Adult ADHD: Sit still for a moment

Posted on May 19, 2012 by

 

Attention-deficit/hyperactivity disorder (ADHD) is a condition that is usually diagnosed in childhood or as a teenager at some point. We often see college students that have been diagnosed with ADHD during their middle school or high school years and then come in to the office to have their prescriptions continued through college. A little less common is when an adult comes in for the first time thinking they may have ADHD.

 

I’ve found that adults will usually come in asking about ADHD when one or two of the following have occurred. #1 Your child has just been diagnosed with ADHD and since it does occur more often in families you do your homework and in listening to the doctors and doing a little googling you say, “hey, wait a minute….I think I have it too!!! #2 Your work is requiring major multi-tasking, deadlines, big projects, etc and you find yourself struggling compared to your colleagues or co-workers. What happens is that often times the ADHD symptoms can be mild enough that you remain “under the radar” and you make it through school, sometimes even grad school, without being diagnosed. For many that are diagnosed in childhood, you do learn to compensate over time so that many “outgrow” the condition and you do not require any treatment in adulthood. However, for about 30% of people with ADHD, the condition does continue into adulthood. It is estimated that about 3-4% of adults have ADHD.

ADHD does always begin in childhood and the symptoms are usually present before the age of 7. However, in diagnosing adults, it’s difficult and unreliable to try and remember how you were at that age. Instead, the American Psychiatric Association is suggesting that symptoms causing impairment be present before the age of 12 when diagnosing adults; even that is pretty tough but it’s better than age 7 I guess.

The symptoms of ADHD are broken down into symptoms of inattention and hyperactivity/impulsivity. You have to meet 6 out of 9 inattention symptoms or 6 out of 9 hyperactivity/impulsivity symptoms. It is now being suggested that in diagnosing adults you only need 4 out of the 9 symptoms instead of 6. Also, the symptoms need to have persisted for at least 6 months and at least some of the symptoms causing impairment must have been present before the age of 7 (or 12 if adult). Additionally, some impairment from the symptoms is present in two or more settings (e.g. school, home, work). Moreover, there must be evidence of clinically significant impairment in social, academic, or occupational functioning. Finally, the symptoms are not better accounted for by another mental disorder such as depression, anxiety, bipolar disorder, or something like thyroid disease, a side-effect of certain prescription drugs or over-the-counter medicines or herbal medicines, alcoholism, substance abuse or exposure to lead.

Here are some general screening questions to consider to see if you might have ADHD:

  • Do you have problems with paying attention and being hyperactive? Have you had these problems since you were a child?
  • Do you have a hard time keeping your temper or staying in a good mood?
  • Do you have problems staying organized or being on time?
  • Excessive impulsivity; saying or doing things without thinking
  • Excessive and chronic procrastination
  • Difficulty getting started on tasks
  • Difficulty completing tasks
  • Frequently losing things
  • Poor organization, planning, and time management skills
  • Excessive forgetfulness
  • Do these problems happen to you both at work and at home?
  • Do family members and friends see that you have problems in these areas?

If you answered yes to some of these questions, consider the formal criteria below. These are the 9 inattention-type symptoms. Remember as an adult you would need to have at least 4 of these:

  1. Difficulty following through on instructions. Failure to finish your schoolwork or duties in the workplace.
  2. Difficulty sustaining attention in tasks.
  3. Loses things needed for activities at school, work and home.
  4. Often does not seem to listen when spoken to directly.
  5. Doesn’t pay close attention to details or makes careless mistakes in schoolwork, work, or other activities.
  6. Difficulty organizing tasks and activities; seems disorganized.
  7. Has trouble with tasks that require planning ahead.
  8. Often forgetful in daily activities.
  9. Easily distracted by extraneous stimuli.

These are the 9 hyperactivity/impulsivity symptoms:

Hyperactivity

  1. Fidgety
  2. Can’t stay seated (you got ants in your pants)
  3. Difficulty engaging in activities quietly.
  4. Feeling of restlessness.
  5. Always “on the go” as if “driven by a motor”.
  6. Talk too much.

Impulsivity

            7. Blurts out answers before questions have been completed.

            8. Difficulty awaiting your turn.

            9. Interrupts people; butts into conversations.

It is possible to have ADHD as an adult even though you were not formally diagnosed when you were young. It is critical to make an accurate diagnosis and not miss some of the conditions listed above that can mimic ADHD in adults. Treatment can be life changing for some and make you much more productive at work and at home. A recent study of more than 150,000 U.S. adults found that current or new use of stimulant medications for ADHD did not increase the risk of serious cardiovascular events, including heart attack, sudden cardiac death, or stroke. So treatment, with proper monitoring, is considered pretty safe.

Additional Sources:

National Resource Center on ADHD

American Psychiatric Association

ADHD review by Familydoctor.org

 

Post R, Kurlansik, S. Diagnosis and Managament of Attention-Deficit/Hyperactivity Disorder in Adults. American Family Physician. 2012;85(9):890-896
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Shingles; not the ones on your roof

Posted on May 12, 2012 by

 

If any of you have seen a family member or friend get shingles, it can be quite painful. Shingles or Herpes Zoster is the reactivation of the chicken pox virus that has been dormant in your body since your youth. The virus is called the varicella-zoster virus (VZV) and when you get it, usually as a child, it manifests as chicken pox. This is a disease characterized by fever, some mild upper respiratory symptoms, and these painful red fluid-filled blisters that pop out all over your body at varying stages. When you get it as a child it’s usually not that bad but if you get it as an adult it can be more painful and sometimes it can even turn into pneumonia. So for many years moms would purposefully expose their children to whoever had chicken pox in the neighborhood so you would just get it and be done with it. Fortunately, since 1995 the chicken pox vaccine, called VARIVAX, has been available and has significantly decreased chicken pox cases around the country.

