How often should women be screened for cervical cancer?  We had a 33 year old patient come in this week for her annual pap and pelvic exam.  She is not currently and has never been sexually active.  She has never had an abnormal pap with her last one being 1/2004.  We told her that if her last two paps were normal, she really only needed to get them every 2-3 years instead of annually.  However, she decided to go ahead and have it done since she was already in our office and since she she'd had them annually in the past.

This interaction caused me to wonder about women's perceptions of pap smears and why this patient chose to go ahead and have it done even though we spent a fair amount of time explaining to her why it was unnecessary.   One study looking at women's perceptions about pap smears showed that many women are not open to the idea of reducing the frequency of their annual pap smears.  Some women are distrustful of the motivation behind decreasing the frequency of pap smears.  Others have concerns about the accuracy of the test.

Let's look at the numbers. 93% of American women over age 21 have had at least one pap smear in their lifetime.  Of women with no history of abnormal smears.  55% have an annual pap.  17% are screened very two years, and 16% are screened every 3 years. 

Take a look at ACOG's recommendations for cervical cancer screening.  Many women still want to have an annual pap smear regardless of current recommendations.  It is important educate them about current recommendations and address their fears and concerns about no longer having annual pap smears if they are unnecessary.

I have had a couple of patients coming in for GERD, who both tested positive H.pylori in the recent past (last 3 months), and received the appropriate treatment.  But now they were experiencing the same symptoms of bloating, acid reflex and burping, all of which had subsided after the treatment regimen.  They were both frustrated because they had thought that they would be free from these symptoms after they took their medicine, and here they are again after a few months.  
 
Could they have become reinfected with the bacteria, or was the bacteria never eradicated?  Should they go through the same treatment, a different combination or none at all?
 
First off, what are the best (most effective) treatments for H.pylori?  For those taking a PPI plus one antimicrobial, either amoxicillin or clarithromycin, the eradication rate is much lower than other regimens (60 to 85 percent).  Bismuth triple therapy (Pepto Bismol 2 tablets, tetracycline, and high dose metronidazole) is able to eradicate the bacteria at a fairly high rate (78-89%), but has a number of unpleasant side effects that may reduce patient compliance. This is not to mention the increasing metronizadole resistence (around 39%) by H.pylori in the United States.
 
A study found that the eradication rates of 46 percent with PPI-based dual therapy, 70 percent with PPI-based triple therapy, 80 with rantidine bismuth based triple therapy, and 76 percent with quadruple therapy.  Thus they suggest that ranitidine bismuth-based triple therapies, as well as quadruple therapies, are the most effective therapies for treating those who fail a previous attempt.

For the best relief, quadruple therapy seems the way to go.  Another study found that a high dose of rifabutin, pantoprazole, rifabutin and amoxacillin could be used as a re-treatment possibility if the PPI based triple therapy is ineffective.  They were able to show an eradication rate of 87 percent.   An even more effective eradication rate was found (95 percent) with a combination of omeprazole, tetracycline, metronidazole, and bismuth subcitrate caplets.

As for reinfection, this is a possibility, although studies have shown that the reinfection rate is low.  There have been many studies showing a small but significant reinfection rate, such these three, which show a reinfection rate as high as 7.6% in one year of followup, another showing 2.4% per patient year, and a third which has a rate as low as 0% (using quadruple therapy and four year follow up).

So, it is clear from these studies that there are a lot of treatments for H.pylori that have evolved over the years, and the most effective means are still under investigation.   This, it is important for patients (and their physicians) to understand that treatment regimines to eradicate H. Pylori, as with all medications, are not 100% effective.  It seems that if a patient continues to have symptoms after treatment, they are most likely due to treatment failure that reinfection.   These patients that I had met had left their doctor's office with the belief that they would be bacteria free and GERD free once they finished their medicine. 

This week, I met a 27 year old woman who was obese (BMI=40.9). Earlier in the year she had experienced periods that were irregular and lasted > 1 month. She was being treated with Metformin for "hard ovaries". She had been diagnosed with Polycystic Ovarian Syndrome (PCOS). Neither my preceptor nor I had heard of Metformin being used in the treatment of this disease. When we spoke to her gynecologist, he told us that Metformin has been used to increase fertility in women with PCOD as well as other beneficial effects.

A review article discusses the effects of clomiphene citrate (CC), which is the standard medication used to induce ovulation in infertile women. This article compares the effect of CC alone vs. CC and metformin and found that the combination lead to 3 to 4-fold higher rates of ovulation and pregnancy in women with PCOS. This review found that Metformin lead to a 50% increase in ovulation vs. placebo in women with PCOS. There are no studies which directly compare Metformin to CC. Metformin has a number of other beneficial effects on women with PCOS. Patients with PCOS tend to be hyperinsulinemic which leads to hyperandrogenemia. With Metformin, all of the patients became normoinsulinemic. LH decreased while FSH increased leading to spontaneous ovulation. Also HDL and total cholesterol decreased significantly and there was a mean weight loss of 4.7%. An advantage of using Metformin instead of CC is that Metformin favorably affects the metabolic profile of patients with PCOS and may lead to decrease in number of patients with PCOS who will develop Diabetes Mellitus type 2 and cardiovascular disease. CC does not have this effect and has several adverse effects associated with it. CC leads to increased numbers of multiple pregnancies, and in rare cases is associated with ovarian hyperstimulation syndrome. CC thickens the cervical mucus and may impede the passage of sperm. CC also has a negative effect on the endometrium because it is an anti-estrogen. Metformin does not hyperstimulate the ovaries but may exert its effect by decreasing Insulin levels, which leads to a decrease in Androgen levels. Currently some physicians are using Metformin as a primary therapy to induce ovulation in infertile women with PCOS. However, much literature still regards Metfomin as a secondary therapy to be used only when CC fails. It seems as though Metformin should be tried as an initial therapy because it can treat more aspects of PCOS as opposed to CC and it appears to be safer.

I saw 2 cases of bacterial vaginitis (BV) this week, and discussed whether or not or how often the women douched. Both told me they douched more around their periods and after vaginal sex, but neither could tell me exactly how often they douched.

Bacterial vaginitis is defined as inflammation of the vagina secondary to bacterial, fungal or protozoan infection, atrophic changes, dermatitis or mechanical factors (especially foreign bodies like IUD's and sexual trauma). It is estimated that as much as 3% of 18 to 35 year olds have untreated chlamydia infection and over 5% have untreated gonorrhea infections. For this reason (and the serious consequences),  sexually active women presenting with symptoms of discharge, odor, pain or burning on urination or vaginal sex or those who report having multiple sexual partners should be evaluated for BV. After STD's (GC, chlamydia, herpes, HIV and syphilis) have been ruled out and the pelvic exam carried out, the vaginal secretions are examined under the microscope for candida on one slide and clue cells on the other. Trichomonas can also be seen. This site has a good picture of a clue cell and a great outline of BV.

Douching is a common practice among women; but, much like cigarette advertising, there is a disconnect between healthful practices and product advertising. This product claims to be "safe, effective, completely sanitary and disposable." What's wrong with that? http://www.amazon.com/exec/obidos/tg/detail/-/B000095SDP/qid=1107720516/sr=8-3/ref=pd_bbs_3/103-4855332-3995867?v=glance&s=hpc&n=507846 but that's advertising. You have to read the fine print to see the manufacturer's warnings that use of the product has been linked with PID, ectopic pregnancy and infertility.

These authors found that 70% of women ages 15 to 24 report douching sometimes and 28% of 20 to 24 year old women report douching regularly. Douching changes the normal vaginal flora. The authors state that "...repetitive douching with a solution containing the bactericidal agent providone-iodine caused more dramatic short-term and prolonged changes in microflora, allowing an overgrowth of pathogenic organisms that have faster growth rates than Lactobacillus species, the predominant normal vaginal flora. More than half of the adolescent girls and young women who douche use commercial preparations, which contain differing combinations of acidifiers, bacteriostatic or antimicrobial agents, and weak surfactants." The overgrowth of pathogenic organisms leads to BV and more serious conditions like PID, ectopic pregnancy and infertility.

These authors disagree about the change in normal flora. They found that the risk of PID in a 4 year study of 1179 women was not associated with base line bacterial vaginosis (69% of healthy volunteers), age, race, education, level of income, smoking, sex during menses, condom use or a history of STD or PID. Only women who had a baseline vaginosis AND 2 or more sexual partners in the previous 2 months were significantly more likely to develop PID. "An absence of hydrogen peroxide-producing lactobacillus was not associated with PID, even among the various subgroups. A baseline diagnosis of G. vaginalis or Gram-negative rod growth above 4 had no association with PID except in the subgroup of women who reported 2 or more sexual partners in the previous 2 months."

What about women who have sex with other women (WSW)—are they at less risk of BV or are multiple other women sexual partners also a risk of BV? These authors say ‘yes!" They studied 1000 women who are lesbian or bisexual, and found that "the prevalence of BV was found to be higher in WSW than in heterosexual women in 2 studies but not another. Epidemiologic studies of risk factors for BV present contradictory findings. The high prevalence we describe is not explained by age, sex with men, vaginal douching, the use of lubricants, a history of pregnancy, or employment status....BV may be sexually transmitted between women. This suggests that female partners of women being treated for BV should also be screened and treated for BV."

Take home messages:
1)      Ask women about frequency of douching, and advise that the more frequently they douche the more risk they have of serious health consequences;

2)      Ask women about the number of sexual partners they have;

3)      Ask lesbian and bisexual women the same questions as your straight women patients.

During the last few weeks, I have been discussing changes in diet with patients who have diabetes, high cholesterol, and high blood pressure, and I have come across a common question: are the rumors about artificial sweeteners true?  Are they associated with cancer? 

In trying to find an answer, I discovered a whole list of artificial sweeteners, some I had never even heard of.  Here is a list of all the artificial sweeteners that are currently being used in the US:

1. Aspartame  = Nutrasweet and Equal, introduced in 1981
2. Saccharin = Sweet N' Low, discovered in 1879 and has been used for 125 years
3. Sucralose = Splenda, discovered in 1976, approved in 1998, and is the only artificial sweetener actually made from sugar
4. Acesulfame-K = Sunnet, used in 90 countries, discovered in1967, but only recently approved in the US
5. Neotame, approved by FDA in 2002

Cyclamate, alitame, stevioside, thaumatin, and neohesperidine DC are artificial sweeteners used in other countries.

