Friday, July 30, 2010

 

bloeddruk

SUMMARY AND COMMENT

Blood Pressure Control in Patients with Diabetes and Coronary Artery Disease

July 20, 2010 | Thomas L. Schwenk, MD

No benefit for lowering BP to <130/80>

Reviewing: Cooper-DeHoff RM et al. JAMA 2010 Jul 7; 304:61


Wednesday, July 28, 2010

 

vitamine D

Reviewing: Thompson MA et al. JAMA 2010 Jul 21; 304:321

Free Full-Text Article

Summary and Comment

Vitamin D and Cognitive Function in Older Patients

Low levels are associated with cognitive decline.

Vitamin D deficiency is associated with several chronic illnesses, but studies of its association with cognitive function have been short and have yielded equivocal results. Data from the well-known InCHIANTI study of older Italian people (J Am Geriatr Soc 2000; 48:1618) were used to determine the relation between cognitive decline among 858 participants (mean age at baseline, 74) and baseline levels of 25-hydroxyvitamin D (25[OH]D). 25(OH)D levels were classified as severely deficient (<10 alt="≥">30 ng/mL [≥75 nmol/L]). Patients were assessed at baseline and every 3 years with several cognitive tests, including the Mini-Mental State Examination (MMSE).

At 6 years, analyses that were adjusted for clinical factors relevant to cognitive functions and for impaired mobility showed that participants with severe deficiency were 60% more likely to experience significant declines of ≥3 points on the MMSE than were participants with sufficient levels of 25(OH)D. Similar relative risks were noted for most secondary measures of cognition.

Comment: Despite appropriate adjustment, these results still could reflect reverse association — i.e., frail patients who are inactive and sun-deprived would have lower levels of 25(OH)D. Editorialists suggest that we move past observational studies and design prospective trials to assess the risks and benefits of vitamin D supplementation specifically.

Thomas L. Schwenk, MD

Published in Journal Watch General Medicine July 27, 2010


 

vitamine D

minder dan 10 microgram per mL is gelijk aan minder dan 25 nano-mol per Liter is erg laag als het over 25-hydroxi-vitamine D gaat.

Bij 30 microgram per dL of 75 micromol per Liter is pas normaal




Een mol is een bepaalde eenheid voor een hoeveelheid stof. Die eenheid ontstaat door simpelweg deeltjes te tellen. Een afgesproken aantal deeltjes noemen we 1 mol.

Dit wordt in onderstaande Bron beter uitgelegd dan ik het kan, dus behalve voorgaande alinea volsta ik met een verwijzing.

Het voorvoegsel n betekent nano. Dat is de eenheid die staat voor een miljardste deel (net zoals milli een duizendste deel is).

Dus een nmol is een nano-mol, ofwel een miljardste deel van een mol.

Die /l tenslotte betekent ‘per liter’.

nmol/l betekent dus nano-mol per liter. Dat betekent dat in 1 liter (bloed, of een andere vloeistof) 1 miljardste deel aanwezig is van het aantal deeltjes dat we een mol noemen


 

PPI proton pump inhibitor

Another Study of Proton-Pump Inhibitor "Withdrawal Symptoms"

July 27, 2010 | Allan S. Brett, MD

Nearly half of asymptomatic volunteers reported dyspepsia after completing a 4-week course of pantoprazole.

Reviewing: Niklasson A et al. Am J Gastroenterol 2010 Jul 105:1531


Tuesday, July 27, 2010

 

Ca blokkers amlodipine


Calcium channel blockers linked to increased heart failure risk


16 July 2010

MedWire News: Calcium channel blockers (CCBs) may increase the risk for heart failure (HF) among patients with hypertension, Canadian researchers report.

“This effect is also observed when comparing CCBs to ACE inhibitors or angiotensin receptor blockers and to beta blockers, and/or diuretics against HF,” say Marcelo Shibata (University of Alberta, Edmonton, Canada) and team.

The researchers reviewed 19 trials with a total of 156,766 patients (mean age 54–76 years) with hypertension who were randomly assigned to receive CCB therapy (verapamil, diltiazem, or a dihydropyridine; n=69,391) or control (ACE inhibitors, angiotensin receptor blockers, beta blockers, or diuretics; n=87,375).

The findings revealed a total of 5049 HF-related events over a follow-up period of 2 to 5 years. An 18% increase in the risk for HF diagnosis was observed among the patients who received CCB therapy, irrespective of the type of CCB used.

Among 16 trials presenting data on myocardial infarction (MI) rates (n=121,404, 3612 MIs), the risk for MI was 4% lower among the CCB groups compared with the control groups.

The team says this means that “the increase in the diagnosis of HF in patients allocated to CCBs cannot be explained by differences in incident MI.”

In subgroup analysis, a 71% higher HF risk was observed among patients with diabetes in the CCB group compared with non-diabetic patients in the CCB group.