For those of us who weren’t that lucky and ended up getting the chicken pox, the virus never leaves your body! It stays in your nervous system along these little nodes close to your spine called dorsal root ganglia. It remains in a dormant state and your immune system does a good job of not allowing that virus to replicate or leave those little ganglia. Anyway, at some point in your life your cellular immunity may become temporarily suppressed, distracted or whatever, allowing the virus to replicate and attack you. This can happen because of stress, trauma, or some other infection where your body gets distracted. This time the disease travels along a nerve path, what we call a dermatome, and you will once again see this red blistering rash appear, many times in these characteristic clusters. It can happen anywhere in your body but only on one side of your body, and usually in 1 or 2 dermatomes at most. If you see it on both sides of the body or occurring in 3 or more dermatomes either it’s not shingles (Zoster) or if it is shingles then there’s something seriously wrong with your immune system. Anyway, the older you get the more likely your shingles episode can be quite painful and incapacitating. Sometimes the area where you got the shingles can remain very sensitive or painful for many months or rarely years after the initial episode; this is what we call post-herpetic neuralgia. An episode of shingles typically will last 1-2 weeks and then resolve. While you have these skin lesions you are contagious. Meaning if someone who has never had chicken pox comes in contact with those skin lesions they will get the chicken pox; ouch! So keep it covered and stay away from the very young, the very old, anyone who has a serious chronic illness, or pregnant women. Finally, shingles can recur. Sometimes, I’ve seen people have it 2 or 3 times. However, most people just get it once.

In 2006 the shingles vaccine or ZOSTAVAX became available and is indicated for those who know they already had the chicken pox and would like to avoid getting shingles. When the vaccine first came out it was indicated for adults 60 and up. In 2011, the FDA approved it also for adult 50-59. If you are not sure if you’ve had the chicken pox we can do a blood test to figure it out. If it turns out you managed to never get the chicken pox then we would actually give you the chicken pox vaccine (VARIVAX) instead. Zostavax should not be given to pregnant women, persons with a primary or acquired immunodeficiency, or to persons with a history of anaphylactic reaction to gelatin, neomycin, or any other component of the vaccine. Herpes zoster vaccine can be administered simultaneously with other indicated vaccines.

Getting the Shingles vaccine reduces your chances of getting shingles by over 50%. If you are still unlucky and get shingles anyway despite the vaccine, your chances of getting that lingering pain after the infection (post-herpetic neuralgia) are much less because of the vaccine.

I highly recommend that anyone 50 or above consider getting this vaccine. I have seen plenty of cases of shingles and it can really disrupt your life and be quite incapacitating for some people.

 

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Fish Oil and Cardiovascular Disease Prevention

Posted on May 7, 2012 by

Fish oil is one of the most popular supplements out there so I wanted to review the current literature on it so you can decide whether or not to take it.

The chemical name for these fats are: n-3 polyunsaturated fatty acids. So you will here the term: PUFA’s, Omega-3 Fatty acids, or just plain old fish oil. The main plant-based form is called Alpha-Linolenic Acid (ALA), and is found in soybeans, canola oil, flaxseed, and English walnuts. There are 2 major types of marine-based fish oils and these are Eicosapentaenoic Acid (EPA 20:5) and Docosahexaenoic Acid (DHA 22:6). High concentrations of these fish oils are found in cold water fish such as salmon, mackerel, tuna, herring, and sardines.

Fish oil hit the spot light when in 1976 there was a study published showing that high consumption of fish oil by the Inuit people living in Greenland was associated with a decreased risk of cardiovascular disease. Since then many more observational studies have shown that consuming a diet high in fish may decrease cardiovascular events. The proposed mechanisms by which fish oil seem to be cardio-protective is that it is thought to have anti-inflammatory, anti-oxidant, and membrane-stabilizing effects. Fish oil will also lower triglycerides when taken in high doses (4gm/day).

When it comes to prospective randomized placebo-controlled trials that we doctors rely upon to really show if there is a cause and effect relationship, the benefits of fish oil seem to be mainly in secondary prevention. In other words, it helps people who have already had a heart attack or stroke (cardiovascular event) and you’re trying to prevent a second event (secondary prevention). At least 4 major trials have shown benefit in this area including: 1. The DART Trial, 2. The LYON Heart Trial, 3. SINGH, et al, and 4. GISSI-Prevenzione Trial. These trials have shown anywhere between a 20-30% reduction in the risk of death related to cardiovascular disease. Unfortunately, we do not have any primary prevention trials yet showing benefit. There are currently several ongoing primary prevention trials that should help clarify whether or not fish oil truly helps those that are currently healthy and have no known heart disease.

So what should we do in the meantime? The current recommendations are that we should be consuming fish at least twice per week especially the dark, fatty fish mentioned above. This mimics the consumption seen in many of the observational trials listed above. This strategy will also help replace consuming less healthful sources of protein such as red meat or processed meats high in saturated fats. For people who don’t eat fish your option would be to consume more of the plant-based Omega-3 Fatty acids listed above and/or take a fish oil supplement. Taking 1 fish oil capsule per day, which is a mixture of EPA and DHA, is approximately 1 gram of fish oil. Taking 1 capsule of fish oil daily is the equivalent of having fish twice per week so take your pick. I prefer the fish myself especially wild salmon which is chock-full of PUFA’s! So if you already have a personal history of cardiovascular disease we know it’s helping you for sure and we recommend you take it. If you’re just a healthy guy or gal looking to do healthy stuff, the jury is still out; we don’t know if it will make a significant impact. We will know more in a year or two when that research trial gets completed. At least we know that taking fish oil does not seem to cause harm except some will get indigestion or belching and some people get the runs. Fish oil does thin your blood a bit so if you are going to have a surgical procedure you should stop it at least 2-4 weeks prior to your surgery. Some will recommend fish oil as a general inflammation reducer and recommend it for anything from stress, arthritis, a cold, or whatever; those indications are even more questionable.

