion, while there is some evidence to support a link between vaccinations and neurodevelopmental disorders, routine vaccination is necessary to eliminate great health threats to developing children.  Ideally, vaccinating everyone creates "herd immunity" whereby the disease is virtually eradicated due to an entire population being immunized.  It is important to note that the studies finding a link (those listed above) dealt with vaccines that either included mercury-based preservatives or were complete cellular-type vaccines.  In my family practice office all childhood vaccines were free of thimerosal or were acellular (DTaP) (table of vaccinations).  The next time a parent comes in with a similar concern I can explain that 1. Vaccines are essential in preventing diseases in your child and the pediatric population, and 2.  The vaccines used in this office do not have ingredients that were shown to cause autism.  More studies are in the works to try and solve this issue, but the fact remains that much good has come about from routine vaccinations and they should be utilized until data proves that the consequences outweigh the enormous benefits.

Often in medicine pharmacology is chosen because of its secondary benefits.  For example, ACE-Is promote cardiovascular health through their anti-angiotensin effects, but they also affect glomerular flow rates, which is thought to mediate the effects of renal disease seen in diabetes.  Thus, when chosing between an ACE-I and a diuretic for diabetic patient, the ACE-I has an advantage over a drug like Lasix thanks to its additional spectrum of activity.

Recently the VA-HIT study was completed.  This study incorporated a head to head trial of two insulin sensitizers, Actos (pioglitazone) and Avandia (rosiglitazone) which in previous trials have both been shown to have similar efficacy with regards to uncreasing insulin sensitivity in peripheral tissue.  The VA-HIT study focused on the effects of these drugs on altering lipid profiles.

http://www.lipidsonline.org/slides/slide01.cfm?q=va-hit&pg=2

It was shown that Actos raises total HDL and decreases particle size of LDL compared to Avandia which did not significantly alter lipid levels when compared to placebo.  This is further discussed (caution!) on the Acots site:

http://www.lipidhealth.org/content/newsletter/vol4no5/pg2.asp

Recent compelling data regarding silent ischemia and increased CAD risk in diabetes heightens the need for lipid control in diabetics.  DM is a disease that promotes a chronic proinflammatory state, which is recognized to be a risk factor for endovascular damage and initiation of arterial plaque formation.  In patients with DM in such a state, proper lipid control seems vital to the health of major arteries, especially the coronaries.

While the data from VA-HIT seems to favor Actos over Avandia (diabetic indications being equal), the jury remains out about end point cardiovascular M&M (morbidity and mortality, not the rapper).  Certainly different anti-hypertensive classes can achieve the same efficacy in getting patients to goal for BP, but there are differences in cardiovascular protection with beta-blockers vs diuretics.  It remains to be seen whether or not Actos actually reduces negative cardiac events better, despite its significant data showing its secondary benefit reducing lipids. 

I would not preferentially choose either TZD at this time.  However, in September data from currently ongoing trials will be published showing M&M, and Actos may be shown to have a clear benefit over other members of its class.  It will be a tense summer for Takeda Pharmacueticals.

Pt with Lyme disease came in asking about Hyperbaric Oxygen Therapy(HBOT) as a potential treatment. Did a literature search and could not find any good evidence of its efficacy, but did find this one article supporting its use. 

This peaked my interest as to what conditions is HBOT useful for and what are the risks involved? An article in New England Journal of Medicine discussed some of the uses.

Clinical Uses of HBOT:

Carbon Monoxide: Use is controversial

Decompression sickness: Primary treatment

Air embolism: Primary Treatment

Radiation Induced Tissue Damage: Use is controversial

Acute Traumatic Ischemic Therapy: Recommended as adjunctive therapy for crush injuries, compartment syndromes and vascular compromise.

Other potential uses requiring more research:  infection, nonhealing ulcer, skin grafts.

As with any controversial form of treatment, its always important to balance the potential benefit with the complications associated with this therapy.

Complications of HBOT: Most of the side effects are mild and reversible and directly related to oxygen toxicity.

Eyes: Reversible myopia: most common side effect

Ears: Otic barotauma (middle ear effusions and tympanic membrane rupture)

Lungs: pulmonary barotraumas

CNS: seizures

So now you're armed with some basic facts of this type of therapy if a patient happens to bring it up.

A young female patient came into the office presenting with abdominal pain, diarrhea, bloating, gas, and nausea over the last several months.   It sounded like Irritable bowel syndrome (IBS).  IBS affects everyone, but younger patients and women are most likely to have it, and it affects women over men 2:1.  The prevalence of IBS in the United States is between 10-15%.  IBS is an important disease to diagnose because IBS costs billions of dollars for the health care system and is a common cause of work absences. 

The diagnosis of IBS is made by having symptoms consistent with IBS and by ruling out other causes.  People with IBS can have varied symptoms, but the symptoms of chronic abdominal pain and changes in bowel habits are the most common findings.  In the 1970s, Manning et al., developed criteria to try to standardize diagnosis of IBS, called the Manning criteria.  These criteria include 1) relief of pain after defecation; 2)looser and increased frequency of stools with pain onset; 3)sense of incomplete emptying; 4)passage of mucus; and 5)abdominal distention.  These criteria are most helpful in diagnosing women and the non-elderly.  The likelihood of IBS is proportional to the number of Manning criteria and the presence of 2 or less of these criteria is strong evidence to rule out IBS.  Our patient had 4 of these criteria, so a diagnosis of IBS was likely.

So what then is the recommended treatment?  My preceptor first recommended getting a allergy blood test for IgG antibodies to see if she was allergic to certain foods and if this could be either causing or worsening her symptoms.  I wondered what the evidence was for food elimination diets based on IgG antibodies?  I found an article discussing this topic.  A total of 150 outpatients with IBS were divided into 2 groups, one receiving a diet free of all of the foods to which they had IgG antibodies, and the other group excluding the same number of foods but not the ones that they had antibodies against. 

After a period of 3 months, the real diet showed a ten percent greater reduction in symptoms (mean difference 39 (95% confidence intervals (CI) 5-72); p = 0.024).  This result increased to 26% in fully compliant patients (difference 98 (95% CI 52-144); p<0.001).  Decreasing compliance of the diet lead to deterioration in symptoms. 

Therefore, food elimination diets determined by IgG antibodies can be effective in controlling IBS symptoms and further studies need to be done in this area.   

A young female patient came into the office presenting with abdominal pain, diarrhea, bloating, gas, and nausea over the last several months.   It sounded like Irritable bowel syndrome (IBS).  IBS affects everyone, but younger patients and women are most likely to have it, and it affects women over men 2:1.  The prevalence of IBS in the United States is between 10-15%.  IBS is an important disease to diagnose because IBS costs billions of dollars for the health care system and is a common cause of work absences. 

The diagnosis of IBS is made by having symptoms consistent with IBS and by ruling out other causes.  People with IBS can have varied symptoms, but the symptoms of chronic abdominal pain and changes in bowel habits are the most common findings.  In the 1970s, Manning et al., developed criteria to try to standardize diagnosis of IBS, called the Manning criteria.  These criteria include 1) relief of pain after defecation; 2)looser and increased frequency of stools with pain onset; 3)sense of incomplete emptying; 4)passage of mucus; and 5)abdominal distention.  These criteria are most helpful in diagnosing women and the non-elderly.  The likelihood of IBS is proportional to the number of Manning criteria and the presence of 2 or less of these criteria is strong evidence to rule out IBS.  Our patient had 4 of these criteria, so a diagnosis of IBS was likely.

So what then is the recommended treatment?  My preceptor first recommended getting a allergy blood test for IgG antibodies to see if she was allergic to certain foods and if this could be either causing or worsening her symptoms.  I wondered what the evidence was for food elimination diets based on IgG antibodies?  I found an article discussing this topic.  A total of 150 outpatients with IBS were divided into 2 groups, one receiving a diet free of all of the foods to which they had IgG antibodies, and the other group excluding the same number of foods but not the ones that they had antibodies against. 

After a period of 3 months, the real diet showed a ten percent greater reduction in symptoms (mean difference 39 (95% confidence intervals (CI) 5-72); p = 0.024).  This result increased to 26% in fully compliant patients (difference 98 (95% CI 52-144); p<0.001).  Decreasing compliance of the diet lead to deterioration in symptoms. 

Therefore, food elimination diets determined by IgG antibodies can be effective in controlling IBS symptoms and further studies need to be done in this area.   

Last week, when I asked one of my patient's what brought her into the office, she responded that she had Alzheimer's Disease.  I quickly flipped through her chart as I saw no diagnosis or medications for Alzheimer's.  So, I asked her who diagnosed her.  To my shock she told me she obtained a kit on-line and had had diagnosed herself at home!!! And so I did some research on this matter...

On google, I quickly found the Early Alert Alzheimer's Home Screening Test which can be purchased for $19.95.  It uses a scatch and sniff like procedure to detect olfactory deficits which is an early predictor of AD.

Okay, so you can easily buy the kits on the web, but do Do-It-Youself Dementia Testing Work?  They examined the Early Alert Alzheimer's Home Screening Test (AHST) which is also available to the public and uses smell identification.  It was found that the validity and the practical utlity of routine screening for people with asymptomatic cognitive deficits hasn't yet been established.  There are also too many other factors not taken into consideration with a home test including age, demographics, and other medical conditions.  Also, the public does not always understand the difference between a screening test and a diagnositic test which causes many frantic visits to the FP doctor the next day (like I witnessed).

Are olfactory deficits really indicitive of AD?  In The Journal of Neruopsychiatry they studied the Pocket Smell Test (PST) in patients with AD, vascular dementia, and major depression in conjunction with the MMSE.  The study concluded that AD patients scored significantly lower than the other two groups on the PST, even after they controlled for MMSE scores with an accuracy of 95%.  Assessment of olfactory can be a diagnostic tool in diagnosis AD vs. major depression in the eldery.

In an interesting study of odor identification tests, significant deficits in olfactory identification were found in early stages of cognitive impairment.  These deficits in olfactory identification increased as AD progressed.  However, odor detection deficits were not apparent until advanced AD.  Thus, they concluded that the hyposmia in AD may not "begin in the nose" as previously thought.  As a result, refinement of the olfactory testing is necessary before it can be a diagnositic tool to evaluate early dementia.

In the follow-up to that study, they studied 90 outpatients with mild cognitive impairment at 6-month intervals.  It was concluded that in patients with mild cognitive impairment, olfactory identification deficits may have value as an early diagnostic marker for AD, especially when the patient has a lack of awareness for these olfactory deficits. 

So maybe the at home tests may have a future?!?!?!

I am sure colon cancer screening has been a huge part of all of our experiences in FP. Colon cancer is the number two cancer killer in the US and is considered a largely preventable cancer. Last week as we talked to more and more patients about screening, I wondered what else we could tell them about prevention.

Overall it appeared that the colon cancer prevention conversation would be a repeat of most other prevention conversations as it is believed that lifestyle, nutrition, and exercise are related to the development of colon cancer. A paper published in 2005 provided a review of current thinking of the relationship between colon cancer and lifestyle. It stated that physical inactivity and excess body weight are associated with increased risk of developing colon cancer. Increased risk is also seen in diets high in alcohol and low in micronutrients, especially folate and methionine. Folate has been shown to be protective although this relationship is still controversial. This review as well as another recently published paper, demonstrated an association between high dietary intake of red and processed meats and the development of colorectal cancer.

Another important dietary factor seen to decrease the development of colon cancer is calcium supplementation. A study published in 2004 examined the association of calcium intake and the development of colorectal tumors. The study compared the calcium intake of participants found to have adenoma of the distal colon with that of participants with a negative colon cancer screening by sigmoidoscopy. After adjustment for known risk factors, a 12% decrease in adenoma risk was found in patients with the highest calcium intake (>1767 mg/d) than for participants with the lowest calcium intake (<731 mg/d). There was a 27% decrease in adenoma risk for participants taking >1200 mg/d than for patients taking no calcium supplement. A paper recently published demonstrated a mechanism for the observed benefit showing that calcium and vitamin D influence the level of apoptosis in the colon. It is believed that decreased levels of apoptosis are associated with the development of colon cancer.

Overall colon cancer prevention is similar to the prevention of many other current health issues. It should be specifically addressed though as colon cancer is a huge killer in the US.

I had a patient come to the office for a routine physical and during the ROS he said yes to vertiginous symtpoms.  I felt very uncomfortable with this because it is not something I had ever had any experience with.  I didn't know much about causes or treatment.  Upon further questioning, I learned that he did some specific movements periodically throughout the day and that they seemed to help his vertigo.  He said he and a friend found them on the web on an ENT site so they tried it and it worked very well.  I had never heard of this so I too looked on the web for articles about these maneuvers.  I found an article that said that these maneuevers were effective when compared to placebo movements.  Although only 22 people were in this study, the Epley maneuver showed significant improvement in symptoms.  Patients rated symptoms 1-10 based on severity before and after maneuvers.  The Epley group reported an improvement of 6 compared to only 1 degree in placebo. 

In the Epley maneuver, the patient sits upright in bed, then falls to one side, then returns to the start, and falls to the other side and repeats several times.  The theory behind this is that benign positional vertigo is caused by debris in the semicircular canals that irritate the hair cells to cause a sensation of movement.  This irritation is what causes the dizziness symtpoms.  The movements, in theory, act to remove the debris from the hair cells, thus alleviating the symptoms.  This study shows hope for patients who have tried and failed the commonly prescribed medications for vertigo such as meclizine, dimenhydrinate, antiemetics and benzos.  These drugs may alleviate symptoms but can cause drowsiness as a side effect.  There are no known side effects to the Epley maneuvers.  Once the extenive malignant differential has been examined such as malignancy, Menierre's Disease, acoustic neuroma, MS, labyrinthitis, and others, benign positional vertigo can be diagnosed.  Given the disabling ability of vertigo and resistance to meds in some patients, this looks to be an effective alternative.  Patients will be happy if they have other options for treatment.

Does the use of even low dose prednisone increase the risk of osteoporosis in otherwise healthy post-menopausal women? 

Glucocorticoids are used in the office for a variety of reasons, which include treating inflammatory and allergic reactions.  In fact, it is routine to switch patients to a long acting steroid for better control of their asthma in the office setting.  In addition, I've seen many patients with rheumatoid arthritis frequently requesting a course of steroids for treating their flare-ups.  Although low doses are safer than higher does, there is still some question as to whether there really is any safe dose in administering a steroid.  In light of this inquiry, a recent study was conducted in 50 healthy postmenopausal women.  This was a double-blinded randomized placebo-controlled 8-week trial where patients were randomly assigned to receive prednisone 5 mg daily or a placebo for 6 weeks, followed by a 2-week recovery phase.  A 5 mg dose was chosen since it is a dose frequently used to treat inflammatory and systemic diseases.  The goal of the study was to determine whether a low daily dose of prednisone affects serum and urine indices of osteoblast and osteoclast activity.  The investigators measured bone formation and resorption activity at weeks 0, 2, 4, 6, and 8.  The results from the study indicate that low dose prednisone significantly decreased serum osteoblast markers (propeptide of type I C-terminal procollagen, osteocalcin) and urine osteoclast markers (deoxypyridinoline).  However, these changes were reversible during the 2-week recovery period.  Therefore, even low-dose prednisone significantly decreases indices and suppresses bone formation in postmenopausal women.   

Bottom Line:  It is well know that high doses of chronic glucocorticoids are known to have adverse effects on bone.  Doses greater than 7.5 mg can cause premature or exaggerated osteoporosis.  However, it is unclear if chronic prednisone doses of 5 mg daily have the same effects on bone.  This study indicates that even 5 mg could reduce bone strength by suppressing bone formation and repair of microcracks that are caused by repetitive mechanical loading.  Therefore even low does prednisone can increase the risk of osteoporosis.  The authors contend that current recommendations for osteoporosis prophylaxis in patients taking low-dose steroids may need to be re-evaluated.  Patients who take a daily dose of 5 mg may require an antiresorptive agent when starting prednisone, although more studies encompassing specific populations (patients with asthma, rheumatoid arthritis, men, and systemic diseases such as lupus) should be carried out in a randomized controlled method to replicate the results of this data. 

When patients come into the clinic with an acute asthma exacerbation, they are usually given a nebulizer treatment.  This practice seems to occur everywhere, but there does not appear to be evidence that this is the most effective and affordable way to treat an asthma attack.  I have heard that nebulizers are not really superior to inhalers for delivery of meds, and found evidence to support this claim.