A review which was published in the Annals of Oncology in January 2004 does a good job of summarizing the history of saccharin, aspartame, and cyclamate and their associated studies.  Many of the publications which reported an associated risk between cancer and aspartame did so by trying to correlate the rising incidence of cancer and the introduction of aspartame to the US.  The article concluded that this was inadmissible in epidemiology, and based on studies done on animals and a case-control study of brain tumors in children, there was no evidence that there was an association between aspartame and cancer.  The article did conclude that there was an association between high doses of saccharin and increased risk of bladder cancer in rats.  However, ascorbic acid (or vitamin C) was also associated with increased risk of bladder cancer in rats, and the association seemed to be more related to the fact that these rodents were sensitive to sodium salts (sodium saccharin and sodium ascorbate).

Unfortunately, there are few epidemiological studies on the newer generation artificial sweeteners such as sucralose, neotame, and acesulfame-K since they were only recently approved by the FDA.   I did find a study done on mice which found that a blend of aspartame and asulfame-K was not genotoxic.  Another study showed that sucralose was not carcinogenic for mice. 

The take home message seems to be that artificial sweeteners are not significantly associated with cancer.  And in fact, they are beneficial to diabetics who need to watch their carbohydrates and are effective sugar substitutes for those who are trying to maintain weight loss. Caution should be given to the newer generation of artificial sweeteners, but so far, things look promising.

    During my Family Practice rotation, I only saw a handful of patients more than once in my short 6 week stint. Usually, they were following up after a URI, or to get their hypertensve medications inceased. One patient I saw more than any other though. She was a 42 year old woman with fibromyalgia. She came in each time complaining of pain all over. While she noticed that it had gotten better compared to when she was first diagnosed, her pain was ever-present. Her chart was filled with different prescriptions for various doses of analgesics, I also noticed that she was started om Amytriptiline a few months earlier. I didn't undersatnd why. Her chart revealed nothing about depression or other psychological problems, and she wasn't being followed by psychiatry. The resident finally told me that she was taking it for fibromyalgia.
    I wondered if it actually worked, and what other things may work for her, and others with chronic pain like this. I came across an excellent article in the Journal of Family Practice, which was a review of the current management options for this condition. It showed evidence suggesting that cardiovascular exercise inreased patients overall sense of well-being by 17%, and decreased tender-point palpation pain by 35%.
    Another review of the management in fibromyalgia syndrome showed strong evidence for the use of the tricyclic amitryptiline in dealing with the improvement of overall sense of wellbeing in patients with fibromyalgia. Patient education regarding their disease was also associated with improved outcomes.
    Most of the articles related to fibromyalgia treatment are either review articles, meta-analysese, or are to small to suggest a benefit for a large group of fibromyalgia patients. There was one randomized double blind trial that showed a significant benefit of using amitryptiline in 208 patients after 1 month; 21% improvement compered to placebo (p = 0.002). This effect unfortunately did not hold after 6 months.
    The best evidence to date then, seems to be a combined approach in treating patients woth fibromyalgia. This approach should include patients understanding of the disease, cardiovascular exercise, and tricyclic antidepressants.

    

I had an odd feeling while interviewing a patient for a routine follow up on depression medicine.  She told me that the meds were not even touching her depression - she had tried almost every medicine out there.  Perhaps because of her visible hopelessness I asked her if she'd ever thought about hurting herself.  She said she thought about it all the time.  I asked her if she'd decided how she would do it.  She said, "I was just going to take all of the medications I have" (she has a lot)...

Suicide is a larger problem than most people realize with a prevalence of 10-12 in 100, 000.  Click here for some more disturbing epidemiology and info.  However, not all depressed people will commit suicide and not all attempters are necessarily depressed (i.e. they may be hearing voices (like Mike) commanding them to harm themselves).  Although it can be associated with depression, suicide is a whole other animal that FP docs need to know how to recognize and treat.

Research on this particular topic is a little difficult to come by.  However, work has been done on developing good screening tools (although I could not get my hands on the actual questionnaire - very sorry about that).  It seems that the screening tools are fairly sensitive in finding attempters.  There were many studies done on different risk factors but you would shoot me if I linked you to all of them.  Suffice to say that there definitely are known risk factors people should be aware of.

There is no study for this - I'm just going to share with you guys some of the wisdom I received while I was training to become an Albany County Rape Crisis hotline counselor: come right out and ask.  "Have you thought of hurting yourself?"  And, if the answer is yes, "Have you decided how you're going to do it?"  And if that answer is yes, then "Do you have the means to do that?"  You're not putting the idea into their heads and most people who are contemplating suicide will answer truthfully because many do want help - especially if they're coming to the doctor.  Those questions will help you determine who's just thinking about it and who is in imminent danger (although, when in doubt...see below).

When dealing with the suicidal patient, the big question is: to admit or not to admit?  The questions above may help determine if the patient is really serious.  Some doctors employ 'No-Suicide Contracts' (similar to contracts used in ending addictions) in cases where the patient seems more contemplative.  This allows for out-patient treatment of the underlying problem.  Young adults, at least, seem to find this treatment acceptable.  It is, however, risky if you're not too sure about how serious they are.  The other option is admission, which could depend greatly on your location.  There may only be a hospital, or a psych hospital may be nearby.  Albany has a really great program called the Mobile Crisis Unit.  They will actually race to someone's house, do an on-location evaluation and bring them back to the CDPC if that is indicated.  911 can connect anyone to this unit while doctors/counselors can call the unit directly.  Unfortunately, I do not have their phone number on me at the moment.  Let me know if you would like it...

At my practice patient counseling during routine physical exams includes suggestion on basement testing for radon. We all heard of radon as been a radioactive gas that can cause cancer with long term exposure. Coming from Connecticut I though that this gas was not so prevalent in other state. WRONG! And here is where my FP practice is located: between New Scotland and Bethlehem. Ouch!

Now what is exactly the significance of having Radon level above 4 pCi/L?
According to the EPA's 2003 Assessment of Risks from Radon in Homes, Radon is estimated to cause about 21,000 lung cancer deaths per year in the US. More than the number of deaths due to drunk driving accidents. Moreover, radon is only prevalent is a handful of states mostly in the North-East whereas drunk driving is universal.

The life time risks of lung cancer due to long standing exposure are described as well in this page. At 4 pCi/L the risks are 73 / 10,000 for a non-smoker and in smoker the risk is 10 times greater. The risk in smokers is such that at levels above 20 pCi/L, 1/4 of exposed smokers will contract a lung cancer sometime in their life time.

I search through the DOH but was not able to find any legal requirement for home owner related to radon. You would think that if a seatbelt or a designated driver was required, routine radon screening should be required as well. It seems until now that is not. While most home buyer will require the screening before acquiring a property, there is no legal requirement, just "recommendations". Even more, I have never heard of standard notification for those like us who lives in cheap rented housing for years. So...

....Have you check your home radon level lately?

For any of us who have or will work at an outpatient clinic associated with AMC, there is a patient physical form which makes life nice and easy.  One of the questions on the checklist refers to the patients sleeping pattern.  I got used to quickly skimming over this subject in Peds clinic, but recently have noticed a multitude of patients complaining of their sleep patterns.                           

So what can we offer to our patients with sleep deficit?

One of the most popular herbal remedies for the alleviation of sleep problems is valerian.  However, studies show no significant difference between valenian and placebo in a sleep EEG.

Studies have shown that Melatonin on the other hand, significantly quickened sleep onset and increasing  results sleep efficiency and sleep duration. In personal experience, melatonin does wonders for jetlag as well.  Melatonin is also known to treat night terrors.

Ambien, is colloquially known as Vitamin A because patients are known to depend on it daily to put them to sleep, Zolpidem is nonbenzodiazepine hypnotic indicated for the short-term treatment of insomnia when used as directed.                                                                   

At a clinically prescribed dosage these sleep inducers have shown to have no remarkable effect on cognitive or attentional functions but increase sleepiness of the subjects.  A high risk of adverse drug reactions have been documented in elder, sick and hospitalized patients.  Several cases have been documented of zolpidem dependence with opioid-like withdrawal symptoms.

A patient presented with continued inadequate sleep hygiene because she intermittently works a night shift.  My mentor decided not to prescribe Ambien for her because she said it needs to be used nightly. This study, however, states that non-nightly administration of zolpidem significantly improves sleep time and decreased awakenings.  Another study actually recommends non-nightly usage of amibien to decrease the risk of tolerance or dependence. 

I wonder what guidelines physicians use to prescribe ambient given this information, because it seems my preceptor is very hesitant to. 

Fish oil (omega-3 fatty acids) is used for a variety of medical conditions.  I was very interested to find out that in one of my patients this week, total cholesterol was lowered from 270mg/dl to 208mg/dl just by being on fish oil and garlic supplements (that patient was against all medications, and would only take vitamins/dietary supplements).  My preceptor prescribes fish oil for all patients with borderline to high cholesterol, regardless of whether the patient is on a lipid lowering medication.  She implements the fish oil into the patient's treatment plan as she does diet/exercise and lipid lowering medications. 

Anthropological studies have confirmed that populations with a diet high in fish have the lowest incidence of hypercholesterolemia and cardiovascular disease.  Though more research needs to be done on omega-3 fatty acids to determine: the exact mechanisms of action, the dosage and the adverse effects related to it, as well as the implications of its long-term use, research so far has shown that EPA (Eicosapentaenoic Acid, found in fish oil) improves endothelial function in hypertriglyceridemic subjects.  In another study it was found that omega-3 fatty acids improve large artery endothelium-dependent dilation in subjects with hypercholesterolemia.  In addition to its cholesterol lowering abilities, fish oil is also an antithrombotic agent.  In a study done at the Women's Hospital in Boston, it was found that women reduced their risk of thrombotic infarction/stroke by taking fish and omega-3 polyunsaturated fatty acids.

Why is it that some of the doctors out there practicing don't seem to pay attention to the evidence-based medicine, or in some cases, basic signs and symptoms.  Take for instance this week, I wasn't going to write on chest pain and cardiac enzymes because I thought it was a fairly exhausted subject.  That is until we had two patients admitted either without enzymes drawn or negative serial enzymes and with no EKG changes.  Why?  Why did we see both of these patients who cardiology had already advised for discharge before we got there?  I think it has something to do with covering your butt. 

Now for the rest of you out there who love the scientific method I ask you this.  36 year-old female with chest pain that lasts for an hour or two, and this has occurred about three times in the past day and a half.  She is obese and has a history of PCOS, type II diabetes and hyperlipidemia.  Her pain improves on sitting up, but that is about it.  So what are you going to do?  Well you probably have seen some literature on the importance of troponins (particularly Troponin I) and CK-MB in detecting MI.  In fact this particular study showed sensitivity and specificity for tropoin I in detecting acute myocardial infarction (not to mention unstable angina) is 100% and 96.3% respectively.  WOW you say, let do that. 