Bang HO, Dyerberg J, Hjoorne N. The composition of food consumed by Greenland eskimos. Acta Med Scand 1976;200:69-73.
Bucher HC, Hengstler P, Schindler C, Meier G. N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. Am J Med 2002;112:298-304.

 

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Polyphenols and Cardiovascular Disease

Posted on April 29, 2012 by

It has been known for quite some time that plant-derived foods and beverages provide cardiovascular benefits. Many observational studies have shown an association between the consumption of plant-based foods including fruits, vegetables, nuts, whole grains, and plant-derived beverages, and a lower incidence of cardiovascular diseases. For years it was thought that these benefits were due to the anti-oxidant properties of vitamins and carotenoids found in these plant-based sources. However, studies completed using these specific substances have failed to show any benefit. So there has now been a focus on a large family of plant-based chemicals (phytochemicals) called polyphenols. Research is now showing that consuming a diet high in flavonoids (a type of polyphenol) will have a positive impact on specific intermediate outcomes such as cholesterol, blood pressure, endothelial function, and platelet function. The research is most compelling for cocoa-derived products and tea; so listen up you chocolate lovers!

 

Polyphenols are a complex group of secondary plant metabolites. They are divided into 5 major types: 1. Phenolic Acids, 2. Flavonoids, 3. Stilbenes, 4. Lignans, and 5. Curcuminoids (not sure how I would say that). The 2 classes that are the most abundant and most studied are the Phenolic acids and the Flavonoids, so let’s talk about them a little more.

Phenolic Acids

This class is further subdivided into hydroxybenzoic acids and hydroxycinnamic acids. Below is a chart showing food sources for these 2 categories:

 

The hydroxybenzoic acid content of edible plants (gallic, salicylic and vanillic acids) is generally very low, with the exception of certain red fruits, black radish and onions. The hydroxycinnamic acids constitute the most abundant polyphenols in our diet because they are present at high levels in many foods widely consumed (coffee, cereals, fruits).

Flavonoids

These are subdivided as detailed on the chart below:

 

The diversity of the chemical structures of dietary polyphenols makes quite difficult the estimation of their total content in foods. Thus, until very recently, the composition tables for polyphenols were very incomplete. A typical diet rich in fruits, vegetables and plant beverages has been estimated to provide about 1 g of polyphenols/day, with significant variations depending on the extent of consumption of drinks rich in polyphenols (tea, wine, coffee, fruit juices). Recently, a new database on polyphenol content in foods has been developed, and is now available online. The Phenol-Explorer database (available at http://www.phenol-explorer.eu) allows retrieval of information on the content of 502 polyphenols in 452 foods (fruits, vegetables, beverages, cereals and spices).

So far the research is strongest for the flavonoid class of polyphenols and specifically the flavanol subclass containing cocoa-derived products (chocolate!) and tea. The most convincing effects were the favorable effects seen on blood pressure and endothelial function. The endothelial cells are the innermost lining of cells in your arteries; these are very important in the development of atherosclerosis (plaque build-up in the arteries). So if your endothelial cells are working properly you are much less likely to deposit plaque in your arteries. So basically, eating dark chocolate and having some tea will lower your blood pressure and keep your arteries clean. Sounds like a win-win situation.

This is, of course, is not to say that the other polyphenols don’t help, it’s just that the other ones have been harder to study. There is ongoing research to figure out how all these plant-based chemicals will benefit us but in the mean time, “it’s all good”. It’s important to get your daily dose of fruits, vegetables, nuts, whole grains, and plant-derived beverages. Variety is key; the more colors the better!

 

Arts, I.C. and Hollman, P.C. (2005) Polyphenols and disease risk in epidemiologic studies. Am J Clin Nutr 81(1 Suppl.): 317S-325S.
Bjelakovic, G., Nikolova, D., Gluud, L.L., Simonetti, R.G. and Gluud, C. (2007) Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA297: 842–857.
Chong, M.F., Macdonald, R. and Lovegrove, J.A. (2010) Fruit polyphenols and CVD risk: a review of human intervention studies. Br J Nutr 104(Suppl. 3): S28-S39.
 Vita, J.A. (2005) Polyphenols and cardiovascular disease: effects on endothelial and platelet function. Am J Clin Nutr 81(1 Suppl.): 292S–297S.
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Cervical Cancer Screening

Posted on April 22, 2012 by

 

Last month, newly revised guidelines for cervical cancer screening were published that I think are important for all women to be aware of. First I wanted to review some data on cervical cancer and the impact of screening, the role of Human Papillomavirus infection (HPV), and finally the new guidelines.

A long time ago, cervical cancer was the most commonly diagnosed cancer in women until Dr. George Papanicolaou came up with his “pap smear” test back in 1943. Because of this test, the number of new cases of cervical cancer decreased by 70% between 1950 and 1970. Between 1970 and 2000, there was another 50% decrease. This has certainly been a great triumph in the field of preventive medicine! However, I still think we could do better as the estimates for 2011 in the U.S. indicated that there would be 12,710 new cases of cervical cancer diagnosed and 4,290 cervical cancer deaths. It turns out that about 50% of women that are diagnosed with cervical cancer in the U.S. have never had a pap smear.

