geoffrey modest medical blogs

3 articles on vitamin supplementation in dec 17th issue of annals of internal medicine. (all with same conclusions). 1. high dose vitamins and minerals post-MI (see  cad mvi not help post MI annals 2013  in dropbox, or  doi:10.7326/0003-4819-159-12-201312170-00004 ). 1700 pts >50yo with MI at least 6 weeks earlier and serum creat <2.  Randomized to high dose vitamins/minerals, with composition designed by alternative med practitioners (vitamins significantly above "daily value" include: vitamins A, C, E, B6, niacin, pantothenic acid, manganese, selenium). results:                 --mostly white males (82% male, 94% white) from Brigham and Duke hospitals  --unusually terrible adherence (which involved 3 pills bid), with 46% discontinuation rates in both the placebo and treatment arms                 --nonsignificant difference in outcomes: 5-year event rates (total death, recurrent MI, stroke, coronary revasc, hosp for angina) in 34.2% on vitamins and 37% on pla

1. The US preventive service taskforce (USPSTF) just released their guidelines for BRCA testing (see  http://www.uspreventiveservicestaskforce.org/uspstf12/brcatest/brcatestfinalrs.htm ). in brief, they suggest: --estimated prevalence of BRCA1 or 2  is 0.2% to 0.3% (ie, 1 in 300-500 women) in the general population of women , 6.0% in women with cancer onset before age 40 years , and 2.1% in the general population of Ashkenazi Jewish women . In a meta-analysis of studies in which recruitment was based on family history of breast or ovarian cancer,  BRCA1  mutation prevalence was 13.6%,  BRCA2  mutation prevalence was 7.9%, and prevalence of either mutation was 19.8% . --A woman's risk for breast cancer increases to 45% to 65% by age 70 years if there are clinically significant mutations in either BRCA gene . Mutations in the  BRCA1  gene increase ovarian cancer risk to 39% by age 70 years, and  BRCA2  mutations increase ovarian cancer risk to 10% to 17% by age 70 years .  -

see below from the FDA.  not just methylphenidate, but also seems to be an issue with  non-stimulant drug atomoxetine. sounds like it can be severe: average age 12.5 and 2 needing surgical intervention.   geoff   Safety Announcement [12-17-2013]   The U.S. Food and Drug Administration (FDA) is warning that methylphenidate products, one type of stimulant drug used to treat attention deficit hyperactivity disorder (ADHD), may in rare instances cause prolonged and sometimes painful erections known as priapism. FDA continues to monitor the safety of drugs after they are approved, and, based on a recent review of methylphenidate products, we have updated the  drug labels 2  and patient Medication Guides to include information about the rare but serious risk of priapism. Patients who take methylphenidate and develop erections lasting longer than four hours should seek immediate medical treatment to prevent long-term problems with the penis.  If not treated right away, priapism can

These guidelines were just published this month by the european society of cardiology in concert with the european society of hypertension (see  htn esc guidelines 2013  in dropbox, or   doi: 10.3109/08037051.2013.812549) .  in general, they are less prescriptive overall or detailed vs. the NICE (Natiional institute for health and clinical excellence of the UK) guidelines (see  dropbox as  htn nice recs 2011, or   http://guidance.nice.org.uk/CG127/Guidance ) general points (my comments in parentheses):                 --need to look at htn in context of overall cardiovascular risk. use the SCORE (or Framingham risk assessment tool). the risk of different levels of hypertension depend on co-incidence of other risk factors (and, from the framingham data, the risk is more than additive with each additional risk factor, such that the attributable risk of hypertension to coronary artery disease is higher in the presence of other risk factors). the presence of organ damage (OD) from h