But wait maybe it takes a long time to see those types of changes in the event of MI and so the window of opprotunity is gone by the time we see elevation.  Oh contraire (sp?) my friend now you pull this little baby out of your hat and see, well now, if CK-MB and Troponin I are both negative at 0, 4 and 8 hours (after admission to the ED) then 99% (95% CI 96%-100%) of patients remain free from serious cardiac events.

Now on an unsarcastic note, these are tests to use only when you are trying to rule out MI.  As seen in this study, an initial EKG was more sensitive than any markers in the first 6 hours. So if you see those ST changes then you have reason to be concerned.  But these two women had normal EKG's.  AAAAHHHHHH. 

Also these simple symptoms could have also helped.  Pain that begins after exertion and is alleviated with rest (neither patient described it this way.)  Pain that is not reproducable (sp?) with pressure (one patient, who fell on his chest and had chest pain, hello broken ribs, maybe chostochondritis).  Anyways, this has been my only and last sarcastic post.  So next time your patient asks what negative enzymes over 8 hours and a negative EKG means, you can say, "Well my friend, you have an outpatient appointment with a stress test."

Since I started this rotation, I have found one single challenge posed to me every single day (usually multiple times in a day). That challenge has been trying to distinguish whether the URI that a patient comes in with is bacterial or viral, and subsequently treating with antibiotics or symptomatically. This question is especially relevant with today's increasing rates of bacterial resistance. Not to mention, answering it helps to treat your patient efficiently and correctly.

While there are clinical signs and criteria for differentiating bacterial vs. viral infections, there is no universally accepted, validated definition of prudent prescribing. For example, the diagnostic criteria developed by microbiologists and infectious disease specialists may seem unrealistic or unacceptable to PCP's. According to the International Forum on Antibiotic Resistance colloquium, prudent prescribing involves a dynamic assessment of the benefits of therapy and the risks based on a dialogue between the physician and the patient. "Indeed, a true risk-benefit assessment of antibiotic prescribing decisions must occur at the individual patient level."

With this being said, I wanted to know if there was any research being done on definitive ways to distinguish the cause of infection. I ran across this article (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11957124), which aimed to find a method to distinguish between bacterial and viral infection by measuring inflammatory markers in the early phase of the illness. They found that in the acute stage of bacterial infections, CRP levels were moderately or highly increased and 2-5A synthetase levels were normal, whereas in viral infections, CRP levels were normal or slightly increased and 2-5A synthetase levels were increased. They propose that the measurement of both CRP and 2-5A synthetase during the acute phase of illness (within 5 days of onset) is of value to determine whether the infection is caused by a bacteria or virus. Of course I am highly speculative as to the use of such testing in an acute setting. The cost-benefit ratio is probably not acceptable and it is not worth delaying treatment to obtain the results. This information may however be a quick way to confirm clinically based guidelines as accurate or not in future evidence-based research. Unfortunately or fortunately, as I've found in this rotation, there is no substitute for sound clinical judgement, experience, and communication with your patients.

Several patients who have come into my family practice this week and last have had significant health consequences due to their heavy drinking. One of them in particular came into the office one day for evaluation of high blood pressure, when further questioning elicited that he was pounding 5-6 drinks a night!

Alcoholism and alcohol abuse are serious problems in the US (2) and alcohol abuse leads to signficant morbidity and mortality.  So what do we do about it? Is it enough to just tell our patients to stop drinking, get some help, or go to AA? Since I have been immersed in the world of free lunches provided by eager drug reps I now believe there is a pharmacological solution to every problem. Let's see if I am right...

The study (sorry, stuck behind the firewall) I looked at was a double-blinded, placebo-controlled RCT that looked at the effectiveness of IM-depot naltrexone (marketed under the trade name ReVia) for the treatment of alcohol abuse. A total of 315 subjects were studied, half of them receiving the IM injections of slow-release naltrexone, in multiple centers in the US. All subjects (classified as alcohol abusers according to the DSM-IV criteria) were also treated with motivational enhancement therapy (MET) during the 12-week duration of the study. Treatment groups received either 3 injections of slow release naltrexone or 3 injections of placebo.

End-points measured were: (1)number of days to first drink of ETOH, (2)number of days to first heavy drinking day, and (3)overall days of abstinence, and (4)total rate of abstinence.  Serum GGT levels were also meaured as part of the study. What was found was somewhat promising...and of course enlightening.

In terms of average days until the first day of heavy drinking (>4 drinks in one setting) there was no signficant difference between the treatment and the placebo group. There's the bad news. The good news: on average the patients in the naltrexone group had a median of 5 days before their first drink vs. 3 days for the placebo group. Not too exciting yet...In terms of total abstinence rate the naltrexone group had an 18% success rate vs. 10% for the placebo group (p<.05). So, about 1 in 5 achieved total abstinence after 12 weeks in the treatment group compared to 1 in 10 for the placebo group. It's getting a little better, right? Lastly the mean number of abstinent days for the treatment group was 52 days compared to 45 for the placebo group. That is about a week longer of abstinence!  GGT levels were not different between the two groups after 12 weeks.

Naltrexone depot is a slow release of nalrexone that was generally well treated by patients and the side effects were not significantly different from those of the placebo group. An interesting point of this study that may be overlooked is that both the placebo group and naltrexone group achieved some level of abstinence and reduction of binge-drinking episodes, a finding that could be attributed to MET.

Alcohol abuse is a big problem and I think it is time we seriously consider the use of drugs like naltrexone and therapy like MET to help patients stay off the wagon (or is it on the wagon?). Post out...  

The other day, we saw a patient with polycystic ovarian syndrome.  She was at the clinic for a PAP smear.  She told us she had PCOS and was been managed by her primary care doctor.  We asked her what medications she was on. She said she used to be on Yasmin but was not currently taking it.  She did not volunteer any further info regarding why she was not compliant.  She mentioned that she does not get her periods.

On observation/physical exam, she is a heavy-set teenager (18) with facial hair.  She also had excess body hair in a male distribution pattern and some acne.   

So, I'm wondering what is Yasmin and why is she not taking it.  Here is what I found.

PCOS is a primary ovarian defect.  Women with PCOS have abnormalities in the metabolism of androgens and estrogen and in the control of androgen production.  There is decreased estrogen levels and consequent anovulation.  The syndrome is variable in its' presentation.  Associated signs include: menstrual dysfunction, hirsutism, infertility, obesity and impaired glucose tolerance.

Some of the mainstay treatments include diet modification and exercise to address obesity.   Metformin for impaired glucose intolerance and infertility (a high likelihood of having ovulatory cycles while on metformin.) Hirsutism: Weight loss (shown to decrease androgen production in women who are obese; therefore, losing weight can slow hair growth) and oral contraceptive (oral contraceptives slow hair growth in 60-100% of women with hyperandrogenemia) and spironolactone

So Yasmine (Drospirenone/EE) is an oral contraceptive (which is supposed to address irregular cycle and hirsutism).  However, according to this study which concludes that Yasmin provides good cycle control for women with PCOS, with an improvement in acne over 6 months but not in other symptoms of the syndrome. I wondered if our patient stopped taking Yasmine because she saw no improvement of her facial her (which seemed more of concern to her than her irregular periods).  I wondered if she was educated on why she was taking Yasmine and if she was given the option of other drugs (mentioned in this study) and spironolactone. Note: Because spironolactone is a class D in pregnancy, an effective form of contraception is required when using these compounds.

The other day I saw a 22 year old  indian female in the office and she had social anxiety disorder. She completely shattered all the stereotypes I had about how a person with social anxiety disorder would look. She was young, attractive, well dressed, very pleasant, and she was married with a son. If I had seen her without knowing anything about her I would never have even guessed that she had social anxiety disorder. The resident I was working with put her on Effexor XR about two months prior and she said it hadn't made any difference so she wanted to try something different although she wouldn't consider counseling because she was too embarassed.

I started to think about what possible medications could be used to treat social anxiety disorder. I found studies on St. John's Wort (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15643100) and Paroxetine (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15520363). 

The St. John's Wort study had 40 subjects (20 for each group) that were randomized to 12 weeks of treatment vs. placebo. The study failed to show any effect of St John's Wort on social phobia.

The Paroxetine study was a multicenter study, placebo controlled study containing 322 patients. This study focused on children from the ages of 8 to 17. This study found that paroxetine was effective and it also didn't have too many side effects.

Ms. B presents to the family practice office with a "personal" question.  After a few minutes of light banter, Ms. B spills into tears telling me that her sister had recently died from breast cancer.  In addition, Ms. B's mother had died from breast cancer.  And if that were not enough, Ms. B's other sister was recently diagnosed with the same form of cancer that killed her other two family members.  Obviously worried about her own mortality, Ms. B sought medical intervention.  As one would expect, she was genetically screened (and found to be BRCA1 positive) and received frequent mammograms.  To date, she has been without any evidence of cancer.

Like most people who are faced with the prospect of a certain illness, Ms. B turned to the internet for more information concerning what she can do to even further limit her risk.  To her surprise, Ms. B stumbled across some information about a prophylactic bilateral mastectomy for high risk women.  Ms. B thus presents at this visit for information concerning this topic.

Certainly, Ms. B is faced with quite a dilemma.  She wanted to know if the mastectomy does, in fact, decrease or limit her risk of developing breast cancer.  If it did, she replied, "I am not sure I could sacrifice the part of my body that makes me a woman."

First, I decided to search the literature for the effectiveness of surgery in limiting cancer risk.  The following article shows that prophylactic surgery does in fact improve survival in women who test positive for a BRCA1 or BRCA2 gene mutation.  Also, if the genetic risk of cancer is high (as it is in Ms. B), surgery also provides a benefit for quality of life.

Now that I knew about the effectiveness of the surgery, I searched for some information on the psychosocial aspect of mastectomy...

A recent article published in the JPRS demonstrated that overall, women who had a prophylactic b/l mastectomy were overall satisfied with the results and fewer than 20% of them reported any complications.  Of course, being that this is the Journal of Plastic and Reconstructive Surgery, these women also received reconstructive breast operations at the time of their mastectomies.  This article also shows that the patients' attitudes concerning the prospect of breast cancer prior to the operation in fact had an impact on their overall satisfaction.  Women who did not worry about developing breast cancer after prophylactic mastectomy and women who did not overestimate their risks of developing cancer had significantly higher levels of satisfaction with breast reconstruction than those who continued to worry or those who overestimated their risk of cancer.