Another great discovery has been the association of the HPV virus with cervical cancer. More than 90% of cervical cancer patients have HPV and 99.7% of cervical neoplasia (cancer + pre-cancer) contain HPV. We now know that HPV causes cervical cancer. The problem is there have been over 100 subtypes described, about 40 of them associated with genital issues. There are about 15 HPV serotypes that are considered “high-risk” or “oncogenic”, meaning they can cause cancer. Two of them, types 16 and 18, cause about 70% of cervical cancers. Gardisil, the first vaccine created to prevent cancer, will protect you against HPV 16 and 18 as well as types 6 and 11. Please review my prior post on this topic.

Although there is still room for improvement in terms of making sure all eligible women are getting their pap smears, there are also many women that may be over screened believe it or not. Over the past decade or two we have assumed that more is better so the medical establishment has advocated annual pap smears as the way to go. It turns out that in countries like the Netherlands, the death rates from cervical cancer are about the same as in the U.S. although they screen a lot less often. There is potential harm in over screening in terms of getting false positive results which may result in unnecessary procedures and risks.

Three major organizations got together to review all the current research and came up with updated guidelines. These organizations are: 1. American Cancer Society (ACS), 2. American Society for Colposcopy and Cervical Pathology (ASCCP), and 3. American Society for Clinical Pathology (ASCP). Separately, the U.S. Preventive Services Task Force (USPSTF) came up with their own recommendations last month, which surprisingly enough, are basically the same. This is weird because the USPSTF usually say something different just to throw everybody off! Anyway, here goes:

1. AGE TO BEGIN SCREENING:21

2. SCREENING FREQUENCY AGE 21-29: CYTOLOGY (PAP) EVERY 3 YEARS.

3. SCREENING FREQUENCY AGE 30-65: CYTOLOGY + HPV DNA TESTING EVERY 5 YEARS (PREFERRED) OR CYTOLOGY ONLY EVERY 3 YEARS (ACCEPTABLE).

4. WOMEN ABOVE THE AGE OF 65 DO NOT NEED ANYMORE SCREENING. Exceptions would be if you have had abnormal pap smears in the past; please check with your Gynecologist.

And one important point that some women are not aware of: If you have had your Uterus removed you do not need anymore pap smears because you have no cervix. The exception would be if the surgeon left the cervix behind which is done occasionally or if the uterus was removed due to cancer or if you had an abnormal pap prior to surgery. Again, please check with your Gynecologist.

And finally, there is a definite value to a well woman exam including breast and pelvic examination with your respective GYN doctors, despite the fact that a pap smear may not be needed. So please continue to visit your GYN on at least an annual basis.

If you currently don’t have a Gynecologist, please visit our website to see our excellent team of OB/GYN’s.

 

Saslow D, Solomon D, Lawson HW, et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 March 14.
USPSTF. Screening for Cervical Cancer. March 2012.http://www.uspreventiveservicestaskforce.org/uspstf/uspscerv.htm

 

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High-Sensitivity C-reactive protein: Should I get one?

Posted on April 15, 2012 by

 

C-reactive protein (CRP) is a nonspecific marker of inflammation in the body. Low level increases in CRP have been associated with atherosclerosis. However, the regular CRP blood test doesn’t detect that so they came up with the “high-sensitivity C-reactive protein (hsCRP) assay or blood test that detects very small increases in this molecule. What is clear is that elevation in hsCRP level is associated with an increased risk for coronary heart disease and stroke. What is more complicated is whether or not it helps us to further risk stratify (figure out who is at high or low risk) beyond the traditional heart disease risk factors and the global risk scores such as the Framingham Risk Score. So what follows is a brief review of this topic and then some recommendations on how we should use this test and who should get it.

It has been known since the 1990’s that inflammation plays a major role in the development of atherosclerosis; the plaque that forms in arteries leading to heart attacks and strokes. Around that same time researchers began reporting associations between hsCRP level and the risk for coronary heart disease, stroke, or both. A few years ago, the Lancet published a meta-analysis of more than 50 studies involving more than 160,000 patients showing that the magnitude of risk associated hsCRP was as large as that of total cholesterol as well as blood pressure. Also, the addition of hsCRP and family history to the Framingham Risk Score, as in the Reynolds Risk Score, has been shown to improve significantly the ability to estimate 10 year cardiovascular risk. Finally, studies done on large patient cohorts, such as Framingham study patients and the Women’s Health Study patients, have shown that the hsCRP level has helped to reclassify patients considered to be at intermediate risk.

The problem is there are some experts in the field who are not convinced that hsCRP is truly an independent risk factor that can further assess risk beyond what the traditional risk factors (smoking, blood pressure, low HDL, etc) can do. This has to do with which statistical model you use to decide if this marker is worthy or not. If you apply what is called the C-statistic or the area under the receiver operating characteristic (ROC) curve, it looks like hsCRP doesn’t add much. The funny thing is, if you do the same thing by adding LDL or HDL to the traditional risk factors, there is also very little change to the area under the ROC curve. Nevertheless, based on this and a few other minor details, the United States Preventive Services Task Force (USPSTF) said in 2009 that hsCRP is bologni and that we shouldn’t order it. The good news is most statisticians are now saying we should be using measures of reclassification in addition to the other standard metrics to evaluate new biomarkers. When you use this metric, most studies are showing that hsCRP is in fact an independent predictor of cardiovascular risk and it is especially helpful in further stratifying those that are at intermediate (moderate) risk (ie- 2 or more major risk factors for heart diease).

The biggest thing to happen to hsCRP was the landmark JUPITER trial in 2008. This was a study in 17,802 apparently healthy men and women who were not diabetic and had an LDL <130. For people who had a hsCRP of 2.0 or more they were randomized to get Crestor 20mg daily (a statin) or placebo. After 1.9 years the trial was stopped early because it showed a 44% reduction in the risk of cardiovascular events including cardiovascular and overall mortality. The shocking thing is that these are people that you would normally not give a statin to.