One study published in England looked at 78 children over the age of 3 admitted to a pediatric ward for an asthma attack.  They were randomly assigned to a B agonist with a spacer (100ug up to 1 hourly) and nebulized B agonist (5 mg up to one treatment hourly).  The group with the MDI was given standardized education on how to use the advice.  There was no significant difference in how long the 2 groups were in the hospital.  However, the group who used the MDI with spacer in the hospital had significantly fewer admissions over the next 12 months.  The MDI/ spacer combination is also cheaper than the nebulizer treatment.  Although this was a small study and not double- blind, I was impressed that the 2 groups did just as well with the acute attack.  I also think that the group that had MDI did better in the long term because they were given formal education and were observed using the device which probably improved their use at home.

Another study was done on adults in an emergency room for asthma.  This study also compared patients given albuterol by nebulizer to those given albuterol by MDI with spacer.  The group given MDI had less time spent in the ED, fewer side effects such as tremor, anxiety and arrhythmias and less relapse at 14 and 21 days.  On PFT's, the MDI group had a greater peak expiratory flow rate and a greater degree of increase in the PEFR after treatment.  This study is also not perfect, as the patients are not double blinded. 

So although I am now convinced that we should be using MDI/ spacer more for treatment of acute asthma in the office and hospital setting, I am not sure why this is not the case.  Perhaps it is because of habit.  I came across several articles about how spacers have really increased the effectiveness of MDI's, so maybe once this catches on this combination will replace nebulizers.

Another interesting fact I came across was that in a study done among interns at Beth Israel Medical Center in NYC, only 5% of them could use a MDI with spacer perfectly.  Luckily this number improved significantly after one- on one training.  This was surprising to me, and I think we could reduce the number of asthma attacks just by making sure we know how to use the thing right and are able to teach proper technique. 

Over the past two weeks our clinic has seen two adult patients  with general complaints of the possible onset of diabetes mellitus.  More specifically, the patients complained of polyuria, nocturia, and polydypsia.  You may ask, "so what's the big deal?"  The big deal is that neither of these patients fit the typical profile of a type 2 diabetic:  both were tall and thin  had very active lifestyles and ate low-carb diets.  Furthermore, neither claimed to have a significant family history of diabetes.

Not too surprisingly, both patients had positive urine dipsticks for glucose and 300+ mg/dL blood glucose levels on fingerstick evaluation.  Although the diagnosis of diabetes could be made, it was unclear what kind of diabetes they may represent and at what stage they were at.  It seemed like they both represented a type known as Adult Onset Type 1 Diabetes but a definitive diagnosis wouldn't be available for some time.  So this got me thinking:  Assuming these patients are early in their development of adult onset type 1 diabetes, should the patient and his/her physician be concerned about the patient's ultimate need for insulin?  Also, do these patients present a challenge in blood sugar management that should be dealt with by a specialist?

To answer these questions I found a couple of studies to indicate that they would eventually need insulin because the gradual progression of their disease would end up destroying the remainder of their pancreatic beta cells, rendering medical therapy useless.  The first prospective study followed 133 patients with newly diagnosed non-insulin dependent diabetes mellitus (NIDDM) and 126 control subjects for an average of ten years.  Of those with detectable autoantibodies like glutamic acid decarboxylase and islet cell antibodies (GAD and ICA indicating adult onset type 1 DM) at diagnosis, between 60% and 67% developed a dependence for insulin within the 10 year period.

The second prospective study followed 569 patients with newly diagnosed NIDDM, of which 10.7% had detectable autoantibodies (GAD65), for the development of insulin dependence.  The study reported that "the presence of GAD65-CAb had a diagnostic specificity for insulin requirement as  high as 99.4% and identified a subgroup of patients with low BMI, low basal C-peptide values, and a need for insulin therapy."  The bottom line here is that this study suggests that those individuals with detectable levels of pancreas-specific autoantibodies are very likely to require insulin in the near future and that those individuals fit a specific metabolic profile and body habitus unlike those of typical type 2 diabetics.

So based on the data available it seems that individuals not fitting the typical description of type 2 diabetics but presenting with new onset adult diabetes are likely to 1) have detectable levels of autoantibodies to pancreatic beta cells, 2) be classified as adult onset type 1 diabetics and 3) progress to the point at which they will REQUIRE INSULIN in the near future.  Knowing this, one can predict that patients such as these would be relatively difficult to manage seeing as their blood sugars would never be stable for long and that eventually they will end up failing an oral medication regimen.  Having said that after identifying some of my patients with similar signs, symptoms and metabolic profile, I would be more inclined to refer them to an endocrinologist for typing and optimal treatment.  Although a family physician should be able to manage most type 1 and type 2 diabetics, asking them to optimally treat a patient with adult onset type 1 diabetes may be asking more of them than what their time will allow.

We had a post-menoupausal woman over the age of 50 with additional risk factors for osteoporosis (ie smoking, white, low Ca intake) who returned to the office for the results of her DXA scan. The woman had a DXA T-score of -1.6. (remember T-score compares patient with a young healthy female reference group) What do we do now? She does not fit the definition of osteoporosis (DXA T-score <-2.5), but appears to be on her way to becoming osteoporotic.

According to the AAFP, the following recommendations should be given even though the patient is not defined as osteoporotic yet:     

So, what pharmacologic therapies really work? According to the Fracture Intervention Trial,  women with low bone mass who do not meet the bone mineral density criterion for osteoporosis, alendronate (FOSAMAX)  is effective in reducing the risk of vertebral fractures. The absolute benefit of this therapy in women with a T score between -1.6 and -2.5 is greater in women with an existing vertebral fracture and/or with other risk factors. The effect of alendronate occurs early. Furthermore, bisphosphonates (aledronate, risedronate) have been shown to be just as effective in weekly dosing as in daily dosing and thus is easier for patients to comply with. One study has shown a superior performance for aledronate vs. risedronate in predefined increases in bone mass density. Both have extremely tolerable side-effect profiles.

Summary:

1. Osteoporosis is defined as DXA T-score of <-2.5. Osteopenia is defined as DXA T-score of <-1.0 - -2.5.

2. Treatment and/or prevention of Osteoporosis includes Calcium, Weight-bearing exercises, smoking cessation, and pharmacologic agents.

3. Aledronate and Risedronate are just 2 of the drugs available in the Bisphosphonates category. Aledronate appears to be superior to risedronate and both have very tolerable side effect profiles.

4. Osteoporosis can be prevented. Thus, treatment should begin in patients defined as osteopenic to prevent the progression to osteoporosis.

 

A postmenopausal female patient presented for an annual physical exam. She has a dual diagnosis of hypertension well-controlled by a hydrochlorothiazide and hyperlipidemia with excellent control by Lipitor. Besides these two medications she takes a multivitamin daily and an 81 mg Aspirin on a daily basis. In response to the inquiry of whether she has any questions, concerns or complains today she wonders if what she has heard on TV about Aspirin is actually true. The news claimed that unlike men, aspirin does not protect women from MI, but only from stroke.

 

 

Daily low-dose aspirin lowers women's risk of stroke but does not prevent heart attacks, according to a new study released this month. Those findings are the opposite of what is known about aspirin's effects on men.

 

 

Recently announced results of the large, primary-prevention randomized trial among women looks at the effect of aspirin at lowering the risk of death from cardiovascular cause, such as stroke and myocardial infarction. The Women's Health Sudy randomly assigned 39,876 initially healthy women 45 years of age or older to receive 100 mg of aspirin on alternate days or placebo and then monitored them for 10 years for a first major cardiovascular event (i.e., nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes).

 

 

Researchers reported a 17% reduction in stroke risk and a 24% reduction in ischemic stroke risk in the aspirin group compared with those on placebo group.

 

 

As compared with placebo, aspirin had no significant effect on the risk of fatal or nonfatal myocardial infarction or death from cardiovascular causes. Subgroup analyses, however, showed that aspirin significantly reduced the risk of major cardiovascular events, ischemic stroke, and myocardial infarction among women 65 years of age or older.

 

 

By contrast, in studies involving men, aspirin has caused a significant reduction in the risk of myocardial infarction but no significant reduction in strokes, the researchers reported. Researchers do not know why aspirin affects men and women differently, the article said, but experts say it may be related to the size of blood vessels leading to the brain, which are smaller than those leading to the heart.

 

 

The results of this study highlight the importance of studying women as well as men in clinical trials, and the need for physicians to consider individual risk profiles when deciding whether to recommend aspirin.

Saturday office hours are for acute visits.  Today, after 16 of these "acute visits", with the majority of them presenting as viral URIs and many of these with related ear pain, I began to question the current thought behind the treatment of ear infections. Specifically, I wondered about the treatment guidelines for acute otitis media (AOM). So with the help of the American Academy of Pediatrics, The Journal of Pediatrics, and UpToDate, this is what I came up with.

Otitis media brings more kids to the doctor's office than anything else. A Medicaid cohort of nearly 90,000 kids under 13 years old estimates that the U.S. spends about $5 billion annually on the diagnosis of otitis media with about half of these costs going to children between 1 and 3 years of age. One study showed that "children aged 0 to 4 years received 53% of all antibiotic prescriptions, and otitis media was the most frequent diagnosis for which antibiotics were prescribed (30% of all prescriptions)." The frequency of this diagnosis, and issues regarding cost and increasing antimicrobial resistance, make otitis worth learning about.

 

Guidelines issued in 2004 by the American Academy of Pediatrics (AAP)  and the American Academy of Family Physicians (AAFP) outline the following:

1. Recommendation: To diagnose AOM the clinician should confirm a history of acute onset, identify signs of middle-ear effusion (MEE), and evaluate for the presence of signs and symptoms of middle-ear inflammation.*

2. Strong recommendation: The management of AOM should include an assessment of pain. If pain is present, the clinician should recommend treatment to reduce pain.

3A. Option: Observation without use of antibacterial agents in a child with uncomplicated AOM is an option for selected children based on diagnostic certainty, age, illness severity, and assurance of follow-up.**

3B. Recommendation: If a decision is made to treat with an antibacterial agent, the clinician should prescribe amoxicillin for most children.

4. Recommendation: If the patient fails to respond to the initial management option within 48 to 72 hours, the clinician must reassess the patient to confirm AOM and exclude other causes of illness. If AOM is confirmed in the patient initially managed with observation, the clinician should begin antibacterial therapy. If the patient was initially managed with an antibacterial agent, the clinician should change the antibacterial agent.

5. Recommendation: Clinicians should encourage the prevention of AOM through reduction of risk factors.

6. No recommendation: There is insufficient evidence to make a recommendation regarding the use of complimentary and alternative medicine for AOM.

Very briefly I wanted to address 3A, regarding antimicrobials.  This guideline provides the option of waiting to initiate antibiotic therapy in specific cases**.  UpToDate makes reference to three meta-analyses [1,2,3] that show modest, if any, benefit to using antibiotics for otitis. These studies showed the following:

• Within 24 hours of the start of therapy, 61 percent of children had a decrease in symptoms whether they received placebo or antibiotics, and approximately 75 percent resolved symptoms by one week.
• Between seven and 20 children would need to be treated with antibiotics to reduce pain after two to seven days in one child.
• Few serious complications occurred in either the antibiotic treated group or in controls. Only one case of mastoiditis occurred (in a penicillin treated patient).

Furthermore, UpToDate reported that "antibacterial therapy prescribed at the first visit may shorten symptoms by one day in 5 to 14 percent of children, but causes side effects in 5 to 10 percent of children."

Bottom line, there is a subset of kids with otitis media that may be better off with a 48-72 hour monitoring period without antibiotics, which may reduce the rate of antimicrobial resistance, decrease unnecessary costs, avoid potential medication side-effects, and provide an equally satisfying outcome.

* Elements of the definition of AOM are all of the following:

1. Recent, usually abrupt, onset of signs and symptoms of middle-ear inflammation and middle-ear effusion (MEE)
2. The presence of MEE that is indicated by any of the following:
1. Bulging of the tympanic membrane
2. Limited or absent mobility of the tympanic membrane
3. Air-fluid level behind the tympanic membrane
4. Otorrhea
3. Signs or symptoms of middle-ear inflammation as indicated by either
1. Distinct erythema of the tympanic membrane or
2. Distinct otalgia (discomfort clearly referable to the ear[s] that results in interference with or precludes normal activity or sleep)

**  Observation is an appropriate option only when follow-up can be ensured and antibacterial agents started if symptoms persist or worsen. Nonsevere illness is mild otalgia and fever <39°C in the past 24 hours. Severe illness is moderate to severe otalgia or fever 39°C. A certain diagnosis of AOM meets all 3 criteria: 1) rapid onset, 2) signs of MEE, and 3) signs and symptoms of middle-ear inflammation.

Antibacterial therapy should be administered to any child under the age of six months, regardless of the degree of diagnostic certainty.

For children ages six months to two years, antibacterial therapy is recommended when the diagnosis of acute otitis media is certain or if the diagnosis is uncertain but illness is severe. Observation is an option for children in whom the diagnosis is not certain and illness is not severe.

For children older than two years, antibacterial therapy is recommended if the diagnosis is certain and illness is severe. Observation is an option when the diagnosis is certain but illness is not severe and in patients with an uncertain diagnosis.

In the clinic, the top three chronic conditions we manage are HTN, DM, and hypercholesterolemia.  Patients come in for a URI, and if they are a "new" patient to the practice, we often draw blood to get a baseline of their CBC, profile I, and often check their fasting lipid profile as well.  Unfortunately, in a society where obesity has become an epidemic, more often than not, lipid profiles are also higher than normal.  So the question is, what do we as healthcare providers tell these patients??   

Hypercholesterolemia is one of the major contributors to atherosclerosis and CAD, the leading cause of death in the US.  The National Cholesterol Education Program of the National Institutes of Health has created a set of guidelines that standardize the clinical assessment and management of hypercholesterolemia.  In May 2001, they released their third set of guidelines, reflecting changes in cholesterol management.  These new guidelines stress the importance of an aggressive therapeutic approach in the management of hypercholesterolemia.  The major risk factors that modify LDL goals include age, smoking status, HTN, HDL levels, and FHx, and the concept of "CHD equivalent" is to introduce conditions requiring the same vigilance used in patients with CAD.  Once LDL cholesterol is at an accepted level, physicians are then advised to address the metabolic syndrome and hypertriglyceridemia. 

Now that we have targeted LDL as the lipid to lower first and foremost, is there any benefit to lowering LDL below the current recommendation of <100 mg/dl?  The Treating to New Targets (TNT) trial was a parallel-group study that randomized 10,003 patients from 14 countries to double-blind treatment with either atorvastatin 10 mg or 80 mg.  During the double-blind period, LDL cholesterol levels reached approximate mean values of 100 mg/dl for the low-dose atorvastatin group and 75 mg/dl for the high-dose group. Randomized patients were followed for an average of 5 years.  The primary end point were the time to occurrence of a major cardiovascular event, defined as CAD death, nonfatal MI, resuscitated cardiac arrest, or stroke.  The large patient numbers in the TNT study and long follow-up ensure adequate power to definitively determine if reducing LDL cholesterol levels to approximately 75 mg/dl can provide additional clinical benefit.  The results showed that reducing LDL to ~77 mg/dl did in fact provide additional clinical benefit in stable CHD patients compared with control of ~100 mg/dl.  The primary endpoint occurred in 8.7% and 10.9% of patients receiving the 80 mg and 10 mg doses of atorvastatin, respectively, representing an absolute risk reduction of 2.2% and relative risk reduction of 22%.  The findings demonstrate the relationship between reduction of LDL-C and reduction of CHD risk shown by previous secondary prevention trials of statins may be extended to very low levels of LDL-C.

In summary, when treating hypercholesterolemia, we should do so aggressively, especially in light of the fact that the major risk factors that modify LDL goals (i.e. age, smoking status, HTN, HDL levels, and FHx) are often multiply present in our general patient population.  In addition to this, in the TNT trial, it was shown that in patients who were already high risk (i.e. with stable CAD), an additional decrease in their LDL below the recommended goal of <100 mg/dl can result in additional clinical benefit.  So although the present guidelines do not specifically recommend pushing patients far below the current recommendation, this study may be key in the future revision of guidelines for the treatment of hypercholesterolemia.  

There I was in the office nearing the end of the day finishing writing my notes when one of my preceptors walks up to me with a funny smirk on his face and asks me, "Have you ever burned a hole in a nail with a paper clip before?". WHAT??!! At first I thought I heard him wrong. I guess the look on my face prompted him to repeat himself.  Sure enough, I had heard him correctly.  He then motioned for me to follow him and the nurse practictioner to an exam room.