Another article supports the findings of JPRS by stating that a prophylactic mastectomy may reduce distress levels in high-risk women and that most women who have had the surgery do not experience psychosocial difficulties.  Women who have had a prophylactic mastectomy are overall satisfied with their decision to have the surgery. 

Of course, every woman is different and this factor needs to come into the decision making process.  Overall, though, if presented with this question in the future, we can safely suggest that the literature supports the effectiveness of the preventative surgery in terms of cancer risk reduction and the psychosocial aspect.

I have seen so many patients with type 2 diabetes (DM2) who are also living with hypothyroidism that I am wondering what the connection is. I read Fazilla's entry on subclinical hypothyroidism as well as Anna's entry on hypothyroidism and hyperlipidemia, and I recommend you read those, too. But, my entry is on the interrelationship between DM2 and hypothyroidism.

 

Let's review some terms. Subclinical hypothyroidism refers to the state of elevated TSH with relatively normal thyroid hormone. The thyroid is (barely) able to produce sufficient thyroid hormone, but it takes much more TSH to get the thyroid to work. Hypothyroidism is the situation in which the patient has elevated TSH with low thyroid hormone. The thyroid is not able to produce sufficient hormone, and the TSH is elevated trying to jump start the thyroid. Fazilla and Anna have written on subclinical hypothyroidism. I am focusing more on symptomatic patients or those being treated for DM2.

 

This study from Israel (not the same study, site or researchers to which Anna refers) determine the prevalence of hypothyroidism and DM2 in 1096 people aged 65 - 92 who live on a kibbutz in northern Israel. They found that 74% of the diabetics (11.5% of the total participant population) were also hypothyroid. 38% of those found to be hypothyroid were subclinically hypothyroid (i.e., they had relatively normal thyroid hormone levels). They conclude that DM2 and hypothyroidism are common disorders in this age group.

 

But are the 2 conditions associated with each other in any cause and effect way? Is there some endocrine dysfunction that leads to both conditions? We know that DM2 causes progressive damage to the vascular bed; but does the damage caused by DM2 lead to hypothyroidism? These researchers from Wayne State U say that cumulative evidence reveals that the endocrine system is not intact in patients with DM2. "It is not clear whether the changes observed in the endocrine system represent a primary defect or reflect the effects of the impaired insulin action and abnormal carbohydrate and lipid metabolism on the hormonal milieu." They go on to say that the function of the entire endocrine system is impaired. The good news, they say, is that good metabolic control and insulin treatment may reverse some of the abnormalities.

 

A case in point is the patient I saw, a 53 year old woman who had a HbA1c of 10.6 (up from 7.8 in 11/04), TSH of 7.3 (up from 2.4) and whose cholesterol was 320 (up from 200). I recommended, in addition to changes to her other meds, increasing her Zocor and Zetia, but the attending said that if we get the patient to adhere to her antidiabetic and thyroid meds, her hyperlipidemia will improve. The attending went on to tell me that whenever she sees a diabetic with hyperlipidemia, she checks for thyroid dysfunction. She says they all go hand in hand.

 

This study shows how important it is to maintain good control of the patients DM2 and hypothyroidism. It was conducted at NY Medical College, and it compares the extent of significant (3-4 vessel) coronary artery disease in 3 groups of patients: those with both DM2 and hypothyroidism, those with just DM2, and those without DM2 or hypothyroidism. They found significant CAD in 90% of patients with both diseases, 40% of those with DM2 alone, and in only 15% of those without either disease. These researchers in Jordan screened 908 patients with DM2 and 304 people who did not have DM2. They found hypothyroidism in 12.5% of the diabetics and in only 6.6% of non-diabetics. But I still have the question: Does one cause the other or do they coexist secondary to lifestyle similarities? This question remains.

 

And do not assume that DM2 can only produce hypothyroidism. When I was presenting the above case to the attending, and asking her about DM2 and hypothyroidism, she told me of one of her other patients. This other lady has long standing DM2 and HYPERthyroidism.

 

The take home message is DM2 is associated with endocrine dysfunction.

Capsaicin for Chronic pain

 

During Neuro clinic at our family practice center, the resident was asked by the patient about any alternative or herbal non-systemic products to alleviate pain.  The patients' father had autonomic neuropathy associated with diabetes and the patient herself suffered from chronic low back pain after MVA 3 years ago.  From the surgery rotation I remembered one of the PM&R physician once prescribe Capsaicin cream for the back pain.  I decided to research this further to evaluate if topically applied capsaicin cream had significant pain alleviating effect.  Such a therapy would be very relevant to patient's health as it could offer a substantial option before beginning systemic therapy which carries a significant potential for broader side effects. I found a meta analysis addressing this very question.

 

"Systematic review of topical capsaicin for the treatment of chronic pain" BMJ  2004;328:991 (24 April),

 

http://bmj.bmjjournals.com/cgi/reprint/328/7446/991

 

 The authors of this analysis studied 9 (6 for neuropathic pain and 3 for musculoskeletal conditions) randomized, placebo-controlled clinical trials comparing topical capsaicin with placebo in total of 1500 patients with chronic neuropathic or musculoskeletal pain. In almost all trials analyzed in this meta-analysis, the capsaicin applied 3-4 times daily for 8 weeks was statistically superior to placebo in achieving 50% reduction in pain from the baseline.  However I should note that placebo response was also significant with almost 38% of the patients reaching 50% reduction in pain.  The authors calculated the NNT and found that in neuropathic conditions the numbers needed to treat at 8 weeks was 5.7, and at 4 weeks it was 6.4.  In musuloskeletal conditions, the NNT was 8.1 at 4 weeks.  On the other hand, significantly more patients on the topical capsaicin had local adverse events of burning, itching, redness etc. than placebo (54% vs. 15%). 

This study is very patient oriented as it studies the effect of a specific modality in relieving chronic pain.  Based on the study's results, it can be safely concluded that topical capsaicin offers a very viable alternative for patients not satisfied with other pharmacological options.

This week I saw two patients with Rheumatoid arthritis. Both had been taking similar anti-inflammatory medications(Cox-2 and/or NSAID's) even though their symptoms seemed to vary greatly in intensity.  One of the patient was newly diagnosed with minimal erosive changes in extremities yet the other patient had clear erosive joint disease and consistent moderate-severe pain.  RA is most commonly diagnosed clinically on the basis of the presenting symptoms.  However, the second patient had brought plain radiographs with her that her rheumatologists had ordered earlier in the week for her joints. After this encounter, I was curious to know the utility of advanced imaging methods like MRI in delineating the extent and severity of moderate-severe RA, thus guiding the treatment accordingly.  Such evidence would be relevant to the patient in finding the specific therapy that is most useful at a particular radiological point in the disease process. Through OVID search I found this article   "Rheumatoid arthritis: MR imaging manifestations" in Radiology. 165(1):153-7, 1987 Oct. 

 

http://radiology.rsnajnls.org/cgi/content/abstract/165/1/153

 

The authors of this preliminary study studied enrolled 17 patients with moderate-severe RA to undergo MRI's to stage the exact changes with bone and soft tissues around their joints.  Their hope was to show that MRI would be able to pick up more specific soft tissue changes in the patients with devastating symptoms and thus can guide the treatments more specifically.  This small study found that MR showed significant interval changes that were not seen on plain radiographs. This study has drawback with the main one being that it's a very small preliminary study with extremely small pt. size, yet I thought it was a good initial study that could be relevant to patients with moderate/severe RA.

A 69 year old female presented to the office with severe (9/10) right flank pain radiating around her side into her RUQ.  She had been in pain for 3 days, but it had worsened significantly over the past day.  When I entered the room she was leaning forward in the chair, which gave her some relief, but was she noticeably uncomfortable.  The pain had been fairly constant and was not associated with eating.  She also mentioned that she'd had a cough.  She is a 40 pack year smoker and drinks a 6 pack of beer each day if she had money to buy it.

She was afebrile and her vital signs were within normal limits.  However, her O2 saturation was 92%.  She was alert and oriented.  Lying down on the exam table made her pain worse.  She had significant hepatomegaly.  On lung exam, rhonchi were heard over her right lower and middle lobes.  She was sent to the ER with a clinical diagnosis of pneumonia.

Seeing this patient and trying to figure out what was causing her pain was a good reminder for me not to close my differential diagnosis too early.  I was thinking of all of the things that cause flank pain and RUQ pain and pneumonia wasn't on my initial list.  However, after getting her O2 sats and hearing the rhonchi the diagnosis became clearer. 

I started wondering about different ways pneumonia presents in elderly patients versus younger patients.  According to one study, "respiratory and nonrespiratory symptoms are less commonly reported by older patients with pneumonia."

It is important to remember that elderly patients with pneumonia often don't present with the typical signs of cough, fever, and dyspnea.  They may present with confusion or a functional decline in daily activities.  The fact that an elderly patients is afebrile or does not have a cough does not rule out pneumonia.  Since the mortality associated with pneumonia is much higher in the elderly, it is important that we diagnosis it and begin treatment as soon as we can.

I recently had a child with Sickle Cell Anemia who was experiencing the beginnings of a "crisis," and was brought in by his mother to see the doctor in order to ameliorate the upcoming problem.  I was interested in learning a little more about how children and their families deal with the disorder, especially when it related to the recurrent painful episodes of vaso-occlusion that they experience.  Treatment, although still an evolving subject, has been thoroughly studied, and a standard of care revolves around the use of narcotics (such as Hydroxymorphone (Dilauded) and Fentynl), as well as many newer treatments, such as potent nonsteroidal antiinflammatory drugs (Ketorolac-Toradol), opioid receptor-binding agents, surfactants that inhibit cell adherence and aggregation, inhaled nitric oxide, anticoagulants, glucocorticoids, and epidural anesthesia.  But what impact does this disorder have on the lives of children living with SCA?  There have been a number of studies looking at this subject, and it is important for physicians to acknowledge, as well as families to understand.

Overall children with SCA normally receive treatment at home, which results in a seven times more incidence of school absence and overall disruption of social and recreational activities.   Using a home-based diary system to examine the impact of SCA on school attendance and sleep, they found that children were absent 21% of the time, half of which was related to pain (two thirds treated at home, the remaining third treated in a hospital.)   

These large number of pain episodes are not obvious to the clinician, since so many of these acute pain episodes are treated at home.  A recent study looking at hematological parameters (such as erythrocyte/ endothelial cell adhesion, including hematocrit, fetal hemoglobin, and adhesion ratio) found that they were valid predictors of the clinical features of SCA pain crises, and purports that these are basically the same phenomena, only a continuum of the same pathophysiology.