The researchers conclude: “The treatment of hypertension with CCBs increases circulating catecholamines that could potentially be involved in the pathogenesis of HF. This information supports biologic plausibility for the effect observed in our analysis and should be tested in future trials.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

Am J Cardiol 2010; 106: 228–235

 

vitamine D

From MedscapeCME Clinical Briefs

Low Vitamin D Levels Associated With Increased Risk for Cognitive Impairment CME

News Author: Susan Jeffrey
CME Author: Laurie Barclay, MD

CME Released: 07/19/2010; Valid for credit through 07/19/2011


processing....

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CME Information

Target Audience

This article is intended for primary care clinicians, geriatricians, neurologists, psychiatrists, nutritionists, and other specialists caring for elderly persons at risk for dementia and vitamin D deficiency.

Goal

The goal of this activity is to provide medical news to primary care clinicians and other healthcare professionals in order to enhance patient care.

Authors and Disclosures

As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.

Susan Jeffrey
Susan Jeffrey is the news editor for Medscape Neurology & Neurosurgery. Susan has been writing principally for physician audiences for nearly 20 years. Most recently, she was news editor for thekidney.org and also wrote for theheart.org; both of these Web sites have been acquired by WebMD. Prior to that, she spent 10 years covering neurology topics for a Canadian newspaper for physicians. She can be contacted at SJeffrey@webmd.net.
Disclosure: Susan Jeffrey has disclosed no relevant financial relationships.

Brande Nicole Martin
CME Clinical Editor, Medscape, LLC
Disclosure: Brande Nicole Martin has disclosed no relevant financial relationships.

Laurie Barclay, MD
Freelance writer and reviewer, Medscape, LLC
Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

Sarah Fleischman
CME Program Manager, Medscape, LLC
Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

Learning Objectives

Upon completion of this activity, participants will be able to:

  1. Describe the association of low levels of vitamin D with cognitive decline in an elderly population studied during a 6-year period in the InCHIANTI Italian population-based study.
  2. Describe the implications of low levels of vitamin D with cognitive decline in the elderly population from the InCHIANTI study for treatment and prevention of cognitive decline.

Credits Available

Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™

Family Physicians - maximum of 0.25 AAFP Prescribed credit(s)

All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation.

Physicians should only claim credit commensurate with the extent of their participation in the activity.

Accreditation Statements

For Physicians

Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

Medscape, LLC designates this educational activity for a maximum of 0.25 AMA PRA Category 1 Credit(s)™ . Physicians should only claim credit commensurate with the extent of their participation in the activity. Medscape News CME has been reviewed and is acceptable for up to 300 Prescribed credits by the American Academy of Family Physicians. AAFP accreditation begins September 1, 2009. Term of approval is for 1 year from this date. Each issue is approved for .25 Prescribed credits. Credit may be claimed for 1 year from the date of this issue.

Note: Total credit is subject to change based on topic selection and article length.

Medscape, LLC staff have disclosed that they have no relevant financial relationships.

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Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact CME@medscape.net

CME Released: 07/19/2010; Valid for credit through 07/19/2011

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There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board.

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July 19, 2010 — Results of a new analysis using data from the Third National Health and Nutrition Survey (NHANES III) show that vitamin D deficiency is associated with an increased risk for cognitive impairment in older Americans.

The findings echo those from a second report from the same group in a different cohort showing that low levels of vitamin D were associated with subsequent cognitive decline during 6 years of follow-up.

Taken together, it appears that, "low levels of vitamin D are just genuinely bad for the brain," lead author David J. Llewellyn, PhD, from the University of Exeter Peninsula Medical School in the United Kingdom, told Medscape Medical News. "That's why we're so excited, because vitamin D supplements are such an obvious thing that we can do something about now."

Dr. David J. Llewellyn

The expected epidemic of dementia with the aging population is already starting to appear, he said, and although long-term strategies are needed, trials that may have a short- to medium-term payoff are urgently required immediately. In that setting, trials of vitamin D for prevention may be a promising strategy, he said.

The results from NHANES III were presented here at the Alzheimer's Association International Conference on Alzheimer's Disease 2010. The results from the Invecchiare in Chianti (InCHIANTI) study appear in the July 12 issue of the Archives of Internal Medicine.

NHANES Findings

Vitamin D was once just of interest in bone health, but recent work has suggested low vitamin D levels may be a risk factor for a wide range of age-associated diseases, Dr. Llewellyn said, including cancer, hypertension, stroke, and more recently, cognitive decline.

It is known that vitamin D crosses the blood–brain barrier and that receptors for vitamin D are found across the brain, but its precise role is still not known, Dr. Llewellyn noted. It does seem to play a role in processes that may be important for dementia risk, including vascular health and amyloid clearance from the brain. Given these associations, he noted, it seems "biologically plausible" that there might be an association of low vitamin D levels with dementia risk and cognitive performance in the general population.