Many unanswered questions remain as to how exactly we should be using this marker and hopefully the ATP IV guidelines due later this year will clarify things. In the meantime, I think the test is most beneficial in identifying people who may benefit from the use of a statin who land in this intermediate risk category. If your risk for heart disease is very low or very high, the test doesn’t help you; it’s for those people in the middle, ie- a healthy 55 year old male with a slightly low HDL at 35.

A few things that mess with the CRP level making it difficult to interpret are: if you are on estrogen, recent infection or trauma, autoimmune or other chronic inflammatory conditions, taking immune-modulating medications, and chronic kidney disease. A level of <1 is considered low risk, 1-3 is intermediate risk, and >3 is high risk. We would use the value of 2 or greater as per the JUPITER trial to decide on the need for treatment. If the value does come out elevated it is recommended that we repeat the level one more time in 2 weeks to make sure it’s a real number.

Thank you for reading; I hope it wasn’t too confusing!

 

  1. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973–979.
  2. Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, Collins R, Danesh J. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis.Lancet 2010;375:132–140.
  3. Ridker PM, Buring JE, Rifai N, Cook NR. Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: the Reynolds Risk Score. JAMA 2007;97:611–619.
  4. Koenig W, Löwel H, Baumert J, Meisinger C. C-reactive protein modulates risk prediction based on the Framingham score. Circulation 2004;109:1349–1353.
  5. WilsonPWF, Pencina M, Jacques P, Selhub J, D’Agostino R, O’Donnell CJ. C-reactive protein and reclassification of cardiovascular risk in the Framinghamheart study. Circ Cardiovasc Qual Outcomes2008;1:92–97.
  6. Ridker PM, Rifai N, ClearfieldM, DownsJR, Weis SE, Miles JS, Gotto AM Jr.. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med2001;344:1959–1965.
  7. Ridker PM, Cannon CP, Morrow D, Rifai N, Rose LM, McCabe CH, Pfeffer MA, Braunwald E; for the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) Investigators. C-reactive protein levels and outcomes after statin therapy. N Engl J Med 2005;352:20–28.
  8. Nissen SE, Tuzcu EM, Schoenhagen P, Crowe T, Sasiela WJ, Tsai J, Orazem J, Magorien RD, O’Shaughnessy C, Ganz P. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med2005;352:29–38.
  9. Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr., Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359:2195–2207.
  10. Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr., Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, Macfadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ. Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial. Lancet 2009;373:1175–1182.
  11. Emberson J, Bennett D, Link E, Parish S, Danesh J, Armitage J, Collins R; Heart Protection Study Collaborative Group. C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20,536 patients in the Heart Protection Study. Lancet 2011;377:469–476.
  12. Sattar N, Murray HM, McConnachie A, Blauw GJ, Bollen ELEM, Buckley BM, Cobbe SM, Ford I, Gaw A, Hyland M, Jukema JW, Kamper AM, Macfarlane PW, Murphy MB, Packard CJ, Perry IJ, Stott PW, Sweeney BJ, Twomey C, Westendorp RGJ, Shepherd J; for the PROSPER study group. C-reactive protein and prediction of coronary heart disease and global vascular events in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). Circulation 2007;115:981–989.
  13. Ridker PM, MacFadyen J, Libby P, Glynn RJ. Relation of baseline high-sensitivity C-reactive protein level to cardiovascular outcomes with rosuvastatin in the Justification for Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER). Am J Cardiol 2010;106:204–209.

 

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Lung Cancer Screening: Is it time?

Posted on April 8, 2012 by

 

We currently have pretty decent screening strategies for both colon cancer and breast cancer; it’s not perfect but it does save lives. Prostate cancer screening is a bit up in the air right now and we’ll talk about that one at another time. Lung cancer screening has come to attention again in the past year because of the recent publication of the findings from the National Cancer Institute’s (NCI) National Lung Screening Study (NLST). Also, one of the major organizations that create guidelines for doctors, the National Comprehensive Care Network, is now recommending lung cancer screening based on the results of NLST. Before we get into that, I wanted to briefly give you some cancer statistics; tell you how bad smoking is so that you’ll quit if you’re currently smoking or basically stay clear away from it; and finally, review the NLST so you can decide if you should be screened.

According to the American Cancer Society (ACS), it is estimated for 2012 that about 14% of cancer diagnoses this year will be lung. The good news is the number of new cases in men has been declining over the past twenty years. In women, the number of new cases has finally started to decline after a long period of increase. However, lung cancer doesn’t like to take prisoners as it accounts for more deaths than any other cancer in both men and women. This year, lung cancer will account for 28% of all cancer deaths. Again, a little good news is that death rates have been declining in men since 1991 and in women since 2003. These improving patterns are as a result of reduction of cigarette smoking over the past 50 years.

Here are the five most common causes of cancer death in the U.S. right now in men and women:

 

WOMEN:                                           MEN:

 

#1 Lung                                                           #1 Lung

#2 Breast                                                      #2 Prostate

#3 Colon                                                        #3 Colon

#4 Pancreas                                                  #4 Pancreas

#5 Ovary                                                       #5 Liver

 

To bring this closer to home, here are the estimates for 2012 in Colorado for men and women combined:

There will be 22,820 new cases diagnosed. The top 5 will be: 1) Prostate (17%), 2) Female Breast (15%),       3) Lung (11%), 4) Colon (8%), and 5) Melanoma (6%).