In order to reduce these adverse effects on education and socialization, a look at children with SCA found that using a method of relaxation and imagery could result in "fewer health care contacts, fewer school absences, and less interference with household activities than on days when they did not practice."

Patients this week seemed especially concerned with their diet, and of particular concern was the contradictory information regarding the effects of eggs on the diet.  Doctors have counseled their patients for years regarding dietary cholesterol, and in the 1970's, the American Heart Association (AHA) recommended that egg consumption be limited to 3-4 eggs per week.  Nowadays, the recommendations are loosening, and patients aren't sure why.  Patients look to their doctors for the facts, and so, I decided to see what I could find. 

According to the AHA Dietary Guidelines which were revised in 2000, it is now okay to eat up to one egg per day as long as the amount of dietary cholesterol is limited to less than 300 mg/day.  FYI, one large egg contains 213 mg of cholesterol. This recommendation has been criticized because eggs contain a large number of nutrients such as folate, riboflavin, selenium, choline and vitamins B-12 and A, which may benefit the population of patients who do not have elevated cholesterol or high risk of heart disease. They are also inexpensive and low in calories.

Eggs have been given a bad rap because of the amount of cholesterol they contain.  However, there are few studies that have found a link between dietary cholesterol and increased risk of cardiovascular disease.  In fact, there is a study that shows no association between dietary fat/cholesterol intake and stroke in men; another study shows no association between dietary fat/cholesterol intake and coronary artery disease in women.  While both are cohort studies that have large populations which give them a lot of power, they both rely on their subjects to report their food consumption accurately.  There are elements of recall bias (relying on patients to report their average daily intake) and selection bias (men and women in both studies are nurses and health care professionals) which may influence the outcomes.  Interestingly, data from these two studies were combined, and this time, the amount of egg consumption was assessed in order to find any association between egg consumption and the risk of cardiovascular disease.  They found that consumption of up to one egg per day was not associated with higher risk of cardiovascular disease among healthy men and women, but there was an increased risk for diabetic patients.

The final recommendation to patients seems to be that if they are healthy, eating eggs is not a bad idea, especially because there are benefits.  But if they are diabetic, have elevated cholesterol or other risk factors that increase their  risk of cardiovascular disease, they should limit their total dietary cholesterol, and that can mean limiting the amount of eggs they eat every week.

This week, I had a morbidly obese patient who could only walk with the aid of a walker. He was unable to clean himself properly because he could not reach or bend down far enough. He was having trouble sleeping flat and now slept in a chair. In the last progress note, he and my preceptor discussed gastric bypass surgery and he was very enthusiastic about it. I brought up this subject with him and he told me that the surgeons him to lose 50 lbs. He stated emphatically that if he could lose 50 lbs, he wouldn't need the surgery. I explained to him that after the surgery, his dietary habits had to change if he were to be successful and by losing 50 lbs he would show his motivation to make such changes. He stated that no one had ever explained that to him. At the end of this encounter, it was clear that he was not interested in gastric bypass surgery if it meant changes to his life.

During this rotation, I have encountered several patients who have had gastric bypass or are considering them. I read an article which discusses the new role of primary care physicians in the process of this surgery. Now, many physicians initally select patients for this surgery by suggesting it to them and referring them to surgeons. Furthermore, PCPs are often centrally involved in the post-surgery followup. I began to wonder about bariatric surgery and its success rate as well as the factors that predict success or failure. I found two articles that deal with long-term outcomes of bariatric surgery. One study  found that "patients who ate three well-balanced meals and two snacks daily; drank water and avoided carbonated beverages of any kind; took multiple vitamins, iron, and calcium; slept 7 hours per night; exercised regularly; and took personal responsibility for weight control were more likely to be successful". We can tell our patients about these characteristics in hopes that they will incorporate these changes into their lifestyles before the surgery and thus be more successful. Another study found that patients with a stronger social network, more success with previous weight loss attempts or who were less distressed by society's perception of their body image were more likely to lose weight.

Much of the obesity literature discusses psychological comorbidities associated with obesity, such as binge eating disorder (BED). Patients must undergo a psychologic evaluation prior to surgery. However when there is evidence of some psychological disorder (as is the case in many obese patients), not all doctors suggest putting the surgery on the back burner until these issues can be dealth with, although there is evidence that patients with BED may continue with the same or modified behavior after the surgery which may lead to failure to lose weight. Part of the challenge here is admitting that some patients do in fact have a psychological disorder (BED) rather that just assuming that all obese patients have no self-control. Another study demonstrated that there was no risk because patients with BED disorder prior to surgery did not demonstrate those behaviors afterwards.  Part of the challenge here is admitting that some patients do in fact have a psychological disorder (BED) rather that just assuming that all obese patients have no self-control. Another study demonstrated that there was no risk because patients with BED disorder prior to surgery did not demonstrate those behaviors afterwards. 

The POEM from all of this is that gastric bypass surgery is not suitable for all patients. Though this information may be out there, many physicians are not discussing this reality with their patients and are setting them up for continued failure and more psychological distress. Primary care physicians will have an increasingly larger role in educating patients about the surgery, the personal modifications needed to be successful as well as what can be realistically expected by patients after surgery. A resource to help determine which patients are suitable for bariatric surgery is the Boston interview for gastric bypass which assesses 7 areas: weight, diet and nutrition history, current eating behaviors, medical history, understanding of surgical procedures, risks, and the post-surgical regimen, motivation and expectations of surgical outcome, relationships and support system, psychiatric functioning. In this article, the interview is included so we can start using it to assess our patients.

Gout is a terribly painful condition that is more common than most people realize.  Your patients will love you forever if you can not only end the pain for them, but also prevent it from happening again.  Thus, treatment has two components: treating the acute pain by decreasing inflammation and preventing future attacks by treating the underlying hyperuricemia (usually due to either underexcretion or overproduction of uric acid).

First line treatment for the acute pain of gout is usually a powerful NSAID.  The doctor I work with went with Indomethacin for the last patient we saw with gout.  Although I could not find studies comparing them to Indomethacin, Naproxen and Lodine are also options with Lodine being slightly more successful. Ketoprofen has also been seen to be as effective as Indomethacin with comparable side effects.  There is also literature showing Etoricoxib to be as good as Indomethacin with fewer side effects but it is not yet legal in the US (?).  With these drugs showing such similar efficacy and side effects, it becomes a matter of trial and error in matching patients with treatments.  However, Indomethacin appears to be tried most often as the first option...

Colchicine use is more controversial.  It can be used to treat acute gout although it has fallen out of favor due to severe GI side effects.  It has been found to be very useful, however, in preventing new attacks - especially when initiating long term therapy with allopurinol.  

This brings us to more long term preventive treatments.  Allopurinol seems to be the the first line treatment.  For people with allergies to allopurinol (and normal renal function), there are also Probenecid and Sulfinpyrazone.  Benzbromarone (sorry - not much info on this one) can be used in patients with renal insufficiency, however, it is not available in the US(?).  I had a very difficult time finding studies to show efficacy in decreasing attacks of gout.  There are studies galore looking at the ability of these drugs to lower serum uric acid, which they can all do, but nothing about attacks (which is what patients would be interested in).  Again, allopurinol seems to be the main treatment option with probenecid being next popular - but that's just my take on it from skimming literature.

Finally, diet!  Alcohol intake as well as foods with high amounts of purine (red meat, liver & scallops) are all thought to contribute to gout attacks.  At least, high intake of meat and seafood have been found to be associated with an increased risk of gout, high dairy consumption is associated with decreased risk and moderate intake of purine-rich veggies or protein has no increased risk.  These are all things to keep in mind as the best treatment for gout is to prevent the attacks from occuring!

This week, one of patient was questioning why he should take so many medications for the treatment of his hypertension. He was on a diuretic, an ACE-inhibitor and a beta-blocker. Like a good student I just recited the lesson. In short all have a direct effect on lowering the blood pressure but each one of them has properties that may reduce long term morbidity or mortality. Beta-blocker more specifically are chosen as first line agent because of their long term effect on cardio-vascular mortality in Caucasians.

 

Looking at the effect of Metoprolol on hypertensive men aged 40-64 years a Sweedish randomized trial showed in 1990 that beta-blockers offer a 25% risk reduction in coronary events in patients on beta-lockers when compared to treatment with diuretics.

 

Well all Beta-blocker do not seem to hold on to these promises. In 2003, a meta-analysis on the efficacy of first line agents showed that diuretics are in fact the best first line agent in reducing long-term cardio-vascular mortality in hypertensive patients, suggesting that other beta-blockers are not as efficient as good old Metoprolol.

 

Because of its more selective action on beta-1 receptors, Atenolol has become one of the most widely used beta-blocker. However its effects on mortality may not be as great as expected. In 2004, the Lancet published a meta-analysis following 6825 and 17671 patient over 4.6 years. The study concluded that despite major differences in blood pressure lowering, there were no outcome differences between atenolol and placebo on all-causes of mortality. Moreover, if there were no major differences in blood pressure lowering when compared to other antihypertensives, strikingly, a significantly higher mortality (1.13 [1.02-1.25]) was found with the use of atenolol treatment when compared with other active treatment.

 

I will then conclude that if you want to treat hypertension with a single medication, diuretics should be your first choice. An alternative would be to use a beta-blocker. Metoprolol remain a good choice because of its noted positive outcome. However, be aware that all beta-blocker have not the same benefit and while some other might work at reducing blood pressure they might not be as good at decreasing long term mortality.

 

This last week in my FP office seemed to be especially heavy in the amount of patients that were seen for flu or flu-like illness. Of all the patients seen, none of them received the flu vaccine and several of them were treated with antiviral medication. After each one of the cases I found myself wondering, "Would it have been any better if they got the vaccine?" "Does it cost more to vaccinate then just treat after the fact?" "Do the patients who are vaccinated have better 'patient-oriented' outcomes?" Then I started to think that it would be better to find the answer on the internet than to keep talking to myself.

To find the answers to my questions I was ablew to locate a study (linked to the abstract) that compared vaccination and treatment (and no treatment) strategies for cases of flu or flu-like illness in the last ten years. They were attempting to measure cost effectiveness of the different strategies as well as more patient-oriented outcomes like days missed from work, loss of productivity, and hospitalizations (cost could also be a large patient-related concern). What they found might interest some of you...