The NP was seeing a patient who had gotten her right middle finger caught in a door a day before. The patient was now suffering from excruciating pain due to the pressure caused by the build up of blood beneath the fingernail - a subungal hematoma.  My preceptor then explained to me that as a resident he learned an effective and simple technique to relieve the pressure caused by the hematoma along with the pain associated with it. - a technique mentioned on this eMedicine page discussing common nail injuries. He uncoiled a paper clip and using a lighter he had borrowed from a member of the office nursing staff he heated up the straight end of the clip.  After about 30 seconds of heating, my preceptor placed the hot end directly upon the affected nail.  The heated paper clip immediately burned through the nail and blood began to be expressed through the nail.  Other than the initial burning sensation, the patient stated that the pain was now much less severe than before.

According to the eMedicine page, the treatment of a subungal hematoma with a heated paper clip or electrocautery (a technique known as nail trepination) is suggested when the hematoma involves 25% or less of the nail plate.  If more than 25% of the nail plate is involved, removal of the nail is suggested.  When recalling the patient treated by my preceptor, it appeared that more than 25% of her nail plate was involved yet my preceptor believed that the use of the heated paper clip was enough.  Was that treatment truly effective? I found an article published in the American Journal of Emergency Medicine that observed in a prospective study the long term outcomes of using nail trepination alone in the treatment of subungal hematomas. The study observed for a two year period a group of 48 patients treated with nail trepination. At the conclusion of the study period none of the patients had developed an infection, osteomyelitis, or nail bed deformities despite the size of their hematoma or the presence of a fracture.  Another study looked at the treatment of subungal hematomas in children. The study divided 52 children into two treatment groups - one group being treated with nail removal and the other group treated with trepination.  The results of the study showed that the complications experienced by the two groups were very minimal and almost identical in rate.  The only difference shown between the two groups was the cost of treatment - with the group undergoing nail removal having an almost six times greater cost of treatment than the group treated with trepination.

In conclusion, nail trepination or use of a heated paper clip seems to be an effective, cost -effective,and safe technique to be used to treat subungal hematomas despite the severity of the injury.

HIV in pregnancy.   retroviral therapy (with attention to page 28) pre-section is advised in situations in which viral load is still detectable.  

How important is retroviral therapy and when should it be given?  This article helped me to draw dual conclusions.  It showed that it was a necessary treatment for HIV positive mothers to effectively lower vertical transmission risk.  The second conclusion was that there was effectively a good and bad time to treat, namely it be given earlier than 1 hour before delivery.  In doing so, transmission rates can be seen to drop.  To do any less would be a substandard of care according to this second article.

So What Now:

For women of expectant age and HIV positive status, begin education early and often.

For those with viral loads requiring therapy, make note of teratogenic potentials.

Lastly remember when all else fails effective therapy is still available in the 11^th hour leading right into delivery.

 

One of the most debilitating progressive diseases affect elderly patients is osteoarthritis.  There have been many studies done to find a better treatment for something that seems inevitable for the elderly patient.  Current non-pharmacological treatments include physical therapy, exercise, and weight management - all focused on reducing pain and improving mobility.  Some of the pharmacological treatments include NSAIDs, COX-2 inhibitors, corticosteroids, narcotic analgesics, and even slow-acting drugs known as the "nutraceuticals." 

I found that many of our patients suffering from OA have switched from the COX-2 inhibitors (because of the recent publicity of its cardiovascular safety profile) and to drugs like chondroitin and glucosamine sulfate.  Upon further investigation of the history of chondrotin and glucosamine sulfate use as a therapy for OA, I found that not only is it a good pain relieving medication, it actually stops and reverses disease progression - something that most of the treatments do not really address.  This study, done in a large cohort of postmenopausal women, found that for the first time a medicinal treatment intervention for OA actually has a disease-modifying effect, rather than just treating the symptoms of the disease.  Actually a knee OA study is currently underway to determine the efficacy of glucosamine sulfate, chondroitin sulfate, glucosamine with chondroitin, compared to placebo and compared to celecoxib.  This would be a great alternative to those patients who fear the cardiovascular side effects of the COX-2 inhibitors such as Vioxx, Celebrex, or Bextra. 

Also in those patients with co-morbidities such as PUD, may not tolerate such drugs in the NSAIDs category.  An evaluation done in another study found that in contrast to NSAIDs, there are no serious or fatal side effects reported for glucosamine.  And also contrary to what the "layman" may believe, glucosamine is safe and does not affect glucose metabolism in any way.  However, I feel that we may be reluctant to approach a patient with this remedy because there is still a need for more randomized controlled studies in vivo to assess its efficacy and long-term effects. 

A female who came to the office s/p nephrolithiasis of unknown etiology (she didn't know what type of stone -- calcium oxalate, struvite, ect).  She said that she heard that cranberry juice prevents future kidney stones from forming.  Since her infection, she has been drinking liters of this juice to make sure it goes away.

I found no study that showed that cranberry juice prevents nephrolithiasis.  Actually, there are studies that show that cranberry juice can actually increase urine levels of oxalate and calcium which could predispose to kidney stones.  

What cranberry juice is efficacious for, is for prevention for UTI's.  Cranberry juice potently inhibits the bacterial adherence of Escherichia coli and other gram negative bacteria.  There are no randomized trials showing its use for treatment of UTI's, but there are randomized trials showing its efficacy for prophylaxis.

One randomized trial with 150 sexually active females divided up 3 groups, each taking different substances: placebo, cranberry juice, and cranberry pills.  Cranberry juice and pills had statistically significantly lower UTI's in women who normally experienced 1 UTI/yr.  Cost savings were greatest for women who experienced at least 2 UTI's/yr.  Since cranberry tablets are more than half the cost of cranberry juice, the study recommended using the tablets for prophylaxis.

The AAFP also commends cranberry juice as a prophylactic UTI complementary medication: "Cranberry appears to be a safe, herbal choice for UTI prophylaxis and has relatively good tolerability."

A large portion of the FP patient population is elderly and osteoarthritis is a very common problem in this population.  I find this problem is often ognored by patients or dismissed as "normal aging."  It may be normal since the vast majority of individuals experience it as they age but that doesn't mean we can't do something about it.  Some of the docs in my practice are big believers in glucosamine as therapy for OA and some are not so impressed.  I decided to take a look for myself and I found an article on Cochrane Database of Systematic Reviews.  (I would link it but I don't think that would work.  Instead, go to CDSR under EBM reviews on the Intranet.  Here is the citation: Towheed, TE. Anastassiades, TP. Shea, B. Houpt, J. Welch, V. Hochberg, MC. Glucosamine therapy for treating osteoarthritis. [Systematic Review] Cochrane Musculoskeletal Group Cochrane Database of Systematic Reviews. 1, 2005.)

Glucosamine is a naturally derived product taken from shellfish, so it is CONTRAINDICATED IN PEOPLE WITH A SHELLFISH ALLERGY.  Other toxicities are rare but are generally related to GI upset and loose stools.

The exact mechanism is unknown but it is postulated that because glucosamine is s precursor for glycosaminoglycans and proteoglycans in articular cartilage, ingestion stimulates cartilage production.  In vitro studies show that glycosamine directly stimulates human chondrocytes.  In vivo animal studies are less clear but 14C-labeled glucosamine delivered IV or po does get metabolized, as evidenced by the expiration of 14-C labeled CO2.  These animals also showed increased cartilage production despite a very small percentage of 14-C distribution in the new cartilage.

One in vivo human study demonstrated that glucosamine administration halted progression of cartilage loss (demonstrated radiographically) over three years.  This suggests that glucosamine may actually be a disease-modifying agent in OA.  There is an additional anti-inflammatory effect of glucosamine but this mechanism is even more mysterious.  The total result is that patients see a significant reduction in pain as well as progression of disease.

In all, studies point to a positive effect from glucosamine 500 mg tid but it may take 6 weeks before patients see pain benefit.  This not only improves patient quality of life but may also reduce their consumption of analgesics.  (And we all know how excessive use of NSAIDs and acetaminophen can turn a patient's minor aches and pains into a medical emergency, right?)

Unfortunately, the patients who need this therapy most (the elderly) may not be able to afford it.  It is not covered by any insurance that I know of and OTC products range in price from $30-60+/month.  These products are available at GNC or other drug stores, but encourage your patients to consult you before starting a praticular brand, as product purity of brands may range widely.  This last point is important because many patients believe (perhaps because advertising says so) that because it is "natural" and OTC it must be safe.  An online site you can recommend may save your patients money and give you an opportunity to examine what they're taking.  Here is a site that one of the office docs recommends to his patients.

We all know the typical uses of B-blockers (post MI, HTN, etc).  They have also been used (without the specific indication) to improve performance on tests.  Do they really help?  

Fortunately we are in luck since studies have been done that explore this very question!  One study stated that "situational stressors and anxiety impede performance on "creativity" tests requiring cognitive flexibility. Noradrenergic agents have been shown to modulate cognitive flexibility as assessed by performance on anagrams."  In an attempt to determine if these findings were attributable to noradrenergic or an anxiety effect, pts were given propranolol, lorazepam, and placebo and then administed a test.  The study showed that for subjects able to solve the anagrams, solution times after propranolol, but not lorazepam, were significantly lower than after placebo.  The results suggested that noradrenergic modulation of cognitive flexibility does not result from a nonspecific anxiolytic effect, but rather is specific to the noradrenergic system.

Another fun study involving ophthalmology surgical residents attemped to address the effect of B-blockers and performance in the OR.  The study concluded that residents who took propranolol 1 hour before surgery had a significant reduction in tremor and anxiety compared to when they took a placebo.   

B-blockers for anyone before the final?!

This week an infant was brought in for a Well Child Visit.  The child was born with Down Syndrome.  During my intake I found the typical associations.  The child had milestone deficits, decreased muscle tone, and strabismus.  There was the typical mongoloid facies, simian crease, and a short fifth digit.  The diagnosis was made intrauterine and so physical therapy and developmental therapy were in place and started early.  During the presentation to the attending I was asked about the most recent thyroid function testing, of which I had no idea about and did not even think about.  Turns out that there is strong correlation between Down syndrome and thyroid function with important sequelae when gone unmonitored and untreated.

This journal article shows that there is an importance in testing not only early but regularly despite continual normal test results.  The question then is "what is the point of testing and how will it affect the patients short and long term morbidities?"  Some immediate effects include dry skin, constipation, and anemia.  Prolonged effects include cognitive impairment and increased coronary artery disease.  Of most interest to me was the decline in cognitive capacity.  For children that are already behind the curve in mental development being able to minimize unnecessary decline is a clear preventable endpoint.

This article showed the difference between those treated for hypothyroidism and those on placebo over a two year time frame with those given thyroxine having a smaller delay in development.  Although not bolstering, the absolute difference seems evidence enough to test and treat.

Now What Factor:

1)      Accurate testing for hypothyroidism can be found here. (at the end there is a short 4 step algorithm to follow.)

2)      Aggressive testing and treatment are important for both physical and mental growth outcomes.

   NOTE:  The following POEM (with the exception of the Footnote) was written without knowledge of a prior POEM on Vitamin E.  I hope to explain some additional findings that might be different than what was previously written, or help to further explain the findings.  See Footnote.

   With so many patients following health news and searching their own information on the web it is understandable that many come into the medical office with questions or concerns about what they have read.  A middle-aged man with a significant cardiovascular risk profile (hypertensive, overweight, family history) came into the office inquiring about vitamin E supplementation after reading about it in the news.  We've heard for years that antioxidant therapy is great for defending against cancers as well as for cardiovascular health.  The proposed theory for cardiovascular benefits is that the antioxidant action of vitamin E (and other antioxidants) decreases LDL oxidation in the arterial wall, thereby diminishing the accumulation of cholesterol esters and decreasing atherosclerosis.

   But, a recent study in JAMA (March 16, 2005) questions an actual benefit of the long-used vitamin in patients with vascular disease or diabetes mellitus.  The study is based on the HOPE (Heart Outcomes Prevention Evaluation) and HOPE-TOO (The Ongoing Outcomes) trials conducted from 1993-2003, which included over 9,000 and 7,000 patients, respectively.  Patients were given a daily dose of 400 IU vitamin E or placebo.  Outcomes included cancer incidence/deaths, major cardiovascular events (MI, CVA), heart failure, unstable angina, and revascularizations.  Results showed no significant difference in cancer incidence/deaths, major cardiovascular events, unstable angina, or revascularizations.  However, heart failure and hospitalization for heart failure were shown to be higher in the vitamin E supplemented group.  The proposed mechanisms are that alpha-tocopherol might turn to a pro-oxidant state, thereby increasing vascular damage.  Another theory is the high dose of vitamin E might displace other fat-soluble antioxidants and disrupt the natural balance of antioxidants resulting in lower cardioprotective HDL.  The authors concluded that vitamin E supplementation should not be used in patients with vascular disease or DM due to the findings of increased heart failure and lack of benefit for other cardiovascular and cancer outcomes.

   A current NCI-sponsored study, the SELECT (Selenium and Vitamin E Cancer Prevention Trial) aims to see if the combination of selenium and vitamin E provide chemoprevention for prostate cancer.  It is based off previous studies that showed a decrease in the incidence of prostate cancer with selenium or vitamin E.  While the SELECT study, to be completed in 1012, may show a positive benefit for vitamin E supplementation for one type of cancer, it does not show information on cardiovascular management.  Other studies have shown a reduced cardiovascular risk with vitamin E supplementation in women; however, they were too short-term to make clinical decisions off of them.

  More studies are surely to come out, but what should we advise our patients in the meantime?  If a patient does not have vascular problems or DM, vitamin E supplementation may provide some chemopreventative benefit against certain cancer types; cardioprotective benefits are questionable for those without significant cardiovascular risk.  However, it may be advisable to eliminate supplementation for cardiovascular-diseased or diabetic patients due to the data of increased heart failure from the HOPE and HOPE-TOO trials.  Until the verdict is out, eating foods with natural sources of vitamin E may be a great way to obtain possible cancer prevention without using a highly concentrated supplement, thus limiting cardiovascular risk.

FOOTNOTE:  The recent article in JAMA involved only patients that have cardiovascular disease or diabetes.  Therefore, it cannot be concluded that Vitamin E is detrimental to the health of non-morbid patients.  In fact, there are a multitude of studies (see above or do a Pubmed search) that show potential benefit to some form of vitamin E supplementation.  The previous POEM's conclusion that "vitamin E supplementation is not beneficial in the prevention and/or reduction of cancer and cardiovascular disease" may be premature; the statement is without regard to other studies present in the scientific literature and is based off one population-specific study.  NIH's Office of Dietary Supplements has a nice website that discusses Vitamin E and previous/current/ongoing studies regarding possible benefits.

FYI: Tthe current RDA for vitamin E, meant only to prevent deficiencies, is 15 mg (22.5 IU) for adults.  Vitamin E is naturally found in many vegetable oils (soybean, sunflower, safflower, olive, canola, etc.), nuts (almonds, sunflowers, peanuts, etc.), and green leafy vegetables

A patient came in this week and voiced concerns about continuing to take Rosuvastatin (Crestor). She had heard about some deleterious side effects on the news. Just a few weeks earlier I had seen an article the Washington Post had run on Crestor and the new FDA warnings. A patient's death in December possibly from rhabdomyolysis fueled an already ongoing debate about Crestor's safety. A watchdog group Public Citizen has petitioned the FDA to ban Crestor and the FDA has been forced to issue an advisory statement and a new product label. The doctor reassured her that the level she was taking was safe and she seemed to leave feeling comfortable. But I wondered what the data said and what all the talk was about.

In reviewing the data I found a paper that compared rosuvastatin with the other widely used statin drugs in its ability to lower non-HDL cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia. Over 2,000 patients enrolled in this randomized open label prospective study and it was found that rosuvastatin was superior in improving the lipid profile than milligram-equivalent doses of atorvastatin and milligram equivalent or higher doses of simvastatin and pravastatin. A review article examined all peer-reviewed articles found in Medline through 2004 and again showed rosuvastatin to have the highest dose-to-dose potency in lowering LDL and raising HDL, thus allowing more patients to achieve the NCEP goals on lower doses of statin. The safety profile of Rosuvastatin was again found to be comparable to that of the other commonly used statins. So the drug is good at lowering cholesterol but is it safe?