There will be 7,190 cancer deaths estimated in Colorado in 2012: 1) Lung (24%), 2) Colon (9%), 3) Female Breast (7%), 4) Pancreas (7%), and 5) Prostate (5%).

So before we get into this new study, let me give you some facts about what tobacco smoke can do for you:

 

 

  • Smoking-related diseases remain the world’s most preventable cause of death.
  • The World Health Organization estimates 6 million smoking-related premature deaths occur each year.
  • 50% of all who continue to smoke will die from smoking-related diseases.
  • In the U.S., tobacco use is responsible for nearly 1 in 5 deaths each year.
  • Smoking accounts for 30% of all cancer deaths and 80% of all lung cancer deaths.
  • Other than lung cancer, here other cancers that smoking can cause: cancers of the head & neck (nasal, oral, vocal cords, lips, etc), esophagus, pancreas, cervix, ovary, kidney, bladder, stomach, colon, and blood (acute myeloid leukemia).
  • Non-cancerous conditions associated with smoking: heart disease, cerebrovascular disease, chronic bronchitis and emphysema, and gastric ulcers.

 

Ok, now the study: The NCI’s National Lung Screening Trial (NLST) was launched in 2002. They randomized 53,454 adults ages 55-74 at high risk for lung cancer into two arms: one group would get an annual Low-Dose Computed Tomography (LDCT) every year for 3 years and the other group would just get an annual Chest x-ray. The high risk patients were defined as current or former smokers ages 55-74 with at least a 30 pack-year history of smoking. For example, this can be 1 pack/day x 30 years or 2 packs/day x 15 years, etc. Also, former smokers would have had to have quit within the past 15 years. In October 2011, the trial was stopped early because it showed a 20% reduction in lung cancer mortality in the LDCT group. There was also a 6.7% reduction in death from any cause. Also, according to Dr. Harold Varmus, Director of the NCI, “the LDCT group did not experience a rate of unforeseen, adverse screening effects that would lead to uncertainty about the balance of benefits and harms”.

The potential harm with screening is getting a false positive result, which means there is a nodule found in the lung but it’s not cancer. This can lead to significant anxiety, additional costs, additional radiation exposure, and possible exposure to invasive procedures. Current issues are: what is the best screening frequency, lung nodule work-up techniques, what about people with other risk factors: history of cancer, lung disease, family history of lung cancer, radon exposure, occupational exposure, 2nd hand smoke exposure. Is LDCT truly cost effective? Many health insurances are not paying for this procedure and it costs about $300.

There are ongoing studies in both the U.S. and Europe that will begin to clarify these issues. In the mean time, although the American Cancer Society (ACS) has not made lung cancer screening with LDCT a formal guideline, they did issue a guidance statement in view of the landmark findings of the NLST. The ACS states the following:

 

“Adults between the ages of 55-74 who meet the eligibility criteria of the NLST and are concerned about their risk of lung cancer may consider screening for early lung cancer detection. With their physician, individuals interested in screening should weigh the currently known benefits of LDCT screening with the currently known limitations and risks and make a shared decision as to whether they should be screened for lung cancer”.

 

And probably the most important point: “SCREENING SHOULD NOT BE VIEWED AS AN ALTERNATIVE TO SMOKING CESSATION”. If you smoke, please consider quitting and if you’re thinking about smoking please don’t!

 

Reduced Lung Cancer Mortality with Low-Dose Computed Tomographic Screening. N Engl J Med 2011.
World Health Organization. WHO Report on the Global Tobacco Epidemic, 2011.Geneva: World Health Organization, 2011.

www.cancer.org

 

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Allergies or a Sinus Infection?

Posted on March 31, 2012 by

 

Many of you have been having the sniffles over the past few weeks as Spring has made it’s presence known. Specifically, there are currently high concentrations of tree pollens in the air, including: a high amount of Cottonwood and Aspen tree pollen, a moderate amount of Cedar and Juniper tree pollen, and a low amount of Elm tree pollen.

Upper respiratory allergies can manifest in various ways and sometimes a viral or bacterial infection could be complicating matters as well. Let’s go over some of the main allergy symptoms and then also review some of the symptoms that could suggest more of an infection that would benefit from an antibiotic.

Allergic Conjunctivitis: dry or watery eyes; red, itchy, and/or burning sensation in the eyes.

Allergic Rhinitis: runny or stuffy nose, nasal and sinus pressure, sneezing, frontal headache.

Post-Nasal Drip: dry cough, worse at night or in the morning, intermittent or chronic sore throat, fullness or pressure in the ears, phlegm stuck in the back of your throat.

Asthma/Airway Hyperreactivity: cough, dry or whitish phlegm, chest congestion but “can’t bring anything up”, wheezing, chest constricted or tight.

With allergies, patients also frequently feel kind of tired or fatigued, “headachy”, and it can affect your sleep, etc.

The following symptoms make me think of an infection:

  1. The fatigue is more pronounced, no energy, you get tired really easy. Many patients will sense this change and know to come in because it “feels like more than just an allergy”.
  2. An increase in the quantity of phlegm production.
  3. A change in the color of the phlegm from white or clear to green or yellow; what we call purulent sputum. (Ok that’s a little gross).
  4. The presence of fever. Most sinus infections occur without fever, however, if there is a definite fever that would argue against this being simply an allergy.
  5. Significant pressure or pain over any of your sinus cavities (forehead, cheeks, or behind your nose/eyes). Symmetric or diffuse involvement of the sinuses is more likely allergy or a virus while one-sided symptoms are more likely bacterial requiring an antibiotic.
  6. Tooth pain.
  7. Loss of sense of smell or taste.
  8. Some patients will get a bad smell in their nose or taste in the mouth and know that their allergy turned into an infection.
  9. Any of the above symptoms for more than 10-14 days suggest more of a bacterial sinusitis.
  10. An initial common cold followed by improvement in symptoms and then a sudden worsening 1-2 weeks later.