In terms of monetary cost, for the 10-yr period the cost of vaccination was the most (239 dollars per person per year) and medical treatment with amantadine was the least at 234 dollars per year. Performing a rapid nasal swab for influenza and then treating with oseltamivir ended up costing about 237 dollars per person per year. Bottom line was that the dollar cost was fairly similar regardless if the patient was vaccinated or treated later. Yes, you are probably not impressed yet.

Here is the jelly in the middle of the donut...When they measured days lost from work and hospitalizations the story gets a little more interesting. After extrapolating the original data from 10 years of studies, it was found that vaccination reduced the amount of workdays lost from influenza by more than half (164 vs. 71)when compared to no intervention! Amantadine therapy reduced the amount of days lost to 139, while the often prescribed tamiflu only cut the lost days down from 164 to 144. The annual rate of hospitalizations was also slashed in half for the vaccination group while it was unchanged when comparing no intervention to tamiflu or amantadine. Get out of here!

In terms of physician office costs, annual vaccination cuts about $1100 yearly (studied as a cohort of 1000 healthy adult workers). There was also less loss of productivity in the vaccination group compared to the others. In summary, vaccination could be expected to prevent 49 cases of influenza per 1000 workers vaccinated, avoiding 93 lost workdays, or 0.09 days per employee, at a net cost of approximately $3 per employee vaccinated. Wow, not bad.

The reason this is important is that so often we focus on the monetary cost of certain tests, medicines, or procedures and forget to look at the big picture. Sure, it costs about the same in dollars to treat someone with amantadine as it would to give them yearly vaccinations. But because we might be treating the wrong illness (flu-like illnesses, influenza type B)people might still end up getting sick and missing work.

Interestingly enough, this research showed that tamiflu was the least cost-effective way to treat/prevent the flu (although they only looked at studies where a rapid test was performed before treating, a practice I would not say is the norm), even though I have seen it prescribed several times just this week.

Yes, I know about the shortage and why people did not get vaccinated this year. Here is some info that might help all of you out there ready to rumble: According to the CDC, there has been a late surge in the amount of influenza towards the end of this January, so they have adopeted some new guidelines for vaccination that might help some of us decide who should get the vaccine right now. 

Hope this helps.

 

This week I saw a 29 year old primigravida woman at 10 weeks gestation. On physical exam, I found her blood pressure (BP) to be 150/82. She was a new patient to the practice and denied any history of hypertension in the past. She will be back to the office next week to have a repeat BP measurement. Because of her nulliparity, she is at increased risk for preeclampsia. I wanted to know if there were any known treatments to prevent this.

I found a number of articles trying to determine whether low-dose aspirin reduces the incidence of preeclampsia. Initial studies were set-up to prevent preeclampsia in normotensive primigravida women. These showed a decrease in preeclampsia but an increase in abruptio placenta. Subsequent studies on women at increased risk for preeclampsia have not shown any benefit. A study in the New England Journal of Medicine found that low-dose ASA did not reduce the incidence of preeclampsia significantly or improve perinatal outcomes in pregnant women at high risk for preeclampsia. Prophylactic ASA use is not currently recommended, however, it is clear that ASA shifts the balance of prostacyclin and TXA2 in a favorable direction. Thus, platelet activation represents only a part of the complex pathogenesis of preeclampsia, which is still a poorly understood phenomenon.

This week my preceptor and I saw a young woman in toe with her nine month old child.  She was here for a well child visit.  She was a very educated woman and warned us that she had come with tough questions.  One of her concerns was about the MMR vaccine.  Her girlfriend had told her about the dangers of vaccines and specifically mentioned the link between autism and the MMR vaccine.  She was reluctant for her child to receive any further immunizations.  My preceptor was very understanding and explained to her that there always is the possibility of negative side effects from the vaccinations such as pain at the injection site, fever, a mild manifestation of the attenuated illness or even an allergic reaction to the vaccine.  He also explained that there were numerous benefits from the vaccinations and explained to me that this was risk analysis: the risks were outweighed by the benefits.

So I looked for studies to see if there existed a link between autism and receiving the MMR vaccine as this woman's girlfriend had warned.  In this retrospective cohort study (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12421889), they examined all the children born in Denmark from January 1991 through December 1998.  They looked at the MMR vaccination records and compared this to the records in which the diagnosis of autism was made in psychiatric hospitals and outpatient clinics throughout Denmark.  Of the 537,303 children in the study, 82 percent had received the MMR vaccine while 0.06 percent of children had been diagnosed with autism.  They go on to explain that the relative risk of autistic disorder in the group of vaccinated children compared to the group that had not received the vaccination was 0.92 and concluded that that MMR vaccination does not cause autism.  However, I also found studies showing that vaccines, such as the MMR vaccine, can do serious harm including this article (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14976450) which explained that a component within the MMR vaccine, called thimerosal, contains mercury.  They found that there was a statistically significant correlation between mercury doses from thimerosal-containing childhood vaccines and the prevalence of autism!  Clearly then, the woman's concerns for her child are legitimate ones and should not be disregarded.

The other day, we saw a patient for a yearly physical.  My preceptor and I did a complete history and physical and all was well.  We asked that famous question: Do you have any other concerns: Patient: You know doctor my right hand has been bothering me.  You see I'm a barber by profession and I use my hand a lot.  He described his symptoms and sure enough he had signs of mild arthritis in his right hand from overuse.

So the doctor tells him: I know something you can use.  It is called Glucosamine.  The patient looked at me perplexed (I returned the look just as perplexed).  I was thinking to myself (You know sometimes I think some doctors just pull medications out of a hat).  Doctor went on to explain: Glucosamine (treatment section of this article) is made by our body.  These molecules help the cartilages in our body to reduce friction from arthritis.  It is an OTC substance (like a food supplement).  In fact I take it myself and it works wonders.  ...I was not convinced.

Next day I see another patient, on her medication list was Glucosamine.  I asked her what she was taking it for.  She answered arthritis.  It works wonders.  Once, I stopped taking it and the pain of arthritis came back.  So I said, I have got to look into this "Glucosamine".

This study states that glucosamine and chondroitin sulfate are non-pharmaceutic alternatives for the treatment of arthritis.  A large majority of patients with arthritic pain are using these alternatives.  These alternatives are popular because of the little or no side effects as well as results (as this study shows) patients are seeing with decreased arthtritic pain. 

Sorry something went wrong with my links below are the respective links

http://www.emedicinehealth.com/articles/5494-1.asp

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15670444

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15023378

RLS is a 34 year old female whom my preceptror sent to have a sleep study after complaints of a constant need to move her legs while in bed.  After talking to neurology she also mentioned a discomfort as the reason for wanting to move (this after my preceptor asked a number of times if there was any pain in her legs).  Now, we have restless leg syndrome, a disease affecting 12 million Americans, possibly more.  In spite of the fairly benign sound of the disease it can severly effect quality of life of the people it effects.

Two things make this disease particularly difficult: the relatively unknown etiology of the disease and the difficulty in treating it.  I say relative unknown because it is thought that although 50% of the cases are idiopathic, the rest can be symptoms of low iron levels, anemia, kidney failure, diabetes, Parkinson's, and peripheral neuropathy (see diabetes).  Some women in their 2nd trimester will develop RLS, which usually resolves 4 weeks after delivery.  In the case of the non-idiopathic causes the RLS symptoms can often be allieviated by treating the underlying condition.

What to do with the other 50%.  Treatment varies but it is generally thought that dopaminergics, benzodiazepines (central nervous system depressants), opioids, and anticonvulsants work best in the medical route.  Changing sleep habits to a time when symptoms are decreased, hot bath, massaging the legs, or using a heating pad or ice pack can help relieve symptoms as well.

Recent research seems to show benefits in levodopa and gabapentin as treatment.  Both studies are small and therefore lack power, but they seem to suggest fairly significant decreses in objective measurements such as leg movements during the night, but also subjective measurement improvment in quality of life and perceived pain.  Levodopa/carbidopa is the medication of choice for RLS, but the severe amount of side effects often associated with all the drugs suggested to treat RLS must always be considered and monitored for.

This week I have seen two women w/ hypothyroidism, both of whom also had hypercholesterolemia.  The relationship between hypothyroidism and hypercholesterolemia, w/ subsequent cardiovascular disease has been long established by research.   However, it's becoming apparent only recently that the patients who have subclinical hypothyroidism are equally at risk for hypercholesterolemia and cardiovascular disease.  Subclinical hypothyroidism is found in 7% to 26% of women (with increasing prevalence as women reach age 60 and 70 years).

In a study done in Israel, subclinical hypothyroidism in middle-aged women was found to be associated with hypertension, hypertriglyceridemia, and elevated total cholesterol:HDL ratio.  This means that atherosclerosis is accelerated in some of these patients, resulting in premature CAD.  In another study done in The Netherlands, it was found that the administration of thyroxine (T4) in hypercholesterolemic subjects w/ subclinical hypothyroidism, there was a reduction in total plasma cholesterol by 0.4mmol/L (15.5 mg/dl).  A significant reduction in both total cholesterol and LDL was observed in a study done in Greece.  Finally, a study done in the UK concluded that patients with subclinical hypothyroidism and hyperlipidemia should receive T4 secondary to its lipid lowering actions.  This means that patients with subclinical hypothyroidism would greatly benefit from thyroxine replacement secondary to the cardiovascular benefits resulting from the lowering of cholesterol.

LB, and adorable 8yo, is here with a 3^rd episode (all within 6 months) of a sore throat, runny nose and vanishing fever.  She does not want to have to stay at home yet for another week or so.  On physical examination, she is playful, her tonsils are grossly enlarged with a tiny spot of exudate.  The doctor performs a throat culture and sends her away with order to remain at home and rest until he gets the result.  I asked him nonchalantly if he is considering a surgical referral for a T or an AT.  He asks me to survey the literature for indications of T or AT.  Here is what I found:
Tonsillectomy is still the most commonly performed major surgical operation among US kids, although it has dropped from 1.4 millions in 1959 to 287000 in kids under 15 in 1996.
The current guidelines by the American Academy of Otolaryngology-Head and Neck Surgery, (Bulletin June 2000 Vol. 19 No. 6) including but not restricted to the following points are:

• Patient with three (3) or more infections of tonsils and/or adenoids per year despite adequate medical therapy.
  
• Hypertrophy causing dental malocclusion or adversely affecting orofacial growth documented by an orthodontist.
  
• Hypertrophy causing upper airway obstruction, severe dysphagia, sleep disorders, or cardiopulmonary complications.
  
• Peritonsillar abscess unresponsive to medical management and drainage documented by surgeon, unless surgery performed during acute stage.
  
• Persistent foul taste or breath due to chronic tonsillitis not responsive to medical therapy.
  