A paper published in 2003 examined the risk to benefit ratio of rosuvastatin (10 to 40 mg) in over 12,000 patients and found that it had a similar adverse event profile as the other statin drugs. Specifically it found that myopathy occurred in >0.03% of patients taking rosuvastatin and no cases of rhabdomyolysis were reported. Similar increases in ALT's were reported for all statin groups. This paper concluded that compared to the other widely used statin drugs up to 40 mg rosuvastatin had a favorable risk to benefit ratio.

Finally one last paper found rosuvastatin to be the most cost-effective statin among the four examined in terms of cost/1% reduction in LDL levels and the cost/patient achieving the ATP III LDL goal. So with some of the data in hand, I feel much more comfortable with the possibility (one day) of prescribing Rosuvastatin. Anyone else hear anything about Crestor?

Today the nurse asked me if I was willing to perform venipuncture all morning.  I explained that I was always willing/ready to perform venipuncture, though I'm no expert, and we would need patients who don't mind multiple sticks and misses.  They told me that those type of patients are imaginary, and set me up in a hot room with all the equipment I'd need, but no lidocaine.  I got to thinking that these poor patients of mine might benefit from some lidocaine, just like we students had during summer orientation.  My dilemma, of course, was that nobody I knew was able to get a flash last summer, which won't fly if you actually need a blood sample.  So I drew all the draws sans anesthesia, came to a computer and researched the subject of pain control and whether the lidocaine increases the difficulty of getting the needle into the vein, as I have been told in the past.  Here's what I found out.  I really needed two studies, so be patient.  I got a reference that showed that subcutaneous anesthesia does significantly reduce pain in those who are having a venipuncture procedure performed, when the needle used is equal to or larger in diameter than a 16 gauge (0=big, 23=small).  Furthermore, I learned that, in this randomized clinical trial, subcutaneous anesthesia did not effect the ability of doctors with less than four years of clinical experience to get the job done one the first attempt, with a p=0.5. 

 

So, when taken together, these two articles support the use of subcutaneous anesthesia in those patients requiring venipuncture with a needle 16-G or larger.  We as students are most likely going to be using 22 or 23-G butterfly needles, which are easier, so we can advise our patients that they won't benefit greatly from anesthesia.        

• POEMs ... the "E" stands for evidence.  Many of your posts cite good evidence, but others cite "expert opinion" .. which is oh-so- 90's ..
• HIPAA
• You don't need to describe an individual patient to make your point well.  Try to make your point without describing one person in particular.
• If you do end up describing on e person (whether real or fictional) ... please don't state the exact age of the patient.  Recall that stating the age with any precision o fless than one year may be considered a violation of privacy. 
• Stating location more specifically than State is also problematic.  So providing information about a given physicians' name (who presumably could be located in a particular City) would not be OK.
• I've edited your posts a tiny bit to keep things "clean" ...
• Overall - I'm impressed with your work.  Keep it up.

After my preceptor and I saw a diabetic patient who had recently began to show signs of hypertension, my preceptor began to pimp me on the issues related to individuals who suffer from both diabetes and hypertension.  When he asked me what drug would I choose first to treat a diabetic with hypertension, I answered without much thought "an ACE inhibitor". To my surprise, he said that recent data has shown that an ARB should be used.  This is the first time I had heard of using anything other than an ACE inhibitor to treat diabetics with hypertension, so like a good 3rd year student (especially and EBM loving ALBANY MED 3rd year student - lol) I decided to look into the literature to investigate this.

Many studies have already shown the effect ACE inhibitor treatment has on decreasing mortality and adverse effects in diabetics - findings that have lead to them being favored as first line treatment.  These findings are mentioned on a page discussing background information on hypertension in diabetics and treatment guidelines from the American Diabetes Association. The ADA's guidelines recommend tailoring treatment based on the clinical presentation of the patient.  For instance, it is recommended to use an ACE inhibitor when treating a Type I diabetic with or without hypertension and with any degree of albuminuria, while an ARB is recommended in a patient with Type 2 diabetes, hypertension, macroalbuminuria (>300 mg/day), nephropathy, or renal insufficiency.  An ARB or an ACE may be used, however, in the treatment of a type 2 diabetic with hypertension and microalbuminuria.

However, the beneficial effects of decreased mortality rate and number of adverse effects shown with ACE inhibitor treatment has yet to be adequetely shown in studies with ARBs.  This fact is discussed in a systemic review published in the British Medical Journal (BMJ) studying the effects of ACE inhibitors and ARBs on mortality and renal outcomes in diabetic nephropathy - a possibly life threatening sequela of hyperetension that diabetics may develop.  The review looked at 43 studies which either compared ARBs and ACE's to placebo or to each other.  The conclusion reached by the study was that there is currently not adequate data available to truly compare and contrast the benefit of using an ACE instead of an ARB and vice versa. However, the study group did find evidence to suggest that ARBs may be more efficacious in renoprotection in diabetic patients.

The finding that ARBs are more renoprotective than ACE inhibitors was disputed however by a study published in the NEJM that compared ARBs and ACE inhibitors in the treatment of Type 2 diabetes and nephropathy.  The study results showed that the ACE inhibitor used (enalapril) displayed better renoprotective results than the ARB used (telmisartan) in the study population of type 2 diabetics with early nephropathy (both drugs were compared on the decrease of GFR over a five year period displayed by their respective study groups)

Based on lack of definitive data to support use of one drug over the other, it would be best to follow the ADA guidelines and base treatment decisions on the individuals specific presentation in order to determine if their hypertension used be ACE'd or not.

Important points

1. Use ACE inhibitors when treating Type I diabetics
2. Consider using an ARB when treating a Type 2 diabetic with advanced renal deficiencies
3. So far, only ACE inhibitors have been shown to be beneficial in the decrease of mortality and adverse effects in diabetics with hypertension
4. Do not always take your attending of preceptor's words as law - try to do your own investigating (No offense to any attendings reading this)  

I am working in an office setting with more than one doctor, so when a patient came in with elevated triglycerides, one doctor recommended Gemfibrozil which is what I thought would be the recommendation.  When I was working with another Doc and she asked me what I would do for a patient with high TG, I smiled and said I would start something like GEmfibrozil.  When she said that this would be okay but she was going with Lipitor, I wanted to see what was out there to back her decision.  The article I found said that Lipitor improved the risk factors associated with athersclerotic disease like LDL cholesterol as we all know.  However, it also improved things like plasma and blood viscosity which could lead to a lower degree vascular blocking.  It also decreased the plasma concentrations of atherogenic lipoproteins.  It did not, however, decrease the triglyceride greatly, 9% with p=0.01.  So while the doctor prescribing this was helping to reduce the patients risk of a coronary event, the desired drop in TG level that she was looking for, is not supported in this literature.  Lipitor has been shown to be great at reducing LDL levels, but in my opinion and the authors of this article, it does not significantly lower TG levels enough to be used as a first line agent for this purpose.

     A patient with diabetes mellitus and metabolic syndrome came into the office last week for his routine physical exam and blood work.  We, of course, took this opportunity to discuss the importance of diet and exercise in improving his health and delaying the appearance of cardiovascular disease.  He asked if taking any dietary supplements would help improve his health.  Specifically, he was wondering if he should be taking daily vitamin E supplements in order to help prevent future cardiovascular events.  He was confused because he had heard that he should take vitamin E awhile back and then more recently, he was told that it could actually cause more damage...so which is it doctor? 

     Experimental data has previously suggested that vitamin E supplementation can play a role in the prevention of cancer and cardiovascular events.  The hypothesis is that antioxidants can reduce atherosclerosis because they can limit low density lipoprotein oxidation on the arterial walls.  Over the last 10 years, numerous studies have been published that have tested vitamin E, C and other antioxidant vitamins and/or combinations on cancer and cardiovascular disease.  Yet consistently, clinical trials have not been able to show an effect of these antioxidant vitamins.  An article in the current issue of JAMA conducted a randomized, double-blind, placebo-controlled international trial of patients at least 55 years old with vascular disease or diabetes mellitus.  These patients were given 400 IU vitamin E (552 patients) from a natural source or a placebo (586 patients).  This study suggested that vitamin E supplementation over the long term does not prevent cancer or cardiovascular events, and may actually increase heart failure risk and hospitalization for heart failure.

     So the answer, at least for now is vitamin E supplementation is not beneficial in the prevention and/or reduction of cancer and cardiovascular disease.

A prepubertal patient presents to the office for a well-child visit. Upon the review of systems patient admits to having frequent headaches with photophobia and sensitivity to noise. Patient and the mother recall that headaches started bothering the patient about a year ago. Headaches last for up to an hour and affect patient's quality of life. The headaches are alleviated, but not completely relieved by O/C Tylenol. Patient's mother denies hx of seizures in a child, but admits to her own history of migranes. Physical exam is unremarkable including normal vision and hearing and absence of neurological deficits.

 

 Should this young patient be sent for an evaluation of the headaches?

 

 

According to the guidelines by Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society there is a lack of consensus concerning the role of diagnostic testing including routine laboratory testing, CSF examination, EEG, and neuroimaging with CT or MRI.

 

There is inadequate documentation in the literature to support any recommendation as to the appropriateness of routine laboratory studies or performance of lumbar puncture.

 

EEG is not recommended in the routine evaluation, as it is unlikely to define or determine an etiology or distinguish migraine from other types of headaches. In those children undergoing evaluation for recurrent headache found to have a paroxysmal EEG, the risk for future seizures is negligible; therefore, further investigation for epilepsy or treatments aimed at preventing future seizures is not indicated.

 

Obtaining a neuroimaging study on a routine basis is not indicated in children with recurrent headaches and a normal neurologic examination. Neuroimaging should be considered in children with an abnormal neurologic examination or other physical findings that suggest CNS disease. Variables that predicted the presence of a space-occupying lesion included 1) headache of less than 1-month duration; 2) absence of family history of migraine; 3) abnormal neurologic findings on examination; 4) gait abnormalities; and 5) occurrence of seizures.

 

Conclusions: Recurrent headaches occur commonly in children and are diagnosed on a clinical basis rather than by any testing. The routine use of any diagnostic studies is not indicated when the clinical history has no associated risk factors and the child's examination is normal.

 

 

 

A patient came in this past week with a long history of fibromyalgia that has been relatively well controlled with various medications but never completely resolved.

Treating a patient with fibromyalgia can be quite challenging. Modalities range from analgesics and antidepressants to hypnotherapy and EMG biofeedback.

This pt tried several different types of treatments over the years including tricyclic antidepressants. Although not uniformly efficacious across studies, a meta-analysis in 2001 showed positive results.

She/he also tried a serotonin reuptake inhibitor which has been shown to have some efficacy in fibromyalgia. A study in the American Journal of Medicine 2002  showed fluoxetine was effective compared to placebo.

 But what about simply exercising for relief from fibromyalgia?

One theory of the pain of fibromyalgia is that these patients have deficient muscle blood flow causing muscle 'spasms'. This suggests that exercise may improve symptoms. In a systematic review of controlled trials of aerobic exercise for fibromyalgia found beneficial effects on aerobic performance, pain, and pressure thresholds those subjects who received aerobic exercise training.

While these results appear promising, it is probably a lot harder to actually get someone to start an exercise program because patients with fibromyalgia often times feel that activity and exercise aggravates their pain. Thus, its going to be really important to work closely with patients to start very slowly and work their way up.

Someone brought an infant in the other day because the baby had a severe case of eczema/atopic dermatitis that did not appear to be getting better.  I talked to Dr. SkinDoctor, a Dermatologist, and asked him if he could give us any advice on how to manage his/her care, and this is what he told me:  

1.  Firstly, if he/she has open wounds that put him/her at increased risk for Staph infection, we might consider prophylactically treating the child with antibiotics.  

2.  Secondly, he recommended using Vaseline, an emollient, on the infant from head-to-toe to maintain skin hydration and reduce water loss from the skin, preventing the dryness often associated with this condition.  This may also help make the child less itchy and uncomfortable.

3.  He also recommended 2.5% (the lowest dose) of hydrocortisone ointment (NOT cream, again to maintain skin hydration) to help bring the inflammation under control.  

4.  Since eczema is a condition that gets worse with itching, he also suggested adding Atarax or Benadryl to the treatment regimen to help relieve the itch.

5.  If the condition still did not resolve, we might consider consulting immunology to search out a possible immunologic etiology of the child's rash.

Although this did not apply to the case I saw (Elidel is not recommended for use in infants younger than two years of age), I was also interested in seeing what studies had to say about Elidel (pimecrolimus),a non-steroidal immunomodulator and one of the newer drugs on the market for the treatment of eczema.  In one study, treatment with pimecrolimus 1% cream demonstrated a rapid improvement of all morphological signs of eczema. In another study, pimecrolimus cream 1% was well tolerated and effective in patients with mild to very severe atopic eczema, with rapid onset of action and no disease rebound after discontinuation.  However, symptoms of atopic eczema did return gradually after discontinuation.

Although Elidel has been shown to be effective in the treatment of eczema, in an FDA Public Health Advisory, the FDA has recently reported a potential link to cancer (skin cancer and lymphoma) with the use of Elidel (pimecrolimus) and Protopic (tacrolimus).  Since the FDA approved Protopic in 2000 and Elidel in 2001, seven cases of lymphoma and six skin cancer cases have been reported in patients, as well as animal testing that has suggested these therapies may cause cancer.  Whether the reported cancers are associated with these products has not been clearly established and further investigation is needed.

"The FDA recommends that healthcare providers, patients, and caregivers consider the following:

Use Elidel and Protopic only as second-line agents for short-term and intermittent treatment of atopic dermatitis (eczema), in patients unresponsive to, or intolerant of other treatments.
Avoid use of Elidel and Protopic in children younger than 2 years of age (our patient above).  The effect of Elidel and Protopic on the developing immune system in infants and children is not known.  In clinical studies, infants and children younger than 2 years old treated with Elidel had a higher rate of upper respiratory infections than did those treated with placebo cream.
Use Elidel and Protopic only for short periods of time, not continuously.  The long term safety of Elidel and Protopic are unknown.  
Children and adults with a weakened or compromised immune system should not use Elidel or Protopic.  
Use the minimum amount or Elidel or Protopic needed to control the patient's symptoms.  In animals, increasing the dose resulted in higher rates of cancer."

Now almost half way through the rotation I've begun to notice that a large proportion of the patients we see in the clinic have "mild hypertension" after we take their vitals during an appointment.  Although a significant number of patients have hypertension listed as one of their chronic medical problems in their charts, this wouldn't account for the frequency with which we identify mild hypertension in the office.  I began to think:  Are the BP readings we take in the office representative of what that persons BP is like throughout the day?

This got me wondering about so-called "white coat hypertension" (WCHT) in our patient population or more specifically:  1) What is it's prevalence?  2) What, if any, is the significance of having it?  3) How should it be treated?  Performing literature searches on this topic was surprisingly fruitful as the topic is clearly the source of endless debate, though three particularly good articles grabbed my attention.  

The first article (White-coat hypertension: a clinical review.) did a good job at describing the overall nature of the issue and provided some relevant details.  It defined WCHT as "the occurrence of blood pressure (BP) values higher than normal when measured in the medical environment, but within the normal range during daily life, usually defined as average daytime ambulatory BP (ABP) or home BP values (<135 mm Hg systolic and <85 mm Hg diastolic)" with a stated range of prevalences from 15% to well over 50% of patients seen in the office setting.

The second article (Cardiovascular outcome in white-coat versus sustained mild hypertension: a 10-year follow-up study.) did an excellent job at illustrating what effect having WCHT would bear on the development of cardiovascular disease when compared to patients with true mild hypertension.  The study followed 479 patients over 10 years and recorded the number of new cardiovascular events among each group.  The study found that although they cannot say that WCHT confers no increase in risk for having cardiovascular events within ten years, the risk when compared to patients with true mild hypertension was relatively benign.  This indicates that WCHT itself is not a significant risk factor in the development of CV disease.

The last article (Isolated office hypertension: A  prehypertensive state?), however, investigated how often individuals with white coat hypertension would end up developing true hypertension (>140/80) over a 5 year period.  The study followed 81 patients over a time period of 5-6 years and monitored their blood pressure for the incidence of elevated blood pressure in the ambulatory setting (home).  After 5-6 years 60 of the 81 patients had a mean 12 hour blood pressure of >140/80, indicating that WCHT may be considered a prelude to mild hypertension in affected individuals.  Although this study suffered from having a relatively small sample size, one cannot argue with the potential significance of the results.