Because sinus infections tend to wax and wane, patients will come in after having symptoms for a few weeks and sometimes a few months. It will feel like its getting better and then it gets worse again, etc.

For many, sinus infections can turn into “bronchitis” or “it always goes into my lungs”. This is what we call Reactive Airways Disease. It’s kind of a form of asthma except it eventually gets better. I will often prescribe an asthma-type inhaler to help with the chest symptoms and if it’s really bad it gets better with a steroid (cortisone).

Anyway, if you’re mainly having allergy symptoms most of you have your own strategies of how to get through the season including anti-histamines (ie- Claritin, Zyrtec, etc) and/or nasal steroids (ie- Flonase, Nasonex, etc).  A sinus irrigation system is also helpful and it may help prevent the progression towards a sinus infection. Options include: Ocean Nasal Spray, Neilmed, or a Neti Pot (yes I said Neti Pot).

Once things turn into a sinus infection, then we go with the following:

 

 

  1. Decongestants: pseudophed or afrin (max 3 days) if needed.
  2. Mucolytic agents (Mucinex).
  3. Sinus irrigation.
  4. Ibuprofen for pain/pressure.
  5. Anti-histamine in the allergic patient.
  6. Nasal steroid for more chronic symptoms or as monotherapy if symptoms are mild.
  7. Oral steroids if symptoms are severe or persistent.
  8. Antibiotics for 10-14 days usually.

Now don’t let those allergies keep you indoors; please get out and enjoy!

 

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Can Aspirin Prevent Cancer?

Posted on March 24, 2012 by

 

The biggest medical news this week has been the 3 studies that were published in a major medical journal called the Lancet from Great Britain. The studies add to the large body of accumulating evidence that aspirin may help prevent cancer.

Large studies in the past looking at the role of aspirin in preventing vascular events such as strokes and heart attacks that we reviewed last week have sometimes shown less cancer deaths as well. The association has been strongest with colorectal cancers and in fact aspirin is recommended to prevent colorectal cancer recurrence and also to reduce the incidence of colon cancer in those that are at very high risk, such as patients with familial polyposis. Prior studies have shown that this association with a lower incidence of cancer occurs after many years of taking aspirin regularly, particularly after 10 years of regular use. The protection also seems to be mainly in “solid tumors” of the “adenocarcinoma type”. The incidence of hematologic tumors such as leukemia’s seems unaffected by aspirin use.

What these newly published studies bring to light is: 1) Aspirin decreased the risk of cancer after only 3 years of use, 2) Aspirin helped prevent other forms of cancer other than just colon; it also reduced the incidence of esophageal, stomach, breast, and lung cancer, and 3) Regular aspirin use helped to limit the spread of cancer in someone who already had it (decreased metastasis). Specifically, the study reviewed 51 randomized trials and found a 15% reduction in the risk of cancer death, a 38% reduction in the chance of getting colon cancer, and a 36% reduction in the risk of developing metastasis in people who already had cancer. The wonder drug is back and it only costs pennies!!!

Before you go to Costco and buy a lifetime supply of aspirin, consider the following limitations:

  1.  None of these studies were designed to look at whether or not aspirin reduces the chances of getting cancer. All the studies reviewed were designed to look at vascular outcomes (heart attack or stroke). So for example, there was no information on what all these patients were doing for cancer preventive screening or surveillance.
  2. The 2 largest ongoing randomized trials, the Women’s Health Study (WHS) and the Physician’s Health Study (PHS) were excluded from the Lancet studies. The WHS involves 39,876 women taking 100mg of aspirin every other day and after 10 years there has been no cancer benefit. In the PHS there are 22,071 men taking 325mg of aspirin every other day and after 5 years there has been no cancer benefit.
  3. Remember that there is a risk of bleeding when you take aspirin on a daily basis.

In conclusion, regular use of aspirin over years may help reduce the chances of getting certain kinds of cancer. This needs to be balanced against the potential bleeding risks. Further studies will need to look at whether or not there is actually a cause and effect relationship instead of just an association. Hopefully, this connection with aspirin will one day lead to a better understanding of cancer that will lead to better treatments and ideally, better preventive strategies. In the mean time, it is not a formal recommendation or guideline at this time that you take an aspirin everyday to prevent cancer. If you are considering taking an aspirin everyday for this purpose, you should discuss the risks and benefits with your doctor so that you can make an informed decision.

 

Rothwell, et al. Short-term effects of daily aspirin on cancer incidence, mortality, and non-vascular death: analysis of the time course of risks and benefits in 51 randomised controlled trials. The Lancet. 21 March 2012 doi:10.1016/S0140-6736(11)61720-0
Rothwell, et al. Effect of daily aspirin on risk of cancer metastasis: a study of incident cancers during randomised controlled trials. The Lancet. 21 March 2012 doi:10.1016/S0140-6736(12)60209-8
Rothwell, et al. Effects of regular aspirin on long-term cancer incidence and metastasis: a systematic comparison of evidence from observational studies versus randomised trials. The Lancet. 21 March 2012 doi:10.1016/S1470-2045(12)70112-2

 

 

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Aspirin in Primary Prevention

Posted on March 17, 2012 by

 

Aspirin, or acetylsalicylic acid, has been one of those great discoveries in the history of medicine. Salicylate-rich plants have been used for medicinal purposes since antiquity. In the 18th century, it became known as willow bark extract and was used to reduce fever, pain, and inflammation. In the late 1800’s it was eventually created synthetically and turned into aspirin; a household name. In the 50’s and 60’s, aspirin was used in pretty high doses and so bleeding complications were a common event. That’s where someone came up with the idea, “Hey, maybe this thing thins your blood and we can use it to prevent heart attacks and strokes”; the rest is history.