• Chronic or recurrent tonsillitis associated with the streptococcal carrier state and not responding to beta - lactamase - resistant antibiotics.
  
• Unilateral tonsil hypertrophy presumed neoplastic.
  
• Recurrent suppurative or otitis media with effusion (Adenoidectomy alone, tonsillectomy added requires one of the indications listed above).
  

According to Burton MJ et al review in the Cochrane Database of Systematic Reviews, no trials evaluating the effectiveness of tonsillectomy in adults were identified. Two trials from Pittsburgh assessed T and AT in children.  The effectiveness of tonsillectomy has not been formally evaluated. Further trials addressing relevant outcome measures are required.
The 1^st trial (need to get actual article from NJEM) in children mentioned concludes that AT has been effective in reducing the number and severity of throat infection but only in children severely affected by recurrent throat infections (7 or more infection a year, each episode associated with an oral temp of at least 38oC or cervical lymphadenopathy or tonsillar/pharyngeal exudates or a positive group A b-hemolytic streptococcus) over 2 years, although many children treated non surgically improved spontaneously.  The 2^nd trial, in children moderately affected by recurrent throat infection, found that T or AT seems not to justify the risks, morbidity and cost associated with the operation(s).
The jury is still out on the indications to perform a T or AT.

I discussed my findings with my preceptor.  He told me that "old habits die hard" and that he does not indicate T and/or AT unless the patient truly meet the condition cited by the American Academy of Otolaryngology-Head and Neck Surgery.  In this case, although it is LB 3^rd infection, she is not ridiculously debilitated each time and group A b-hemolytic strep was cultured only once.  So he'd rather wait!

In the FP office I'm working in we see a number of new mothers. In one of my encounters with a mother and her child, the topic of breast feeding came up. The father of the child thought breast feeding was awesome because that would mean saving money on formula, the mother on the other hand wanted the doctor's opinion. I started wondering what I would say if a mother asked me about breast feeding.

We all took pediatrics so we know all the benefits breastfeeding has for the baby however I was a little suprised to see the amount of benefits breast feeding has for the mother. Breast feeding decreases the mother's risk of breast cancer, endometrial cancer, and ovarian cancer. Most of the benefits obtained with breast feeding aren't significant unless the mother breast feeds for around a year. That is a long time for anyone to breast feed but if the patient knows the benefits, it might be something she'll consider.

Varicella is a highly contagious viral disease, belonging to the herpesvirus family. Following infection, VZV remains latent in neural ganglia, and may cause zoster if reactivated. While a generally mild, irritating disorder in childhood, varicella tends to be more severe in adults. Healthy individuals may develop complications such as bacterial superinfections, pneumonia or encephalitis.

            In 1995, the Varicella vaccine was introduced to the United States.  Studies show the live attenuated Oka strain vaccine to be highly immunogenic and well-tolerated amongst the general pediatric population as well as amongst immunocompromised children, with seroconversion rates ranging from 94 to 100% and 53 to 100%, respectively.  A cost-analysis showed that respectively, 68% and 57% of chickenpox-related hospitalizations and deaths could be prevented with a 90% coverage rate. Vaccination costs are 40% less than the cost of chickenpox treatment costs, implying that savings are incurred from both a societal and a health-system perspective.

However, a study conducted in France concluded that there is a possible shift of the disease to older children and adults.  Also, without natural exposure earlier in life,  the vaccines protection would decreased in adulthood and zoster in elderly could increase. Recent reports suggest that a booster dose or a two doses regimen would be better for adequate immunization in childhood.

Today I had the pleasure of speaking with and examining a 42 year old gentleman who told me his butt itched. He didn't have any changes in bowel habits, nor fever, nor blood on the toilet paper. I asked what he did to relieve it, and he told me he scratched, but now, even that wasn't working. On exam, there were no anal or rectal masses, and the stool occult blood smear was negative. There was no discharge, or gross lesions. The only finding was an inflamed looking anus, with scant dried fecal matter surrounding. The man ended up going home with a prescription for 1% hydrocortisone cream and recommendation to use baby wipes. I was intrigued. I too have the occasional bout of pruritus ani. So far, not severe enough to send me to my doctor, but certainly annoying.

I found a wonderful article detailing the various causes, and some treatment ideas. The most common causes are infectious in nature, usually candida, Staph aurus, HSV, scabies and pinworms to name a few. These usually present with infectious stigmata, possibly vesicular lesions with  HSV, burrows with scabies and little worms tha run away and hide with pinworms.

Contact dermatitis is another common cause of anal pruritis. Soaps, deoderants, rubber, poison ivy and propylene glycol are commonly recognized irritants in many cases. Hot baths, although soothing can actually further exacerbate the pruritus.

Other causes may include poor anal sphincter tone, which may lead to occult fecal leakage. Of course hemorrhoids are another cause of pruritus, but this is usually associated with pain, possibly blood, and compressible mass on physical exam. Thongs and tight jeans have also been implicated in perianal and perivulvar pruritus, recommendations are  to wear some sensible, absorptive cotton panties.  Foods, such as chocolate and tomatoes have also been implicated.

So, how is this best managed? Another article compared simple washing to using local corticosteroids in 72 patients with a wide variety of causes for their pruritus. There was no significant difference between the two treatments. With this in mind, it seems that simply educating people in hygeine, and recommending hypoallogenic type baby-wipes may help avoid some of the side effects of steroids and provide some much needed relief for some of your patients..

Otitis Media is wicked common .. here's a New York State Guideline ... who knows where the AAP/AAFP guideline is?  Should we use antibiotics in the treatment of AOM?  Whats' the diff between AOM and OME??

     A 45 year old male patient with long-standing poorly controlled Type 1 DM (HbA1c 9.4) presents to the clinic with severe pain in his left shoulder and a limited range of motion.  The patient states that about one year ago, he was lifting a refrigerator out of a box and suddenly heard a large "pop" in his shoulder.  At this time, the patient noted severe pain and limited range of motion in the affected shoulder.  Being stubborn about seeing doctors, the patient refused to seek any medical attention.  For about 3 months, he learned to comb his hair with his right hand as he was no longer able to raise the left (and dominant) arm above his shoulder.  Also, the patient states that he was plagued by severe pain, especially at night.  The shoulder was stiff and he was seriously limited in his range of motion.  Finally, he sought orthopedic help, who, after an MRI, diagnosed him with a rotator cuff tear.

     At the time of the patient's visit, he was given a steroid injection and told to use 600 mg of Motrin three times a day to help alleviate the pain.  The patient states that this therapy did help him for a few months, but recently, the pain has returned and is "worse than ever."  He describes the pain as a sharp, throbbing sensation in the superior, lateral, and anterior portion of the shoulder.  He is unable to abduct his arm past 90 degrees.  His rotator muscles are weak and painful.

     The patient presents today wondering if surgery is an option for alleviation of his pain and overall improvement of his symptoms.  He was told one year ago by orthopedics that surgery is the treatment modality of choice in a patient his age.  After a little research, however, I discovered a good POEM that may suggest otherwise, depending on what he believes surgery will achieve.

      The purpose of the present study was to determine the long-term results, failure rates and successes of surgical rotator cuff repairs in people age 50 years or younger.  What this POEM actually shows is that overall satisfaction for rotator cuff repairs is not that great.  Although some subjects of the study reported excellent satisfaction following surgery, the majority reported unsatisfactory results.  In addition, the majority of subjects reported little or no improvement in range of motion following the surgery.  However, what was accomplished by having the surgery was long-term pain relief.  Having these data handy would have been very helpful to the patient that presented to the clinic where I am working.  I think it is important to explain to young patients undergoing a rotator cuff repair that realistically, although their pain will improve from the surgery, they will still be limited in their range of motion.  If they are only looking for pain relief, then surgery will be successful.  However, improvement in range of motion and overall satisfaction may not be achieved.

 

It becomes almost second nature to order tests we don't need.  Debate about the benefits of screening PSA are commonplace among medical arenas, but the debate about screening TSH is a much less common one. 

Articles outline the sequalae of leaving subclinical hypothyroidism untreated.  Progression to overt hypothyrodisim, myocardial infarction, stroke, impaired ventricular function, an increase in low density lipoprotein cholesterol and a decrease in high density lipoprotein, enhancing the risk for development of atherosclerosis and coronary artery disease, ovulatory dysfunction and infertility are amongst the list. 

    For all the above listed reasons, many studies  mandate screening every patient.  Other studies,  however, enforce that without clinical signs of thyroid disease, and even if isotope and imaging studies were conducted, it is still difficult to decide whether there is direct correlation to thyroid function.  For this reason, routine screening for thyroid disease with thyroid function tests is not recommended for asymptomatic patients. This excludes people of higher-risk: people with family history of thyroid disease, elderly persons, postpartum women, and persons with Down syndrome.

         If screening is performed, thyroid-stimulating hormone (TSH) is the most sensitive and specific.  A study conducted in Spain showed that 27% of participants with subclinical hypothyroidism progressed to overt thyroid failure within a mean 32 months. 

    This and other studies indicate that thyroid hormone replacement therapy slow the progression of coronary heart disease and overt hypothyroidism.

      While the debate continues regarding whether screening should be conducted on people without symptoms of hypothyroidism, if screening is conducted, it seems most appropriate to treat subclinical hypothyroidism to wane associated illnesses.  A screening lipid profile might also be appropriate if TSH levels are higher than normal.  However, if physicians who are screening TSH choose not to treat or monitor abnormal values, and instead only treat when the patient comes in with symptoms, then what is the benefit of screening at all?  

So, I keep passing by this door at my clinic that has a sign that reads OMT. I asked one of the residents what it stood for. She told me it was something the D.O.s use called Osteopathic Manipulaive Therapy. They employ stretching and muscle positioning to treat structural musculoskeletal problems. They use it alot for people with back pain. I was curious, M.D.s don't have the best history intreatng back pain, maybe the D.O.s are doing a better job.

In a 1999 study, osteopathic manipulative therapy ( including stretching and positioning) was compared with standard medical care (including NSAID's, muscle relaxants and heat) in the treatment of lower back pain.  178 patients complaining of lower back pain of less than 6 months duration were randomly assigned to one of the two treatment groups. After 12 weeks of either intervention, outcomes were measured using the Visual Analogue pain scale, range of motion testing, and questioneers assessing how often the pain occured, and how much it interfered with daily activities. These assessments were performed by  people other than the physicians delivering the care, as a control.The study showed no statistically significant difference between the osteopathic or standard care group. There was however, a difference between the groups in the amount of medication given for the back-pain.  NSAIDs were prescribed to 54.3% in the standard group, compared to 24.3% in the osteopathic group (p <0.001). Muscle relaxants were given to 25.1% of the standard group compared to 6.3% of the osteopathic group (p<0.001).