When taken as a whole, the data on WCHT suggests that there is the potential for individuals with WCHT to develop mild hypertension within a matter of years with a debatable increase in risk of developing CV disease.  In light of these data it is recommended that physicians and health care professionals initially refrain from actively treating WCHT with pharmacotherapy but encourage home blood pressure monitoring and careful follow-up for the potential development of true hypertension.  These recommendations, although controversial, will certainly help to make decisions concerning management of WCHT easier when seeing patients in the office setting.

Many of the patients I see present with lower back pain (more than I thought I would see!). Most of the time we keep them out of work for a couple of days and send them to rehab and most get better. I've heard that is detrimental to keep patients on bed rest and that instead they should be doing as much physical activity as tolerated. So, I decided to look up the benefits of rehab and physical activity for patients with lower back pain.

When considering rehab vs. no rehab, one article found that in the setting of 181 general practices and 63 community settings for physical treatments around 14 centres across the United Kingdom, spinal manipulation (ie rehab) is a cost effective addition to pain management for back pain in general practice.

In terms of limiting one's activity, controlled studies conducted in the United States showed a benefit of functional restoration in patients with low back pain, especially on return to work. A randomized parallel group comparative trial demonstrated the effectiveness of a functional restoration program on important outcome measures, such as sick leave. Though there were no significant difference in the intensity of pain, the quality of life and functional indexes, the psychological characteristics, the number of contacts with the medical system, and the drug intake, patients took fewer sick days after functional restoration (ie-returning to normal level of activity) than with just rehab.

Another quick FYI looking into alternative treatment, a randomized controlled clinical trial evaluating the role of accupressure vs. physical therapy found that acupressure is another effective alternative medicine in reducing low back pain, although the standard operating procedures involved with acupressure treatment should be carefully assessed in the future.

An elderly patient had just gotten her bone density scan results which revealed that she was developing osteoporosis.  She had tried taking fosamax and evista and reported that she had to stop both due to side effects.  She was wondering if there was anything that she could take besides those two medications.  She also hated taking pills. 

Having just heard about Forteo from a drug rep, I decided to throw this out as an option.  She wasn't crazy about having to take a daily injection, but she worried a little less when I told/showed her the needle was the size of an insulin needle. 

But does it really work?  One study showed that after a median of 19 months of therapy, new or worsening  vertebral fractures occurred in 21 of 448 patients (4.7%) in the placebo group compared with 3 of 444 patients (0.7%) in the 20 mug/day teriparatide group.  This study inferred that the risk of developing a new or worsened grade 3 vertebral fracture was reduced by 86% (P < 0.001) in patients treated with 20 mug/day teriparatide.

Another study showed a reduction in fracture risk associated with previous treatment with teriparatide, 20 and 40 microg, was 41% (P = .004) and 45% (P = .001), respectively, vs placebo. The absolute reduction from the onset of the study to the 18-month follow-up visit was 13% for both doses. However, it was noted that osteoporosis drugs were used by 47% of women during follow-up, with greater use in the former placebo group (P = .04).  It was still concluded that persistent fracture protection of previous teriparatide therapy was evident.

While this drug sounds promising, the 5 year study results are just coming out.  It will be much longer before all adverse side effects are really know (Vioxx anyone?).  Plus, this drug is expensive and I am not sure if all insurances cover it.   

All day long, I hear my preceptors telling their patients to drink at least 8 glasses of water a day.  I also hear that for every glass of caffeine, they need 2 of water.  So, I began to wonder if all this drinking really is necessary? 

The 8 glasses of water rule began when the Food and Nutrition Board recommened approximately "1 mm of water for each calorie of food" which would average about 64 to 80 ounces a day.  However, the next part of the recommendation was "most of this quantity is conatined in prepared food."  So, it seems that America only listened to the first half of this recommendation.

According to Family Practice News, 8 Glasses of Water a Day is no longer the Mantra.  Most healthy individuals remain adequately hydrated by allowing their thirst to dictate their intake. 

Additionally, I found that caffeinated drinks (coffee, tea, and soda) DO count towards your daily total.  Dilute alcholoic beverages as beer also count toward your intake if taken in moderation.  Their diuretic effect has been found to be only transient in nature.

Thus, drinking whenever you are thirsty is an adequate guide of how much your body needs.  Looking at the color of your urine is also helpful.  If you are not taking vitamin B2 (which turns your urine bright yellow), then your urine should be very light yellow.  A deep yellow is an idication that you are not intaking enough.

OK...so 8 glasses is not necessary, but can it be harmful?  According to many experts it can.  "Even modest increases in fluid intake can result in 'water intoxication' if one's kidneys are unable to excrete enough water (urine). Such instances..have led to mental confusion and even death in athletes... and in ordinary patients."

Other disadvantages of a high water intake: (a) possible exposure to pollutants, especially if sustained over many years; (b) frequent urination, which can be both inconvenient and embarrassing; (c) expense, for those who satisfy the 8 x 8 requirements with bottled water; and (d) feelings of guilt for not achieving 8 x 8.

So, let thirst be your guide and do away with the 8 glasses of water a day!!!

A young female patient presented to the office with an acute asthma exacerbation, which she believes was triggered by the cold air.  The patient was also 26 weeks pregnant and has an inhaler at home but concerned about using it during her pregnancy.  In addition, the patient was also very wary about taking any medications during her pregnancy.  Although the use of certain medications should be limited and avoided altogether, it is essential to keep asthma under good control in the pregnant patient in order to avoid maternal and fetal hypoxia.  In fact, it has been shown that persistent poor control of asthma is associated with pregnancy induced hypertension, preeclampsia, pre-term delivery, low birth weight, as well as increased rates of cesarean sections. 

Changes to beta 2 adrenoreceptor responsiveness and the impact of high levels of circulating progesterone in the airways may account for the effects of asthma exacerbations in pregnancies.  My preceptor then explained that inhaled therapies are the first line treatment and studies have shown that they are safe in pregnancies. 

When considering safety and efficacy of asthma treatments in the pregnant patient, is it better to stick with an inhaled corticosteroid or go straight to an oral bronchodilator?   I found a study that compared the effectiveness of an inhaled beclomethasone dipropionate to oral theophylline for the treatment of asthma exacerbation requiring medical attention.  This was a prospective, double-blind, double placebo controlled randomized clinical trial of 385 pregnant women with moderate asthma.  The women were split into 2 groups, 194 in the beclomethasone cohort and 191 in the theophylline cohort.  The results from the study are as follows:

1. There were no significant differences in treatment failure, compliance, or proportion of peak expiratory volume less than 80% predicted.
2. There were no significant differences in maternal or fetal outcomes.
3. However, the theophylline cohort had significantly higher incidences of discontinuing the medication due to side effects and also required serum monitoring.
4. The theophylline cohort also had higher incidences of study visits with forced expiratory reserve volume (FEV1) less than 80% predicted.

The investigators favored the use of inhaled corticosteroids for moderate asthma during pregnancy, as it resulted in improved FEV1 and prevented the potential for discontinuation due to side effects. 

A male quadragenarian presented with lumbosacral back pain of 2 days after intensively working on his hands and knees.  After ruling out other causes of acute back pain -- with history, reflex testing, tandem gait, straight leg test, and the like -- the pathology appeared muscular in nature.

I was wondering which of the following would best decrease his pain and decrease recovery time:

1.) resuming normal ADL's 2.) stretching and strengthening exercises OR  3.) prescribing bed rest (and giving a sick note for work)

I discovered a Helsinki study which divided 186 patients with acute low back pain into those three groups.  The article states patients resuming normal activity fared better than those prescribed bed rest or exercises:

"After 3 and 12 weeks, the patients in the control group had better recovery than those prescribed either bed rest or exercises. There were statistically significant differences favoring the control group in the duration of pain, pain intensity, lumbar flexion, ability to work,... and number of days absent from work."

An AAFP article (and props to the small group that presented LBP in class) has good summaries of methods and treatments of LBP. 

As the study suggests, we told the patient to resume normal ADL's. 

Pharmacologically, we actually prescribed Naproxen and Carisoprodol (Soma), a centrally-acting muscle relaxant much like Neurontin, which the patient has had success with before. 

Take home message: Continue normal daily activities and don't prescribe bed rest for acute LBP!

I am working in a large practice with multiple providers, all of whom seem to take a slightly different stance on the benefit of screening for prostate cancer and which tools they use.  Given that my personality is one that wants a single best answer for a given question, I set out to figure out what the best protocol is for screening so I could go back to sleeping at night.  What I found was even more confusing and frustrating and I instantly saw why everyone in the practice took a slightly different approach to prostate cancer screening.  After sifting through conflicting reports and studies I settled on the literature review compiled by the United States Preventive Service Task Force.  I will try to share with you a simplified version of the evidence I found.

1.  Prostate cancer is a significant cause of mortality.  In fact, it is the second leading cause of cancer related deaths among men in the United States.  In 2002, 189,000 new cases were diagnosed while 30,200 died from it.  

2.  Despite the high ranking among cancer deaths, prostate cancer does not have a very high mortality rate after diagnosis.  The average lifetime risk for American males of being diagnosed with prostate cancer is 15% while the risk of dying of prostate cancer is only 3%.  One study comparing prostatectomy with nothing found that only about 9% of men die of prostate cancer over 8 years if left untreated.  The vast majority of cases are diagnosed in older populations (>75% are over age 65).  This is generally a slowly progressive cancer.  Therefore, men are more likely to die with the disease than from the disease. 

3.  Mortality is more closely related to grade than stage.  Only 5 to 10% of cancers detected by screening are poorly differentiated.  I found no evidence of a relationship between prevalence of tumor grade with patient age.  Mildly to moderately differentiated cancers often take a decade or longer to progress to clinically significant disease.  Therefore, catching the disease early is not as important as just catching it.

4.  Sensitivity of testing is variable.  DRE is limited to examination of posterior and lateral walls of the prostate and detects fewer than 60% of cancers when used alone.  Using PSA with DRE increseases sensitivity (if PSA > 4.0 ng/ml is used, sensitivity is between 63 and 83%). 

5.  Specificity declines with age because BPH and prostatitis cause elevations in PSA and are related to aging.  One study reported that PSA > 4.0 ng/ml is 98% specific in men in their 6th decade but only 81% in men in their 8th. 

6.  Modified PSA techniques including PSA density (the ratio of PSA level to prostatic volume), PSA velocity (the rate of change of PSA level through time) and percent free PSA (level not bound to serum protein) do not improve diagnostic accuracy.

7.  Once an abnormality is detected by screening, you have to do something about it, so a patient gets biopsied and then treated.  The risks and benefits of treatment are a separate discussion but as illustrated above, untreated patients usually die of something else without incurring risks of surgery including erectile dysfunction, urinary incontince, or bowel dysfunction.

8.  Any positive result, be it true or false, may cause undo anxiety and worry and expense on the part of the patient.  This alone is an undesirable patient outcome and may create a reduction in quality of health, especially in the case of false positive results.

So what?  There are several factors that must be considered when initiating a screening program.  The disease in question must have an asymptomatic phase in which it can be detected and there must be a benefit to treating it while in this phase (rather than waiting for symptoms to develop).  The detection of prostate cancer by present screening methods is a bit shaky, especially in at-risk populations, rife with false positives and negatives.  Additionally, there is no clear evidence that early detection of prostate cancer leads to improved outcomes.  Therefore, the USPSTF issues an I recommendation (insufficient evidence to support or refute) for prostate cancer screening.  In conclusion, I am no closer to understanding what the right thing to do is about this matter, but I hope I've given you enough information to counsel your patients and help them understand this confusing issue.

Invasive Pneumococcal Disease (IPD) has been declining in recent years thanks to the widespread use of pneumoccoal vaccines in the pediatric population.  Recently at the clinic I found myself struggling to catch up on current vaccine protocols for infants (not having had pediatrics yet!).  A mother asked about the pneumococcal vaccine for her 1 year old child and the immunization was both recommended and delivered at that visit.

Curious abou the safetly and efficiacy of the vaccine, i searched UpToDate and came up with this report http://www.utdol.com/application/topic.asp?file=pedi_id/4932&type=P&selectedTitle=42~68.  The 23 capsular vaccine is designed to provide immunity against approximately 90% of all pneumococcal species and is recommended for for children ages 2-5, as they are of school age and have sufficient immunological response.

However the common 23 capsular vaccine does not reportedly provide immunity against nasopharyngeal Strep nor does it lessen the incidence of acute otitis media.  It has been reported to reduce the severity of symptoms as well as chronic otitides however.  And in cases of HIV+ children, the vaccine has been shown to be only 25% efficacious vs. 80-95% efficacious in immunnocompetent children.

What this information shows, as well as a report from the Journal of Pediatrics from January 2005 from the Massechusettes Dept. of Health by Hsu, et al (could not provide a hot link, I apoligize.  Try OVID terms "pneumococcal vaccine" + "pediatric recommendations" and limit to ENGLISH and FULL TEXT) is that while regular administration of the vaccine has reduced IPD in children, discretion must be used.  For example, children with sickle cell anemia may also derive benefit from the octavalent vaccine and cultural issues such as ethnicity may also warrant attention.  Hsu et al note a higher proporation per capita of HIV disease in blacks and hispanics in the Bay State, which should give a physician of such patients pause for thought in administering the vaccine, for though it's safety is high, the benefit to such children is reduced and they may need more intesive care with thought towards alternative preventive stratigies.

 

This past week, I learned a new way to "prescribe" exercise to the patients that really needed it badly, suffered from metabolic syndrome, or even diagnosed with a pre-type 2 diabetes condition.  My preceptor brought out his prescription pad and wrote down "walk 2 miles/week" and handed it over to the overweight patient whose fasting sugars were "pre-diabetic."  I asked him why he wasted prescription pad paper on something that could have been verbally instructed, but he said that in addition to verbal advice, a written goal-oriented exercise prescription has been shown to be a useful tool to motivate patients to increase their physical activity.

As far as the evidence based medicine shows, written advice, known as the "green prescription," was shown to significantly increase the recreational physical activity in the patients received both verbal advice and written advice.  This study involved over 450 patients randomized to either verbal advice alone or both verbal and written advice.  Over the next 6 weeks, those that received the "green prescription" increased their physical activity significantly more. 

How about the general practitioners prescribing this "green prescription"?  A study showed that the GP's were comfortable discussing and prescribing exercise and felt that they were a "valuable tool to formalize and document mutually agreed exercise goals."  However, they believe that time constraints were a major reason why this tool has not been in widespread use.

A survey done with GP's in other parts of the world identified some reasons for not using the "green prescription."  Reasons included:  compliance issues, time restraints, and the belief that this may be patronizing or simplistic.  

This intervention with verbal advice and written exercise prescription also proved to be cost-effective in another study.  It was found that cost of converting one additional "sedentary" adult to an "active" state over 12 months would cost only $1,756.  The montly cost-effectiveness ratio for total energy expenditure was about $11 per kcal/kg/day.  So verbal and written physical advice given by GP's is in inexpensive and an efficient way (and also creative) to reduce long-term cardiovascular morbidity and mortality.   

          It wasn't long after multiple willing patients agreed to subject themselves to two DRE's, one from the doctor and one from myself, that I started to question the utility of this exam.  Soon thereafter, I encountered a 40+ year-old patient who was not excited about the prospect of undergoing this examination altogether and decided to forgo it.  Dissatisfied with the lack of EBM-based-encouragement offered to the reluctant patient I decided to attempt to find out for myself some facts about DRE's, PSA and screening for prostate cancer.
            Prostate cancer is a valid concern for the American male with an average of 16% being diagnosed with and 3% dying from prostate cancer, making it the fifth leading cause of death in men over the age of 45.  The risk is significantly higher in black males and those with a positive first degree family history.  The dramatic prevalence of the disease underscores the need to improve our ability to diagnose and treat it early in an effort to decrease the mortality rate.  Unfortunately the jury is still out regarding the utility of screening PSAs and DREs for prostate cancer.
            According to UpToDate ("Screening for Prostate Cancer", sorry that I can't hyperlink this one), "there are currently no convincing data from randomized controlled trials of [prostate] screening that show benefits on morbidity and mortality."  So although a DRE in combination with a PSA may increase the detection of prostate cancer they have not been shown to improve a patient's outcome. The American College of Physicians, the American Urologic Association, the American Cancer Society and others have differing views on whether or not to screen. The U.S. Preventive Services Task Force (USPSTF) doesn't commit to either camp determining  "that the evidence is insufficient to recommend for or against routine screening for prostate cancer using prostate specific antigen (PSA) testing or digital rectal examination (DRE)."
            Therefore, since there are potential negative side effects associated with screening, both mental (i.e. anxiety) and physical via unnecessary procedures, and potential benefits through early detection and treatment (though not clearly proven to be beneficial) it is our responsibility to inform patients of the current debates regarding screening and assist them in making an informed decision based upon their risk factors.  The following recommendations from the Annals of Internal Medicine may be helpful in this process.