 so, here is my brief (ie, briefer than usual) review of JNC-8 (see  htn jnc8 jama2013  in dropbox, or doi:10.1001/jama.2013.284427). this is a short 14-page document, recommending the following: --in people over 60 years old, initiate drug treatment to lower BP to <150/90 (but okay to keep at systolic<140 if already there based on prior guidelines and if well-tolerated, per expert opinion, though no clear benefit to doing so) --in those younger than 60, begin drugs to lower diastolic <90, mostly based on really old studies from the 1970s, which only looked at diastolic blood pressure. this recommendation is stronger for those 30-59yo than 18-29yo (ie, no RCTs showing anything in the younger group) --in those younger than 60yo, use a systolic goal of <140 (expert opinion, since lack of studies, as in last point) --in those >18yo with CKD (chronic kidney dz, with GFR<60, or people of any age with alb/creat ratio >30), treat to lower BP to <1

the NY times had a front-page story on "the selling of attention deficit disorder", one of a recent series of health care expose-type articles (see  http://www.nytimes.com/2013/12/15/health/the-selling-of-attention-deficit-disorder.html?nl=todaysheadlines&emc=edit_th_20131215&_r=0 ). their basic points: --dramatic increase in diagnosis (made in 15% of high school aged children!! -- second only to  asthma -- with # of kids on meds increasing from 600K to 3.5M in past 20 years) --increase in meds coincides with intensive drug company campaign to publicize syndrome and promote pills as therapy, including widespread advertising to parents/kids: using celebrities on TV to promote diagnosis, defining ADHD to include "childhood forgetfulness and poor grades as grounds for medication, that, among other benefits, can result in 'schoolwork that matches his intelligence' and ease family tension", "subsidized 50,000 copies of a comic book that tries

Although gastric acid is required to cleave vitamin B12 from ingested dietary proteins, and the same parietal cells that produce acid also produce intrinsic factor, studies have been mixed as to whether acid suppressive therapy leads to low vitamin B-12 levels. a large community-based case-controlled study was done by Kaiser Permanente North California comparing 26,000 patients with an incident diagnosis of vitamin B12 deficiency with 185,000 without (see  PPI and B12 deficiency jama 2013  in dropbox, or   doi:10.1001/jama.2013.280490).  Results: --Vitamin B12 deficiency was more commonly diagnosed in patients with at least a 2 year supply of PPIs compared to nonusers (OR, 1.65). --among people taking PPIs for at least 2 years, those on a higher dose (greater than 1.5 pills per day) had a higher OR of 1.95, as compared to those who were on lower doses of less than 0.75 pills per day, with OR of 1.63, and a statistically significant trend. --a similar trend was found with peo

Although the vast majority of epidemiol studies have found HDL to be cardioprotective, there have always been some concerns.  HDL is comprised of a diverse group of lipoproteins with significant metabolic heterogeneity.  there were a few older studies finding a "pro-inflammatory HDL", which predisposed people to heart disease (see my lipid powerpoint, slide 106, which cites small studies from 2003 and 2009). the clinical trial of  Torcetrapib, a cholest ester transfer protein inhibitor, dramatically increased HDL but was not cardioprotective. the researchers suggested that the HDL was somehow deformed. (this large torcetrapib trial overwhelmed a meta-analysis  last year  in BMJ, suggesting no benefit to raising HDL). in any event, there is a likely very illuminating article from harv school pub health (see  lipids inflam hdl apoC3 jaha 2012  in dropbox). they had found before that there was occasionally a small apolipoprotein (apo C-III) on some lipoproteins causing a pro-in

several people have asked what i consider a reasonable approach to lipid management. i have been following the lipid literature at this point for several decades, since i have always felt that heart disease was a manifestation of our industrialized society and abnormal lipids (from the attendant changes in lifestyle) was a principal component of atherosclerotic disease. my approach over the past decade or so involves developing a general sense of atherosclerotic risk as follows: --the major part of the overall gestalt of a person's risk is the traditional risk factors: age, smoking, hypertension, and lipids (with smoking being the strongest remedial component -- we can't do a lot about age). --existence of atherosclerotic disease to me is an indication for very aggressive lipid management, independent of the lipid levels. in this category i have always included strokes (data on positive effect of statins is at least a decade old), as well as PAD or other atherosclerotic v