We know that aspirin is a must for anyone who has had a prior heart attack, stroke, transient ischemic attack (TIA), or unstable angina; this is what we call secondary prevention. There is a 25% reduction in the risk of a recurrent vascular event and an 18% reduction in the risk of dying from a “vascular” cause. Since this would be the most common cause of death in someone who already has vascular disease, we know that aspirin reduces total mortality, or in English, aspirin prolongs your life!

The role of aspirin is also very clear in the setting of an acute heart attack and also when undergoing coronary revascularization such as bypass surgery or angioplasty.

Things become a little more complicated when considering the use of aspirin in a healthy population that has never had a vascular event; what we call primary prevention. A meta-analysis of 6 large trials published in 2006 showed a 12-14% reduction in the risk of “composite cardiovascular events”; this is all the endpoints (fatal and non-fatal cardiovascular events) combined. However, when you weed things out a bit there was no decrease in the risk of cardiovascular death; so the benefit is not as great as with secondary prevention. This is important because if you’re looking at a much smaller benefit, you really need to think about the risks of aspirin, which is of course, the bleeding.

Other interventions for reducing the risk of cardiovascular events and death are pretty clear such as taking medication to lower your blood pressure (If it’s high), taking a statin (if you need it), and smoking cessation (that’s always a good choice). If you think about potential side-effects of the above, they are pretty minor or at least manageable in comparison to having a major bleed. Aspirin-induced bleeding is mostly from the gastrointestinal tract (GI tract) and although most bleeding outside of the GI tract tends to be minor (i.e. – a nose bleed), very rarely the bleeding can occur in a critical area such as the eye or the brain (intra-cerebral hemorrhage). Fortunately, these things are rare but let’s review the most recent meta-analysis on this topic.

Just published in the Archives of Internal Medicine is a meta-analysis of 9 trials, involving 102,621 patients, studied over a 6 year period. They had very similar results to the other big primary prevention trial showing a 10% reduction in the risk of cardiovascular events. The biggest contributor to that decreased risk was a 20% reduction in the risk of non-fatal heart attack over a 6 year period. Again, there was no benefit on decreasing the risk of cardiovascular death. Of note, this analysis found no reduction in the risk of stroke. As far as bleeding, there was a 70% increase in the risk of total bleeding (intestinal or extra-intestinal, minor or major) and a 31% increase in the risk of “significant” bleeding. Significant bleeds were defined as: 1) non-fatal intra-cerebral bleeds, 2) retinal bleeds, 3) fatal bleeds, and 4) bleeds requiring hospital admission or blood transfusion. To put it into perspective, you would need to treat 162 patients with aspirin over a 6 year period to prevent one non-fatal heart attack, while you would have 1 significant bleeding event for every 73 patients treated over a 6 year period. So for every non-fatal heart attack you prevent you get about 2.5 bleeding episodes; those odds don’t sound so great.

The current guidelines from the U.S. Preventive Services Task Force (USPSTF) published in 2009 state the following: “Aspirin should be considered in men aged 45-79 and women aged 55-79 for the primary prevention of a cardiovascular event if the perceived benefit of aspirin outweighs the potential harm caused by an increased risk of gastrointestinal hemorrhage”. In addition, the studies reviewed by the USPSTF showed that in men the protection was mainly against a heart attack while in women the protection was mainly against stroke. I’m not sure if they specifically looked for that in this most recent trial.

In conclusion, the decision to take a daily aspirin to prevent a first heart attack or a first stroke is a little complicated. The more risk factors you have for cardiovascular disease the more likely it is that aspirin will be of benefit for you as long as your risk of bleeding remains low. Certainly a discussion with your internist is warranted before deciding to take aspirin on a regular basis.

A few final important points:

1. Aspirin 81mg daily is all you need; taking a higher dose does not provide more benefit and what it does is increase your risk of GI bleed. Of note, bleeds outside of the GI tract can occur at any dose, it is not a dose-dependant effect like with GI bleeding.

2. Taking a buffered or enteric-coated aspirin does not protect you against bleeding. These formulations may decrease stomach irritation but at the end of the day it still inactivates your platelets thus raising your bleeding risk.

3. Taking a daily proton pump inhibitor (ie- Prilosec, Prevacid, etc) will decrease your risk of GI bleeding when taking aspirin. This is something to consider in people who have had a history of GI bleeding (ie- an ulcer) and are at significant risk for a cardiovascular event and would like to take a daily aspirin.

4. Taking aspirin on an every other day regimen is associated with a lower risk of bleeding and the more recent studies reviewed suggest the cardiovascular protection is maintained.

5. Finally, be careful taking NSAIDS (Ibuprofen, Naproxen, others) with aspirin. This causes two problems. First, it quadruples your risk of bleeding (especially GI bleeding) and second, depending on when you take it, it will eliminate any cardiovascular benefit the aspirin was providing. If you have to take an NSAID, make sure you take your aspirin first thing in the morning and then wait 2 hours before taking an NSAID.

  1. Aspirin for the prevention of cardiovascular disease: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2009;150:396-404. Abstract
  2. Seshasai SR, Wijesuriya S, Sivakumaran R, et al. Effect of aspirin on vascular and nonvascular outcomes: meta-analysis of randomized controlled trials. Arch Intern Med. 2012;172:209-216. Abstract
  3. Berger JS, et al. Aspirin for the primary prevention of cardiovascular events in women and men. JAMA 2006; 295:306-313

 

 

 

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