"All men who are considering having digital rectal examination and PSA measurement should understand the potential risks and benefits of screening and participate with their physicians in deciding whether to be tested. Before any testing occurs, patients should be fully informed about the following:
1. Prostate cancer is an important health problem.
2. The benefits of one-time or repeated screening and aggressive treatment of prostate cancer have not yet been proven.
3. Digital rectal examination and PSA measurement can both have false-positive and false-negative results.
4. The probability that further invasive evaluation will be required as a result of testing is relatively high (see Table 1 in part II of the background paper).
5. Aggressive therapy is necessary to realize any benefit from the discovery of a tumor.
6. A small but finite risk for early death and a significant risk for chronic illness, particularly with regard to sexual and urinary function, are associated with these treatments (see Table 1in part II of the background paper).
7. Early detection may save lives.
8. Early detection and treatment may avert future cancer-related illness."
Hopefully questions surrounding prostate cancer screening will be answered upon completion of two ongoing clinical trials, the American Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial and the European Randomized Study of Screening for Prostate Cancer. But until their completion we must assist patients in making informed decisions based upon available research.
P.S.  PSAs can be measured immediately after doing a DRE.

 

 

 

A young female patient came in because she wanted to be checked for STI's and pregnancy.  She has had the same sexual partner for several years, and although she does not have other sexual relationships her partner does.  She is worried because she does not want to take birth control and her partner does not like to use condoms.   While the temptation may be to advise this patient to find a new boyfriend, I realized that my responsibility was to provide her with information about all of her options and what she can do to minimize her risk of STI's and unwanted pregnancy.  I had a hard time thinking of what she could do in this situation.  My preceptor told her about the female condom as an alternative to try. 

            The female condom was developed over 10 years ago to enable women to have more control over protection from STI's, primarily HIV.   While there are still studies in progress regarding its effectiveness in preventing infection transmission, it looks promising.  Three studies were done in the field, including a brothel in Thailand, which showed disease transmission rates for the female condom to be as low as for the male condom.  A randomized crossover trial was done in Brazil to compare male and female condoms in which PSA levels were taken in the vaginal fluid after intercourse as a measure of semen transmission.  The rate of low- level semen exposure was higher with female condom use, but the rate of high- level exposure was the same for both.  The authors of this study believed that the low level exposure was insignificant in terms of pregnancy risk and HIV transmission, which requires many copies.  However its risk of other STI's is unclear. 

            In terms of ease of use and comfort, a study showed that both men and women preferred the male condom to the female condom.  However, the author of this study pointed out that the female condom is less commonly used and these results could in part be due to the subjects being more familiar with using male condoms.

            One major pitfall of the female condom is the price- running from $2.50 to $3.50 they are much more expensive than the male condom.  They can be found at many pharmacies or ordered online.  As with any contraceptive method, the clinician should be aware of how to use it and explain it to their patients.

            So although it is not a perfect solution for this patient, I think the female condom is a good alternative for her to be aware of.  Even if it might not be easier or more comfortable than the male condom, it may give her more control if she is not able to convince her partner to use a condom himself.   Although I am not convinced based on these studies that it is as good as the male condom in preventing STI's, it is certainly better than no barrier.  Also, it is made out of polyurethane and not latex, and is allegedly hypoallergenic which may make it a good alternative for some people.  I hope that this patient will use it, but I have a feeling that the high cost may be a deterrent.

Today I met with an extremely friendly young lady who is suffering from a viral URI.  This is not an uncommon thing to happen to me.  This particular woman had several problems which she wished to address while at the clinic, one of which was her depression.  After asking her about the "sigecaps" stuff we all remember from psych, I asked her if she was experiencing any changes in her sex drive.  Her eyes lit up.  She explained to me that her libido was wrecked and that her lack of desire was causing problems for her and her wonderful fiancé.  The depression had improved greatly, though, with the SSRI treatment she was receiving, so she didn't want to switch to another drug.  What to do, I asked myself.  I turned to PubMed, which is a great resource for medical professionals, to find an answer.  I found an article from the Journal of Clinical Psychiatry which addressed the very question I was asking.  The article is a "placebo-controlled, double-blind comparison of bupropion sustained release (SR) as an antidote for sexual dysfunction versus placebo in 42 patients with selective serotonin reuptake inhibitor (SSRI)-induced sexual dysfunction."  This article was really great for me, as Dr. Jones had just talked with us about the possibility of adding buproprion to the treatment regimen of patients on SSRI treatment experiencing sexual side effects.  The authors concluded that buproprion acts as an antidote to SSRI induced sexual side effects, giving patients increased desire to engage in sexual activities, and increased frequency of sexual encounters, when compared with placebo.  The woman left with a prescription for Wellbutrin and a new outlook on life.  So keep this in mind next time a patient reports that the SSRI they are taking is mucking with their libido, they will thank you for it.

   How jealous can a patient make you?  This was the fist thought that crossed my mind when a young adult came to the clinic because he was traveling to the Caribbean for a week right in the middle of a great Northease snowstorm.  He was interested in obtaining any necessary vaccinations as well as malaria prophylaxis. While explaining primary prevention to the patient was necessary, medical prophylaxis is still recommended.  Primary prevention of malaria focuses on preventing mosquitoes from biting in the first place and includes wearing long sleeve shirts and pants, using an insect repellant with DEET, and sleeping with permethrin (insecticide)-treated insect nets.

   One large item of interest about malaria prophylaxis is the fact that the region of travel determines what specific medical regimen is necessary due to different resistances and sensitivities of Plasmodium to the various medications.  The CDC's malaria website has great fact sheets for both patients and providers about malaria prophylaxis and treatment.  The actual CDC prophylaxis page has information on which medication to take, dosing, directions, side effects, and other useful information.  You can also go to the CDC Traveler's Health website, search the specific region of travel, and find a great deal of information about recommendations, precautions, and other relevant information about that area.  In general, patients traveling to Mexico, the Caribbean, Central America, the Middle East, and Eastern Europe should use Chloroquine.  If traveling to Africa, South America, India, Asia, or South Pacific, you need to choose between Atovaquone, Mefloquine, Primaquine, or Doxycycline; these areas have Chloroquine-resistant Plasmodium.

   Regarding one of the prophylactic medications:  One systematic review of Mefloquine trials was performed to determine the efficacy and tolerance to malaria prophylaxis with mefloquine.  It showed that while the efficacy of mefloquine is great, its high side effect profile might hinder use for traveler during long periods of stay.  Common side effects included headache, nausea, dizziness, trouble sleeping, and anxiety.  Also, due to slow elimination mefloquine may stay in the body for many weeks after discontinuance of the drug.  Therefore, it is important to look at the side effect profile of these medications as they are not equal as far as patient comfort level goes.

The Bottom Line:

1. Counsel patients on primary prevention (especially because of #3)
2. Search for the correct region of travel for the specific medical prophylaxis
3. Realize that some meds have greater side effects than others, which might cause the patient to not use them during extended travel.
4. If a patient contracts malaria while laying on a Caribbean beach, switching from pina coladas to gin and tonic because of the quinine content in the tonic water will NOT be effective for treatment!  see here

I saw a patient in the office recently with a history of DM Type 2, hyperlipidemia, and s/p CABGx4.  He has had trouble with taking statins (severe myalgias) and was looking into alternative methods to lower his cholesterol.  He had heard about an herbal supplement called "red rice yeast" (I later found it is actually red yeast rice but he was close enough) and was wondering if we knew anything about it.  He had gone to a health food store and wanted to buy it but the person at the store said that he MUST consult his doctor before taking it.  Way to go health food guy!!  Neither my preceptor nor I had ever heard of anything like that and so we could not help him out.

I started by finding some general information posted by the University of Maryland Medical Center.  Red yeast rice is made by fermenting a type of yeast (Monascus purpureus) over red rice and has been used in China as a food and medicinal since 800 AD.  It has recently been found that red yeast rice contains HMG-CoA Reductase Inhibitors.  Some preparations contain 10 different monacolins, including monacolin K which is identical to lovastatin.  Even with this information the FDA still classifies it as a supplement and not a drug.

Then, I needed to know what sort of human studies had been done on red yeast rice.  One double-blind, placebo-controlled, prospectively randomized 12-week trial published in the American Journal of Clinical Nutrition, looked at 83 healthy subjects with hyperlipidemia.  These subjects took red yeast rice (2.4 g/d) or placebo and followed a certain ADA diet.  At 12 weeks, the group receiving red yeast rice had a decrease in total cholesterol of 40 +-21.  This was significantly more than the placebo group.  The HDL did not change in either group.  As for safety, there were no serious adverse effects in either group and there were no significant differences in liver function tests at 12 weeks.

It is important to keep in mind that red yeast rice is not regulated as a drug by the FDA and different preparations may contain different amounts of active substance as well as byproducts.  This study found that 7 of 9 preparations had measurable concentrations of a toxic fermentation byproduct.  Also, only 1 of the 9 they studied had all 10 monacolins.  This makes it clear that a study done with one preparation may not be generalized to all.

So, what have we learned:  Red yeast rice lowers cholesterol and is safe in healthy subjects for 12 weeks of use.  It appears that red yeast rice might be a good supplementation for someone with hypercholesterolemia who is otherwise healthy and not already on a statin.  On the other hand, it is a little scary to me to be recommending an OTC statin of a potentially unknown dose.  Also, I would be cautious about giving red yeast rice to someone who experienced adverse effects on statins since they both contain HMG-CoA reductase inhibitors.

I want to acknowledge that the outcome of the article (cholesterol numbers) may not at first seem patient-oriented, but I argue that it is. My patient with known CAD is worried about his elevated cholesterol and the consequences this will have on his health.  He is also looking for a way to improve his health without the debilitating side effects he has experienced with certain statins.

A patient presented to the family practice office complaining of a painful rash. It seemed to the patient that the rash appeared on a patient's right arm after he/she was taking a bath to soothe the back pain. The patient claims that the reason the rash appeared on the skin is most likely due to the harsh water. The water softening system was broken in the patient's house for a couple of days and the harsh salts were not filtered out.

Careful inspection revealed the classical dermatomal distribution of the erythematous maculo-papular rash on the patient's right arm and right side of the chest. And surprisingly to the patient was not due to the "harsh water, but due to the reactivation of the varicella-zoster virus.

Both acyclovir and valaciclovir are available for treatment of acute herpes zoster to speed rash healing and decreases pain and ocular complications. Which one of these is a drug of choice?

In a randomized, double-blind, multicenter study, the safety and efficacy of both drugs were compared in immunocompetent adults aged > or = 50 years with herpes zoster. Patients were evaluated for 6 months. The intent-to-treat analysis (1,141 patients) showed:

• The limited oral bioavailability of acyclovir necessitates frequent dosing.
• Valaciclovir for 7 or 14 days significantly accelerated the resolution of herpes zoster-associated pain compared with acyclovir; pain durations were 38 and 44 days, respectively, versus 51 days for acyclovir.
• Treatment with valaciclovir also significantly reduced the duration of postherpetic neuralgia and decreased the proportion of patients with pain persisting for 6 months (19.3 versus 25.7%).

However, 

• There were no differences between treatments in pain intensity or quality-of-life measures.
• Cutaneous manifestations resolved at similar rates in all groups. 
• Adverse events were similar in nature and prevalence among groups, and no clinically important changes occurred in hematology or clinical chemistry parameters.

Both antiviral drugs have demonstrated efficacy in the treatment of herpes zoster in immunocompetent patients. Based on the above study it can be concluded that unless cost is an issue, valacyclovir (1000 mg three times per day for seven days) was associated with more rapid resolution of acute neuritis, a shorter duration of PHN, and had a lower pill burden. If, however, cost is an issue, then ACV (800 mg every four hours [five times/day] for seven to ten days) may be preferred.

 

A woman was seen in the clinic for her Depo-Provera shot. As well as a script for the next dose, the physician wrote a script for a calcium supplement and questioned the woman's calcium intake. I wondered why.

 

One study I found compared the effects of hormonal contraception, including medroxyprogesterone acetate (Depo-Provera) and oral contraception, and nonhormonal contraception on bone density. At 24 months, it was found that women using Depo-Provera and oral contraception had a 5.7% and 3.2% loss in bone density, respectively. The bone density loss noted in Depo-Provera users differed significantly from that seen in both the oral contraceptive group and the control group. The bone density loss seen in the oral contraceptive group did not differ significantly from the control group.

 

Another study examined bone density changes over 24 months in women using Depo-Provera for the first time. A decrease in hip and spine bone density was found after the initial injection with further loss noted with each subsequent injection.

 

Thus it appears the physician was correct in prescribing a calcium supplement for patients using Depo-Provera. The necessary calcium intake changes over time and it a good idea to know how much calcium your particular patient needs. In 1994, the NIH published a consensus statement on the optimal calcium intake for both men and women of various ages. This should be used when recommending calcium supplemention to your patients. 

Folks - I'm enjoying reading your posts.  Sounds like you are all learning well.

A few reminders:

• Your posts won't appear right away.  We have to review them before they appear - so that we can confirm that you are being responsible and not posting PHI in any way.  We'll edit them a tiny bit if necessary.  For example,  I removed references to the exact age of a child on one post .. as it wasn't really necessary to say exactly how old the child was. 
• Anyone can read what you are writing.  Your preceptor, your mom, and your colleagues.  Don't say anything you wouldn't be proud of.
• Try not to just enter the URL of a document like this:  http://www.google.com
• Hyperlink the words like this.
• Thanks and keep up the good work.

     We had a patient that came into our office that said that one week ago, she just felt unwell.  Then, she had developed very painful red lesions on her neck and scalp, just on the right side of her body.  She said that she had a lot of trouble getting dressed and could not wash or comb her hair because it was too painful.  This sounded like a classic case of herpes zoster and this diagnosis is made clinically.  Our patient asked us if she was contagious and could transmit this virus to her children.  The answer is that she can infect someone who is not immune, causing varicella, especially while she has visible lesions.  She also wanted to know what the potential long term complications could be.  Postherpectic neuralgia is one of the most common complications of herpes zoster.  Postherpectic neuralgia is defined as significant pain or dyasthesia 3 months or longer after having herpes zoster and results from damage and changes within the nervous system. 
     The doctor that I am working with mentioned that sometimes anti-convulsant medications could be used to treat postherpetic neuralgia.  I found an article about a double-blind, placebo controlled 7 wek study that looked at the effects of gabapentin in treating postherpetic neuralgia.  The study used 354 people who were given 1800 mg of gabapentin, 2400 mg of gabapentin, or placebo and measured change in average daily pain diary score as a primary outcome measure.  The researchers also examined other outcomes such as weekly sleep interference score.  The results were that pain scores and sleep interference measures showed significant improvement with drug vs placebo.  The difference vs. placebo was 18.8% for the 1800 mg dose (95% confidence interval 10.9-26.8%; P<0.01) and 18.7% for the 2400 mg dose (10.7-26.7%; P<0.01). In conclusion, the article found that gabapentin was well tolerated and was an effective treatment for postherpetic neuralgia.

 

 

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11690735

This past week, we had a patient who I thought had an otitis media (OM), more commonly known as an ear infection.  This made me wonder if ear infections put individuals at risk for deafness or hearing loss, especially children who are more often affected than adults.  In light of this, I also think it is important to know what to tell parents about ear infections.  

In this study, the investigators evaluted the etiology of deafness in 840 deaf primary school children.  At the end of their evaluation, they concluded that preventable ear disease, such as ear infections, are important health problems among children because these diseases can affect the real level and type of deafness, so determining early diagnostic criteria, ear diseases and minor abnormalities is important for early rehabilitation. Infections can also be treated in prenatal or postnatal periods to avoid complications that may lead to hearing loss.