This study did not assess the efficacy of either study as compared to doing nothing. The pathophysiology of lower back pain is such that it may simply resolve on its own with time. The study also didn't look at the difference in costs ofthe modalities. It may be that osteopathic manipulation, is more expensive than medication, because of reimbursement for the D.O.s time. The one thing this paper did show is that osteopathic therapy utilizes less medication. This is undoubtably an important difference, especially when considering the side effects of long-term use of NSAIDs and muscle relaxants, like GI upset, bleed, neutropenia, hepatic injury and so on.

A number of patients with chronic pain from osteoarthritis came in to the office for check-ups last week, many of them complaining that they were still having a lot of pain in their joints.  They had stopped taking Celebrex (celecoxib) and Bextra (valdecoxib), because they believed that these drugs might cause heart attack and stroke.  Since Vioxx (rofecoxib) was taken off the market  on September 30, 2004, there have been many questions regarding whether or not Celebrex and Bextra should also be taken off the market since they are in the same class of drugs as Vioxx.  Patients wanted to know if it was safe for  them to continue taking their medications.

Currently, there are no indications for patients to stop using Celebrex and Bextra.  A recent study showed that while doses of Vioxx > 25 mg was associated with a elevated risk of MI, Celebrex was not associated at any dosage. Another study showed that Vioxx is associated with new onset of hypertension, but again, it also showed that there was no association with Celebrex and new onset of hypertension.  A metaanalysis of trials that compared Bextra with a non-selective NSAID and placebo showed that there were no differences in incidence of cardiovascular thrombotic events between the 3 groups.

There has been some suggestion that there is an increased risk of MI associated with Vioxx because it was compared to naproxen which may have a cardioprotective effect.  However, the case-control study that shows this effect is retrospective, and the decision to prescribe naproxen versus an NSAID may have been based on perceived cardiovascular risk.   

An alternative to Bextra and Celebrex for patients who remain wary is Tylenol.  A meta-analysis of 10 randomized clinical trials shows that Tylenol reduces the pain of osteoarthritis in patients, though it is not as effective as NSAIDs.

Selective-COX-2 NSAIDs are currently indicated for the pain and inflammation of osteoarthritis, acute pain in adults, and menstrual pain in patients with histories of  gastrointestinal bleeding/ulcers.

Most of us starting to read this might have no answer for my title question. However, I sought to find an answer after seeing this 56 y/o man who came into the office this week for a recheck of his blood sugars and control of his type 2 diabetes.  When I looked at his old meds, it showed that he had been on chromium in the past, but not anymore. When I asked the doctor why he stopped the chromium or if it was effective he shrugged and said, "You know, I am not really sure." EBM searching to the rescue!

The therapeutic use of chromium has been debated, and the possible mutagenicity of the compound has been studied without much general conclusion.  In fact, there are multiple studies going on now aimed at finding a definitive answer (and even a grant by the NIH!). Here is the study I found that might prove beneficial to treating a certain class of type 2 diabetics.

In 1997, researchers from Beijing, China studied 180 men and women from the ages of 35-65 who had diagnosed type 2 diabetes for less than 10 yrs in a randomized, placebo-controlled, double-blind study. The patients were grouped into three categories: 1. receiving 100 micrograms of chromium picolinate twice a day, 2. receiving 500 micrograms twice a day, or 3. placebo group. The patients who were selected all had fasting blood sugars between 106-229 mg/dl and no other major health problems.

The main results were: 1)fasting blood sugars at 4 months were 20% lower in the 1gram/day group compared to placebo (130 vs. 105), 2)mean hemoglobin A1c levels were 8.5% for placebo, 7.5% for low-dose Cr, and 6.6% for the higher dose Cr (a decrease of ~22%)at 4-month follow up. Interestingly enough, there was no significant change in weight between the Cr and placebo groups at 2 or 4 months. No adverse events or toxicities were reported by subjects in the study.

What does this all mean? Keep in mind that patients in this study were free of major health problems and they all had BMIs between 24-26 (slightly overweight).  Also, their fasting blood sugars were not excessively high as some patients in poor control of their type 2 diabetes have. For now, I believe you have to choose your patients wisely if they come to you asking about the possible benefits of chromium picolinate. It is not a "cure" for type 2 diabetes but it might be beneficial for the patient in the early stages of mild-moderate diabetes who wants to use chromium, diet, and exercise modifications to get a hold of their sugars.

Chromium picolinate is available over-the-counter at most health food stores (and on-line)for about 20 cents per 200 mcg tablet.  This translates to a little less than a dollar a day to take as much as 1gram/day. Not too bad and cheaper than the meds!

 

This week we saw a patient who wanted a test for chlamydia because his partner had recently been diagnosed with it. I was able to learn quite a bit from his case. Within the last year, his partner had been tested for
chlamydia and tested negative. Even though they were mutually monogamous since before that test, his partner now tested positive. There are two methods of testing for chlamydia, one involves a cervical swab or urethral swab while the other is a urine test based on a first void specimen. A study compares the sensitivity and specificity or each method and found that using ligase chain reaction (LCR) genital swabs were more sensitive at
detecting Chlamydia trachomatis  than urine specimen however both methods were sensitive and specific enough to be employed for diagnosis of Chlamydial infection. Urine specimens have an advantage over urethral swabs because of the level of discomfort experienced by men during this procedure. Urine specimens also have an advantage over cervical swabs performed during routine Pap smears because they are less time-consuming and more comfortable for the patient.

We decided to treat this patient without testing to determine if he in fact had chlamydia. As we learned last year, there is a high rate of coinfection of chlamydia and gonorrhea thus we treated both. According to our lectures, the treatment of choice was doxycycline (100 mg BID for 7 days) with ceftriaxone or ciprofloxacin to cover gonorrhea. During the period of treatment patients must abstain for sex so as to prevent (re)infection of partners. It was exciting to learn that one dose of Azithromycin (1g) was also considered effective treatment for chlamydia and gonorrhea. Despite this, we still prescribed our patient with one dose of Ciprofloxacin (500 mg) to cover gonorrhea. This treatment regimen should significantly improve compliance and decrease the rates of reinfection. I found two studies (Study
1:, Study 2) which found that both treatment protocols are equally effective in treatment of Chlamydia infections.
We have learned a lot about the complications of chlamydia infection which most notably include PID and infertility in women, as well as epididymitis, prostatitis and conjunctivitis. I found a study which suggests that chlamydia may cause direct damage to sperm and may contribute to male infertility as well. In vivo studies provide conflicing evidence as to whether fertility is decreased in men with chlamydia infection, acute or past. However, in vitro studies provided direct evidence that sperm coincubated with chlamydia trachomatis have
decreased motility and premature death. This is hypothesized to occur by different mechanisms One, the lipopolysaccharide (LPS) in chlamydia may induce apoptosis by increasing the amount of reactive oxygen species (ROS) present in the sperm. ROS could also lead to DNA damage. Also, chlamydia LPS may bind to CD14 receptors present on sperm to induce the changes that lead to decreased motility and premature death. Overall
what is important is that there is a possiblity that men may suffer from decreased fertility if they are infected with chlamydia. This presents a new angle for us to discuss chlamydia with our male patients. Most of the complications of infection are female-centered and some males may not think it's important to be tested and treated for chlamydia because it does not affect them. However, by sharing this information with our patients we may be able to convince them that they should be tested
regularly and treated for chlamydial infections because it may affect their fertility as well as that of their female partners via PID. Now here are some pictures
of chlamydial infections. Chlamydia is a reportable disease in New York State.

This week in the clinic I followed up on a 21 year college student that had injured his neck while playing ice hockey. He was transported and seen in the ED (ER) the weekend prior. He was placed in in-line stablization with his helmet still on before being transported to the hospital. It turned out that he only had a muscle sprain without any significant c-spine injury. I got to thinking and I was curious to see if anyone had compared protective equipment from different sports and how well they protected from certain injuries.

As luck would have it, I found an article that compared head movement in backboard-immobilized helmeted football, lacrosse and ice hockey players. In the study, athletes were immobilized on backboards as per protocol. Three motion analysis HiRes cameras followed retroreflective markers placed on the helmet and bite mouthplate to measure relative head and helmet motion. The mean range of head motion for football players was 4.88 degrees (n = 9, SD 2.07), lacrosse players 6.56 degrees (n = 9, SD 1.61), and ice hockey players 5.54 degrees (n = 12, SD 1.19). The article concluded that the rotational head motion seen inside standard immobilized lacrosse and ice hockey helmets is similar to that seen in football helmets. This supported the safety of prehospital stabilization of the potential cervical spine-injured ice hockey and lacrosse athletes with in-line stabilization and helmet in place. I found this article to be patient oriented because we all either participate in sporting activities or know someone who does. This simple piece of info could prevent a permanent neurological injury. The moral of the story...Keep your helmet on.

*** The Blog is telling me "error on page" when I try to insert my link. Instead you can copy and paste this link to view the article: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11403119

A 33 year old patient, physically fit with an active lifestyle, proper diet per him, no family history of hypertension (HTN), was diagnosed with HTN 6mo ago during a check up visit.  He was medically treated for 5 mo and his blood pressure (BP) returned within normal limits.  The treatment was discontinued.  He now presents for a follow up visit. His BP is back in the 150s/100s.  The pt has no significant past medical history.  His social history is unremarkable except for his new position, started 1 year ago, that he finds extremely stressful.  Lead me to wonder, can professional stress impacts blood pressure so much? 

Stress is more and more recognized as an important factor in the disease process.  Stress has been shown to induce transient elevations in BP (Mancia G, Parati G. Reactivity to physical and behavioral stress and blood pressure variability in hypertension: Handbook of hypertension, vol. 9: behavioral factors in hypertension. Amsterdam: Elsevier; 1987, pp. 104-122.).  But can professional stress induced a chronic elevation in BP?

Fauvel JP et al concluded that stress could be associated with high BP at a short term and could explain high blood pressure in a long run only in stress-sensible subjects.

There is no real consensus in the literature because there are so many factors to consider (ages, nature of profession, perception of high and low job demand, individual perception of stress, individual coping reaction to stress...) and the mechanisms to explain the causality of stress on elevation of BP are so complex.  Moreover, important methodological problems still need to be appropriately solved.

What is your personal opinion on the matter?

As for the patient above, stress management was proposed and he was back on his previous meds but at lower doses.