Another article I found discusses the importance of developing a vaccine to help prevent bacterial OM.  OM is the most common childhood illness seen by physicians with bacterial and viral infections being the single most important cause.  The most common bacteria responsible for infections of the middle ear are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis, and antibiotics have been widely used to treat these infections.  Although it rarely results in death, there is a significant level of morbidity and economic burden.  Also, given the high prevalence of this disease and the increasing incidence of microbial resistance to antibiotics, there is a need to develop alternative therapies such as vaccination.  An efficacious vaccine would require combining protective protein antigens from all three causative bacteria listed above, and a combined bacterial-viral vaccine formulation would produce the most profound and sustained impact on reducing the incidence of OM.

My third patient of my first day was diagnosed with bronchitis and was sent home WITHOUT antibiotics. My preceptor then proceeded to show me a folder with notes she has kept from visits to urgent care by her patients. Diagnosis after diagnosis was bronchitis and treatment after treatment was antibiotics. Is this good medicine?

 

My preceptor feels very strongly that antibiotics are not indicated in acute bronchitis unless the patient has been having symptoms for more than 3 weeks. Why?   According to AAFP, up to 95% of upper respiratory infections are viral. Moreover, most will resolve on their own and antibiotics have not been shown to shorten course of illness or provide symptomatic relief.  So why do practioners prescribe antibiotics to patients? Many argue its to satisfy demanding patients requesting antibiotics. One study found that significant associations with antibiotic use were found for geographic location and number of patients under care. On the other hand, he use of diagnostic tests significantly lowered the risk of prescribing antibiotics.  Appropriateness of antibiotic prescription was reported in 39.0% of cases, with geographic location, physician's gender and diagnostic tests being the factors more predictive of appropriate antibiotic use. There is still excessive antibiotic use for ARI and therefore, effective strategies for changing diagnostic and therapeutic behavior are needed.

 

Furthermore, there are significant dangers to over-prescribing antibiotics. One study found that the emergence and spread of resistant bacteria are related to antibiotic use on an individual and on a community level. Most respiratory tract infections are self-limiting conditions, and recent evidence shows that antibiotics only slightly modify the course of most respiratory tract infections. The practitioners should focus on patients with more severe symptoms who might benefit more from antibiotic treatment.

 

How will this help you with your patients? By explaining to your patients that is not efficacious, cost-effective, or safe (ie-increasing resistance) to prescribe antibiotics, you can help your patients and the rest of the population by maintaining our current antibiotic efficacy and keep the cost of medical care down. Patient education is always beneficial (and maybe they won't leave the office angry and go to urgent care to get abx?)

 

My third patient of my first day was diagnosed with bronchitis and was sent home WITHOUT antibiotics. My preceptor then proceeded to show me a folder with notes she has kept from visits to urgent care by her patients. Diagnosis after diagnosis was bronchitis and treatment after treatment was antibiotics. Is this good medicine?

My preceptor feel very strongly that antibiotics are not indicated in acute bronchitis unless the patient has been having symptoms for more than 3 weeks. Why?   According to AAFP,up to 95% of upper respiratory infections are viral. Moreover, most will resolve on their own and antibiotics have not been shown to shorten course of illness or provide symptomatic relief.  So why do practioners prescribe antibiotics to patients? Many argue its to satisfy demanding patients requesting antibiotics. One study found that significant associations with antibiotic use were found for geographic location and number of patients under care. On the other hand, he use of diagnostic tests significantly lowered the risk of prescribing antibiotics.  Appropriateness of antibiotic prescription was reported in 39.0% of cases, with geographic location, physician's gender and diagnostic tests being the factors more predictive of appropriate antibiotic use. There is still excessive antibiotic use for ARI and therefore, effective strategies for changing diagnostic and therapeutic behaviour are needed.

Furthermore, there are significant dangers to over-prescribing antibiotics. One study found that the emergence and spread of resistant bacteria are related to antibiotic use on an individual and on a community level. Most respiratory tract infections are self-limiting conditions, and recent evidence shows that antibiotics only slightly modify the course of most respiratory tract infections. The practitioners should focus on patients with more severe symptoms who might benefit more from antibiotic treatment.

How will this help you with your patients? By explaining to your patients that is not efficacious, cost-effective, or safe (ie-increasing resistance) to prescribe antibiotics, you can help your patients and the rest of the population by maintaining our current antibiotic efficacy and keep the cost of medical care down. Patient education is always beneficial (and maybe they won't leave the office angry and go to urgent care to get abx?)

Atrial Fibrillation is common and sometimes patients will not even know they have it.  This was the case over this past week when a middle aged gentleman came in for his first physical in several years.  As is customary for this age gropup, a routine EKG was obtained and the patient was found to be in A Fib.  Upon seeing this EKG, the physician asked me what should we do for this patient. This article (link fixed) discusses the recommendations for treatment of A Fib.  The article states that rate control with chronic anticoagulation is more effective than rhythm control.  The article recommends  using atenolol, metoprolol, diltiazem or verapamil for rate control as opposed to digoxinn because digoxin is only good at rest where the others are also good during exercise. DC cardioversion and conversion with medications are both appropriate options. Finally, most patients converted to sinus rhythm do not need placement on rhythm maintenance because the risks outweigh the benefits.  I feel that this article is helpful in that it gives a pretty clear picture of what should be done for a patient with this diagnosis.  Most can easily make the diagnosis based on EKG findings, but actually knowing what to do from there may not be so easy.  I feel that this article gives us some direction in where to go once the diagnosis has been made.

My office does a lot of Pap smears.  They use lubrication on the speculum for all woman, regardless of their age.  In my GYN outpatient, it was beat into my head not to use lubrication on the speculum as it interferes with the pap results.  I was taught only to run warm water over the speculum.  So, even though my FP doctors insisted it didn't interfere with the results, I was very hesitant. 

I found an interesting article in the Journal of Family Practice studying water vs. gel lubricant in a retrospective review of medical records.  It included 615 women, 50 whom were pregnant, 49 that were menopausal, and 42 that had undergone a total hysterectomy.  They concluded that a thin coat of water-soluble gel applied to the outside of the speculum did not affect either the adequacy or the interpretation of the cytology.  The study also argued that use of lubrication may increase compliance if discomfort is minimized.   Overall, the make the following recommendations:

PRACTICE RECOMMENDATIONS

• Gel should be considered a viable option in obtaining Pap smears to ease insertion, minimize discomfort, and perhaps help maintain regular interval sampling compliance. Physicians choosing to use gel should be careful to apply only a thin layer to the outer blades of the speculum.
• Because approximately two thirds of false-negative smears are related to inadequate sampling, be sure to obtain cells from the transformational zone, where cancer is known to develop.

Then, I wondered if the recommendations in FP journals differed from OB/GYN journals. I found they did not differ.  For example, in Obstet Gynecol, five clinics to water-soluble gel or water only lubrication for cervical cytology collection in a randomized, double-blind study.  It was concluded that using a small amout of water-soluble gel lubricant on the outer surface of the bottom blade doesn't affect cervical cytology results in women.

One additional article seconds the idea that many women avoid annual pap smears for fear of pain.  So, I guess since the lubrication doesn't affect pap smear results, it should be used in all women!!!

 

  
   A middle-aged women presents to the clinic with a two week history of plantar heel pain.  The pain is partially relieved with ibuprofen.  She denies any previous history of similar pain or injury.  Suddenly she realizes that the pain started right about the time she got her new (poor quality) high-top work shoes. Hmmm...

For more information about Plantar Fasciitis, eMedicine has a great summary of the condition.

I am working in a region (on planet Earth) that hosts a large number of retirees and thus I see many creatures that may or may not be Homo sapiens of advanced age in the practice (also on planet Earth) on a daily basis.  One very common ailment that I have seen in many of these same creatures at some point in the last three thousand years is hypertension. 

Diagnosing hypertension in the elderly may be trickier than it sounds.  One might think that taking an office BP of 170/70 would be sufficient.  If one did that, one would be wrong.  According to an article taken from the American Academy of Family Physicians (AAFP) website, BP must be determined by the average of at least two measurements at two or more office visits.  The patient should be seated comfortably whenever BP is measured for consistency and accuracy.

Once you have determined that your patient's BP is consistently elevated, you have to decide how to treat.  The challenge of treating older people who already take 10 medications per day is that they often don't want number 11 (especially when they are asymptomatic) so you have to convince them it's a good idea.  If they are resistant to adding a medication (lifestyle modification first, then thiazides, then B-blockers, then ACE/ARB or Ca-channel blocker) you can tell them that controlling systolic BP significantly reduces risk for morbidity and mortality due to MI and stroke.  When they agree to be treated, start one medication and titrate up to the maximum dose before adding another medication.  Once you have maxed out three meds, you've done pretty much all that is indicated. 

And even if you have got your patient on maximum doses of everything in the PDR and their office BPs are consistently 170/70 in the office, there are still potentially confounding causes other than true hypertension that result in an elevated BP: white coat hypertension and pseudohypertension.  The first is relatively easy to diagnose: teach the patient to monitor BP at home and find out what happens.  The second is a little trickier to confirm and very common in the elderly.  PseudoHTN occurs when significant atherosclerosis results in calcified arterial walls that do not compress with the BP cuff -- intraluminal pressure may be WNL but the systolic reading may be 180 or higher.  The significance of these apparently refractory cases of HTN may be that the patient's "HTN" is treated aggressively based on faulty data, therefore the patient may experience increased episodes of orthostatic hypotension leading to injury or death from falls, car accidents, etc.  Therefore, it is vital to ask patients about symptoms of orthostatic hypotension, especially when you are beginning or altering their therapeutic regimen. 

Hypertension is an extremely common problem in the US that is grossly undertreated.  Screening in the primary care setting and appropriate management are vital for patient mortality and overall quality of life (nobody wants a stroke that leaves them hemiparetic).  There is a lot of information out there but I encourage everyone to skim through the article linked above -- it's short, to the point, and very readable.  In closing, I want to wish you good luck with the rest of the rotation and I hope all of you are having fun. 

A concerned parent who had brought their child into the office for a checkup expressed concern about the possibility of a child developing autism after receiving the MMR vaccine.  They wanted to know if I could give them any information that proved the MMR vaccine was safe, because they had heard conflicting reports.  A literature search revealed the following article.

This retrospective cohort examined children born in Denmark from January 1991 to December 1998.  The MMR status of children in the study was obtained from the Danish National Board of Health while information on the child's autism status was obtained from the Danish Psychiatric Center Register which contains all diagnostic information from psychiatric hospitals, wards, and outpatient clinics.  The study showed that of 537,303 children, 440,655 children had received the MMR vaccine.  316 children with a diagnosis of autism and 422 with a diagnosis of other spectrum disorders were identified.  After adjusting for confounding variables, the study concluded that the risk of autism and other spectrum disorders was not increased in vaccinated vs unvaccinated children (relative risk 0.92 vs 0.83 - both at 95% confidence intervals).  No association was found between the age at vaccination, time after vaccination, or calendar period at the time the vaccination was received and the development of autism.  This article provided strong evidence against the MMR vaccine causing autism.

Knee pain is a common office complaint, which I first handedly witness during my first week in the clinic.  I had seen 6 consecutive patients in one day, all complaining of knee pain.  Most of the complaints were due to work related injuries, accidental falls, and joint pain in the elderly.  However, I did have one young patient who stated she might have strained her knee while running.  She has been running for many years and is the only type of exercise that she enjoys.  She runs 3x/day, which has kept her blood pressure in good control as well as increasing her stamina.  She emphasizes that running is the only form of physical activity that she does.  After examining the patient, it was determined that she had a mild muscle strain.  We relayed the importance of proper stretching prior to running, recommended Naproxen for the pain, but I also wanted to look for evidence-based data that demonstrated beneficial, preventive measures.  This led me to investigate the data out there on knee injuries pertaining specifically to runners.  I found two articles that suggest wearing foot orthotics and a knee brace can reduce knee injuries and prevent the development of anterior knee pain in young runners.  The first study looked at custom-molding of foot orthotics compared to a control condition.  The article found that the combination of medial posting and custom-molding of foot orthotics resulted in a reduction in maximum foot eversion and ankle inversion, while increasing the vertical loading rate.  While this was a small study with only 21 volunteers, the potential for foot orthotics for reducing injuries is encouraging.  The second study focused on wearing knee brace as an effective measure to prevent anterior knee pain.  The study looked at 27 subjects in the brace group and 33 in the non-brace group.  Although the incidence of anterior knee pain syndrome increased as the intensity of the exertion increased, the study found that as a whole, the brace group did comparatively well compared to the control group.  The data suggests that consistently wearing a brace may reduce pain syndrome in young runners.

I saw a young man in the office who recently contracted HSV 2 from a female associate with whom he had recently enjoyed several intimate encounters.  He was unaware of said woman's condition, failed to adequately protect himself, and had an outbreak shortly after the aforementioned adult activities.  He expressed an interest in starting on Valtrex because he saw a commercial on TV about daily therapy to help decrease the frequency of future outbreaks.  I agreed that his decision was a sound one, and told the patient how I felt.  He wanted to know if he could engage women in intercourse in the future without transmitting to them his newly acquired condition, as the commercial he saw reported that viral shedding may occur even in the absence of symptomatic lesions.  I knew he needed my help, so I went to computer to analyze some patient oriented evidence that matters to this young man in need.  I will share this information with you now, such that future patients/students/physicians might benefit from my labors.

This article followed 1484 immunocompetent, heterosexual, monogamous couples: one with clinically symptomatic genital HSV-2 and one susceptible to HSV-2 for eight months.  The effected individuals were treated with 500 mg of valacyclovir once daily or placebo.  The research team hypothesized that once daily valacyclovir treatment would decrease viral shedding and thus decrease the transmission rate among the couple, when compared to the placebo group.  This hypothesis proved to be true and differences in viral shedding and transmission were significantly significant.  Viral shedding, mearsure by the presence or absence of HSV 2 DNA in genital secretions daily, was detected 2.9% of days in the valacyclovir group, versus 10.8% of the days in the placebo group (p<0.001). Transmission was measured a 1.9% in the treatment group versus 3.6% in placebo treated patients (p=0.04).  Thus I informed the patient that, even though viral shedding and transmission of HSV-2 can only be prevented by abstaining from intercourse, he could reduce the risk by taking daily valacyclovir 500mg.  I instructed him to always discuss his HSV with potential sexual partners, and to always use a barrier type contraceptive.

This week I saw a preteen patient for a Well Child Visit.  There were no other complaints except for a recurring, persistent headache.  The patient had inconsistent relief with Tylenol.  There was also some blurry vision during the headaches, sensitivity to light, nausea without vomiting, and localization was mostly to the occipital region, less in the frontal region.

Migraine and tension headache was high on my differential (malignancy flashed before my mind but I thought otherwise without neuro deficits).  The symptoms sounded more migraine and less tension.  Treating migraines in adults I knew at least a little about, however in the pediatric population I was lost.

I came across this article (Go through Schaffer for the full article, pay attention to the first table).  The article  evaluates acute episodic treatment primarily, preventative measures are inconclusive.  Summarized the article states that over the age of 6 ibuprofen and acetaminophen worked over placebo.  In children over 12 sumatriptan, in the form of nasal spray, was better than placebo.  Although triptans are often indicated in adults they were found inferior to the aforementioned therapies.  Again although prophylactic treatment is available in the form of flunarizine, it is inconclusive.

The bottom line here is to:
1) accurately assess migraine in children
2) accuratley treat migraine in children; i.e. adult treatments are not equivocable across the age spectrum
3) not forget supportive therapies such as sensory deprivation and even a cool cloth to the forehead.
4) consider behavioral therapies

I saw a patient in the office with persistent trochanteric bursitis.  For about 2 months, she had tried NSAIDs and hot/cold packs with minimal relief.  So, my preceptor decided it was time to try a corticosteroid injection into the bursa.  I was curious about how long her relief from the injection would last.  I found a very helpful article on this topic.

This study looked at 75 patients with trochanteric bursitis.  They were divided into three groups, each receiving a different dose of betamethasone and the same dose of lidocaine injected into the bursa.  The outcomes of the study were severity of pain and functional limitation due to pain (very patient oriented!).  77.1% had improvement in pain at week 1, 68.8% at week 6, and 61.3% at week 26. 

I came across an interesting fact in a different article.  They found that some women with greater trochanter bursitis actually present with chronic low back pain and sciatica, and corticosteroid injection into the bursa may help resolve their symptoms.  Keep that in mind next time you have a patient with low back pain.

Take home message:  About 60% of patients with trochanteric bursitis will have continued symptom improvement 26 weeks after steroid injection.  

For some good, brief info on trochanteric bursitis and other musculoskeletal d/o, check out these guidelines . 

A child came to the office with a sore throat.  His throat is erythematous with no exudates.  He has cervical lymphadenopathy.  He has no cough and no known exposure to strep pharyngitis.  Is this strep throat? 

For a useful  guideline for evaluating the likelihood of strep throat based on clinical findings click here.

We did a rapid strep test in the office, which came back negative.

Most pharngitis is viral and requires no treatment.  However, given the potential complications of untreated strep throat it is important to make this distinction. 

The gold standard for diagnosing strep throat is throat culture.  However, this takes 24 hours and most patients want to know right away whether they have strep or not so they can begin antibiotics if needed and get to stay home from school.  So many practitioners use the rapid strep antigen test, which gives results right away. 

The sensitivity of the rapid antigen testing used to be relatively poor compared to culture.  However, the rapid detection has improved.  Do patients with negative rapid test results need to be cultured?

A retrospective study was done by studying laboratory records of patients with rapid strep testing in an office setting from 1996-1999.  There were 11,427 rapid tests done, with 26.6% positive and 73.4% negative.  Of the negatives, 98% were sent for culture, yielding only 2.4% positive results. 

The rapid strep tests are better than they used to be, and it is now usually not necessary to follow up a negative test with a culture.

(sorry, but the link to the study can only be done through Albany Med)

 

I've never been particularly good at infectious disease type questions on exams and the same holds true in the clinical setting--especially when it comes to management.  So far in this FP rotation I've had plenty of opportunity to exercise my inadequate knee-jerk reaction to ID cases which has given my preceptor plenty of opportunity to straighten me out.

This case is one such example of a patient with respiratory symptoms consistent with acute bronchitis that raises a question of to treat the underlying infection or just let it run it's course and treat the symptoms:

A 45 year-old married white female presented to our clinic complaining of a six day history of a heavy, productive cough that has neither been resolving nor worsening over the past two days.  The onset of her symptoms were sudden as she first noticed them upon awakening first thing in the morning last week.  The second day she noticed that her cough began bringing up clear and green-colored phlegm.  Associated symptoms include a mild sore throat that was present from the beginning but resolved after day three and loss of her voice for part of the second day.  The patient denied any chest pain, dyspnea, fever, chills, nausea, vomiting or diarrhea.  Sick contacts include two coworkers that had cold-like symptoms two weeks ago.  She is a life-long non-smoker and only rarely uses alcohol.  The physical exam was unremarkable aside from faint rhonchorus breath sounds and occasional coughing.  Otherwise HEENT were all clear.

In cases such as these it is not always clear whether to treat the patients with antibiotics or not.  My preceptor told me that if he feels that a patient's symptoms are severe enough, he will cover the patient with antibiotics just to be safe, however, more often than not these kinds of patients don't need antibiotics and probably shouldn't receive them.  In this particular patient's case we opted to treat the patient with azithromycin to cover many of the possible bacterial etiologies of acute bronchitis.  But was this what the evidence indicated would be best?

I did some literature searches and discovered that indeed the most common etiologies of acute bronchitis are viral and not bacterial.  Therefore, it is assumed that coverages with antibiotics would do little to change the outcome of the infection.  One article in particular that was published in Lancet in 2002 (Azithromycin for acute bronchitis: a randomised, double-blind, controlled trial) investigated this issue by randomly treating 220 individuals with acute bronchitis with either azithromycin or low-dose vitamin C for 5 days in addition to dextromethorphan and an albuterol inhaler.  By day 7 the two groups of patients were indistinguishable with respect to health-related quality of life and similar in frequencies of adverse effects of treatment.  The results of the investigation suggested that there was no benefit to treating most cases of acute bronchitis with azithromycin when compared to low-dose vitamin C.

In light of this study and other suggestions in the literature it appears that antibiotic treatment (at least azithromycin) of acute bronchitis is often not necessary and will likely only waste precious health care dollars.  This recent experience in the clinic and the literature I have reviewed has been helpful in teaching me how to approach the patient with acute bronchitis and how not to panic every time I hear a patient cough.

Pt came to the office earlier in the week complaining of 10 days of a dull constant pain in the maxillary sinus area. He/she did not have any other associated facial pain, teeth pain, purulent discharge or fever.

 Sounds like sinusitis to me. But knowing when to treat with antibiotics or just symptomatically is really important. Being one of the top ten diagnoses in outpatient practice, if everyone just throws antibiotics at every acute sinusitis, resistant bacteria may become a problem. Further, most acute sinusitis infections are viral reemphasizing the fact that antibiotic use has to be carefully administered.

 Unfortunately, differentiating between bacterial versus a viral infection is not easy in the initial presentation because there is a lack of specific clinical features and effective diagnostic tests distinguishing the two.

 
The following articles discuss what symptoms may help separate viral versus bacterial sinusitis, how to manage the disease and what treatment options are available.

 Annals of Internal Medicine

American Family Physician

 
Key distinguishing symptoms of bacterial etiology: presence of symptoms for at least 7 days/ purulent nasal discharge along with maxillary tooth or facial pain (especially unilateral)/ worsening of symptoms after initial improvement.

 The pt symptoms described above was considered viral in nature and was treated symptomatically.

 By learning a few diagnostic features that distinguish acute viral versus bacterial sinusitis we'll be helping to prevent resistant infections for this common diagnosis.

127. It was the first fasting blood sugar over 126 in an older patient with a history of pre-diabetes. Granted, 127 is not off the charts, it's not even diabetes yet, but type 2 DM typically has an insidious onset and frequently has already incurred some silent damage by the time it presents clinically. My preceptor and I discussed what would be the most appropriate next step. By this time I'm thinking "here's my chance", 2 fasting sugars>126 = DM, this patient is likely heading that way, let's get more blood work, maybe diagnose him, encourage diet and exercise, possibly start him on a low dose oral hypoglycemic agent, get him to the eye doctor, check out his feet, start him on a statin, an ACEI, aspirin, check a microalbumin, and send him to a diabetes educator. I was thinking that if this patient does have diabetes (the sixth leading cause of death in America), taking some aggressive action now could reduce this patient's risk for serious comorbidities in the future and potentially help him retain his good health for what may easily be his remaining 10-20 years of life. My preceptor disagreed. "This is a healthy guy", why scare him and complicate his life by throwing all this at him now. Last year his fasting blood sugar was 123, we'll tell him that it's essentially unchanged and check him again in a year.

I'll cut to the chase. A study done on insulin-dependent diabetics showed that aggressive glycemic control, not to beat a dead horse, "delays the onset and slows the progression" of nephropathy, neuropathy, and retinopathy related to diabetes. It also led to 2-3 times the "normal" rate of hypoglycemic episodes. Bottom line, while you don't want to go sending patients to the emergency room by overtreating their DM, patients should know that if their blood sugar is consistently uncontrolled that they risk damaging their eyes, kidneys, nerves, and heart and possibly dying prematurely as a result. They should know that good control of their blood sugar (via diet, exercise, and medication) can limit the harmful affects of their disease and prolong their life.

Because heart disease is the leading cause of death in the US, costing more than $350 billion dollars in 2003, screening for this chronic disease may prove to play an important role in decreasing its mortality rate as well as the costs in today's medical world. Whether it is smoking, high LDL chol levels, family history of early heart disease, HTN, or diabetes, it seems that every patient we see fits the picture of one or several typical risk factors that contribute to the development of this disease. Mortality from CHD has considerably diminished since the 70's and there are still an increasing number of clinicians that recommend screening for asymptomatic CHD screening It has been documented that asymptomatic adults definitely benefit from risk factor modification with relation to their degree of CHD risk (RF modification). In addition, there were instances in our clinic as well as others around the country where patients would request screening for themselves. It may be the patient's belief that early detection of CHD "saves lives," but the stress test, also known as the exercise tolerance test (ETT), is a common request from patients. I learned that there are several factors to consider before sending the asymptomatic patient to a cardiologist for a stress test even if he/she has no risk factors; these issues include cost-effectiveness, patient satisfaction, and health maintenance. The idea behind early detection of CHD is that by identifying patients at early stages of the disease may improve prognosis (early screening), and especially prevent clinical scenarios such as acute MI, unstable angina, or sudden cardiac death. It has been proven that the presence of asymptomatic CHD during an exercise tolerance test would predict an increased risk of an unexpected coronary event within 10 years (ETT). However the controvery on the use of the exercise tolerance test (ETT) in screening asymptomatic patients has been surrounding the predictive value of this test and its low pretest probability. The sensitivity of ETT for predicting CHD events from 3 to 12 years in the future ranges from 40% to 62%. The PPV of ETT ranges from only 6 percent to 48 percent (PPV).  Specifically in the population I was studying, the yield of ETT in detecting severe CHD in asymptomatic middle-aged men is estimated to be merely 0.5 percent (ETT middle-aged men) and the PPV for future CHD events in cohort studies also falls into a range of only 6 to 48 percent. With respect to the asymptomatic patient, those at higher risk for CHD events have a higher prevalence of severe CAD, therefore the positive results on ETT would obviously be more likely. However, it is uncertain whether this increased PPV increases the detection of people with severe CHD to an degreee that invasive procedures such as PTCA or CABG would be of any benefit (mainly mortality). According to the U.S. Preventive Services Task Force (USPSTF), it is negatively recommended to use "routine screening with resting electrocardiography (ECG), exercise treadmill test (ETT), or electron-beam computerized tomography (EBCT) scanning for coronary calcium for either the presence of severe coronary artery stenosis (CAS) or the prediction of coronary heart disease (CHD) events in adults at low risk for CHD events." USPSTF This was because the USPSTF found limited evidence that ETT could detect asymptomatic adults at increased risk for CHD events apart from the usual CHD risk factor classification. And because false positives could potentially cause harm (causing an unneccessary and expensive intervention cascade), and exceeds the potential benefits, it is a practice that is statisically not satisfying USPSTF2.  Besides any false-positives that this test can provide, there was no other documented potential harms of this screening tool. However, we cannot forget that the ETT has been a cornerstone of detecting heart disease in our symptomatic population and it may still be unclear of the benefits it serves as an early clinical screening tool in the asymptomatic patient.

How important is exercise? I had a patient in his fifties who was diagnosed with diabetes about 2 years ago. I wanted to relay to him the importance of exercise on increasing his life span.

I found an article discussing the decrease in mortality among diabetics when walking over 2 hours/week. This study sampled 2896 adults and controlled for sex, age, race, smoking, comorbid conditions, and BMI. Lowest mortality rates were for those who walked 3 to 4 hours/week and for those who reported moderate increases in heart and breathing rates. One death per year may be preventable for every 61 people who walk at least 2 hours per week.

Take home messages:

• moderate increases in heart rate and respirations seems to be more beneficial than strenuous activity. -
  
• Anything over 2 hours per week seems to decrease a diabetic patient's risk of death.

Very exciting being thrown into the lion's den. On my first week my attending said "there's a patient in room 6, go work them up. We'll see if you get it". As the young female patient presented with chest pain, a differential a mile wide and written on the chalk board of ME-500 flashed across my brain, but the post-prandial, retrosternal burning quality of the pain, associated with nausea helped me narrow the differential rapidly. Having arrived, at the satisfaction of my preceptor, to a fairly solid piece of ground, namely that of heartburn, a discussion of intervention ensued. When treating any disease, is it medically appropriate to begin with lower doses or less efficacious therapy and titrate up until symptomatic relief is achieved or is it better to use larger guns, rapidly control the Sxs and then titrate down to the barest dose necessary? In this instance, given the disruptive nature of this woman's complaint we opted to use a high dose PPI (Protonix) instead of low dose PPI or an H2 blocker. This article  tested this question in a head to head prospective comparison of omeprazole and ranitidine. The study found that this specific PPI has equal safety and therapeutic efficacy vs. ranitidine but may achieve greater efficiacy potentially through easier (qD) dosing regimens (thereby improving adherence). While specific therapies for specific ailments in different patients clearly require individualized thought by the physician, the treatment of mild to moderate GERD seems one instance where the "big guns" may safely be brought out as first line therapy for rapid control of disease and symptomatic relief.

After a long day of interviewing patients, I was relieved to review the chart of the last patient my preceptor and I were to see and read that her appointment was to review her blood pressure and write prescriptions for medications she was taking for osteoperosis and urinary incontinence, respectively. I viewed the vitals taking by the nurse and was happy to see that her recorded BP was well within the accepted range. I then thought to myself "What a great way to end the day - with such as straightforward patient". These are words I hope to never utter again!

While interviewing the patient, I inquired about the medications she was currently taking.  While answering my questions, she mentioned the medication that she had been taking for urinary incontinence and noted that it had not been as effective as it had been in the past. She noted that in the past few months, she has experienced occassional episodes of incontinence despite regularly taking her medication.  At this time, I took the opportunity to ask her about other symptoms such as dysuria, increased frequency, increased urgency, and hematuria - in order to rule out a UTI that we've all heard over and over and over again are so prevalent in the elderly population.  She denied all these symptoms and said that she did not believe that the incontinence was significant enough to worry about or tell the doctor. (WHEW!! Close call there - or so I thought).  While presenting to my preceptor, I mentioned the patient's reported episodes of incontinence despite her medication and thoughts that a change in dosage or medication may be in order.  I then told him that the patient denied other urinary symptoms (i.e. dysuria, increased frequency).  However, my preceptor decided that it would be best to still obtain a urinalysis in order to more definitively rule out a UTI and because he was aware of her history of UTI's (a piece of history I did not obtain from my encounter with the patient).  Sure enough, the results of the U/A taken showed that the patient's urine was positive for nitrites and large amounts of leukocytes and my preceptor wrote her a prescription for Bactrim. So a "routine" blood pressure follow up ultimately became an opportunity to treat a UTI.

But wait a minute! When did urinary incontinence become a presenting symptom for a UTI?  I thought we had learned to ask about dysuria, frequency, and/or urgency in order to work up a possible UTI?  This experience made me wonder how common urinary incontinence is associated with UTI's - especially elderly women.  I found a study that observed the frequency of UTI's in healthy post-menopausal women.  The results of the study showed that an increased risk of UTI is associated with postmenopausal women with a history of UTI and those who experience urinary incontinence - with history of prior UTI associated with the highest observed risk.

For those who are interested in more information on UTI's or would like to refresh their memory on information learned in the past, this page should be helpful. ( I apologize for the length of the page, but a menu bar is located on the left hand side of the page with links to each specific topic addressed)

Based on this experience, I will never ever take a patient encounter lightly again and I will make sure to keep a UTI in mind when dealing with patients in the future who complain of incontinence.   

Did Dr Forman teach you how to make an entry?  He didn't? 

I'm not going to teach you how to do it either ... go watch the tutorial right now.  (for some reason - it only works if you click the url .. then let it load .. THEN "reload" the page by clicking the reload/refresh button in your browser. 

• Welcom, folks.   I'm sorry that I couldnt be there last week.  
• This post is a little reminder about the exercise - with some instructions on how to make your posts, how to grade your colleagues, etc.

• Recall that this exercise is for you to find and describe an article that relates POEM to your colleagues.

  Patient Oriented Evidence (that) Matters.

  So .. when I score a post, I consider the following:

  • 3  stethoscopes  for good, interesting writing and efficient use of hyperlinking.  This includes accurate analysis of the article (you interpret it correctly) and describe it well.   The useful article will provide us with RELEVANT and VALID information with little work.
  • 1 stethoscope for Patient Oriented information.  This means I can explain it to grandma -- and that she will think it's important.  Example: an article that describes lower risk of death for treatment of hypertension with beta-blockers.  Death is a patient oriented outcome.  Example of something that is NOT patient oriented:  a study that demonstrates lower LDL with statin use.  Get it?  Grandma doesn't know or care about her LDL.  LDL is the intermediate outcome.  She cares about death, or MI or stroke.   A medication that lowers LDL by 600% but caused liver facilure and kills 80% of those who take it would look GREAT if we look at the LDL .. but would look pretty bad if we look at how many patients are alive at the end of the trial.
  • 1 stethoscope for a study that presents Evidence that Matters.  Is the study relevant?  You don't have to say "this study is relevant because ... "  (so please don't) ... The reader should be able to interpret relevance easily.  In general .. this means that the topic is relevant to the practice of family medicine, and to the question you have posed

  As you see - I'm heavily weighting the quality of writing and presentation.  If you don't write something well - the readers won't read it and your efforts will be wasted.  Patient Oriented Evidence is also important - as it's a core component of what we're trying to teach you: a method of discriminating between information that is important and relevant to your patients .. vs information that may be interesting .. but may not be relevant or important.

•