It is estimated that about a billion people worldwide have vitamin D levels considered insufficient (<75>

A previous paper using data from NHANES III did not find an association between vitamin D levels and cognitive performance (McGrath J, et al. Neuroepidemiol. 2007;29:49-54), but the researchers speculated this may have related to methodology — specifically, the choice of cognitive tests included.

The previous paper used only delayed verbal memory from the Mini-Mental State Examination (MMSE) and the East Boston Memory Test, Dr. Llewellyn said. "I threw everything in, because I was interested in whether this would be a more stable representation of these individuals' cognitive status."

The researchers also adjusted for a wide range of variables, including vitamin E levels, family income, more extensive measures of physical activity, and obesity.

A total of 3325 adults aged 65 years or older had complete cognitive assessments and blood samples available; cognitive impairment was defined as the worst 10% of the distribution of combined scores. Vitamin D levels were divided by cut points previously established for bone health, from severely deficient (<25>

Compared with those patients with sufficient levels of vitamin D, those participants who were very vitamin D deficient had a 6-fold higher risk for cognitive impairment, with a doubling of risk still for those who were considered deficient (≥25 to <50>

"We see some attenuation in the fully adjusted model, but this is still a relatively large effect size, I think it's fair to say," Dr. Llewellyn noted. "People [with severe vitamin D deficiency] have about 4 times higher odds of cognitive impairment, and again the trend across groups remains significant."

NHANES III: Risk for Cognitive Impairment With Severe Vitamin D Deficiency vs Sufficient Levels

Model Hazard Ratio 95% Confidence Interval P for Trend
Unadjusted model 5.97 2.82 - 12.6 <.001
Fully adjusted model 3.94 1.49 - 10.43 .017

When they restricted the analysis to only the memory items, there was still a trend across groups, although it was no longer significant (P = .18), which may explain the previous null finding, Dr. Llewellyn noted.

Further prospective data on this link are needed, he told the meeting here, "and we also need to consider whether the enormous expense of a trial is now justified."

At a press conference here, Dr. Llewellyn noted that they are now in the early stages of designing the protocol for a vitamin D trial, probably a dose-comparison trial, to see whether supplementation might have an effect in preventing progression among those with early cognitive impairment. Of course, "it will be funding-dependent," he added wryly.

Dr. William Thies

William Thies, PhD, who moderated a press conference here featuring this paper among others, pointed out that since 2 previous trials treating cognitive impairment with vitamin D have been negative, "I think prevention is the logical place to go, but typically you're dealing with 5 to 10 times as many people and you're following them for a much longer period of time, so the cost-escalation is often 10 to 20 times what it is for treatment."

InCHIANTI Findings

In a separate analysis published in the Archives of Internal Medicine, Dr. Llewellyn and colleagues looked prospectively at the relationship between vitamin D and cognitive decline in the InCHIANTI study, a population-based study conducted in Italy between 1998 and 2006.

"To our knowledge," the researchers write, "no prospective study has examined the association between vitamin D and cognitive decline or dementia."

The InCHIANTI study included 858 adults aged 65 years or older who completed interviews, cognitive assessments, and medical examinations, as well as providing blood samples. Cognitive examination was done using the MMSE, with substantial decline defined as 3 or more points. Trail-Making Tests A and B were also used, with substantial decline defined as the worst 10% of the distribution of decline or as discontinued testing. Assessments were done at baseline and then at 3 and 6 years.

Again, the researchers found that those severely deficient in vitamin D (<25>

Severe deficiency was also associated with the risk for substantial decline on the Trail-Making Test B, but no significant association was seen with the Trail-Making Test A.

Fully Adjusted Risk for Substantial Cognitive Decline for Severe Vitamin D Insufficiency vs Sufficient Levels, by Cognitive Test

Test Hazard Ratio 95% Confidence Interval P for Trend
MMSE 1.60 1.19 - 2.00 .02
Trail-Making Test A 1.16 0.65 - 1.84 .44
Trail-Making Test B 1.31 1.03 - 1.51 .04

"If future prospective studies and randomized controlled trials confirm that vitamin D deficiency is causally related to cognitive decline, then this would open up important new possibilities for treatment and prevention," Dr. Llewellyn and colleagues conclude.

Just a Marker of Poor Health?

In an editorial accompanying the Archives of Internal Medicine article, Andrew Grey, MD, and Mark Bolland, MBChB, PhD, from the Department of Medicine at the University of Auckland, New Zealand, are cautious in their assessment of the vitamin D link with cognitive decline and other health problems.

Results from recent observational studies, they write, "have prompted calls for widespread treatment of individuals with low levels of vitamin D and the establishment of public health programs aimed at raising the population levels of vitamin D to 'healthy' values."

Despite the preliminary evidence that components of vitamin D may have a favorable effect in certain diseases, "it seems intuitively unlikely that a single hormone could play a substantial role in preventing or ameliorating the diverse range of diseases that have been linked to low levels of vitamin D."

Instead, a more likely explanation is that low vitamin D is a marker of overall poor health — low sunlight exposure, low physical activity, high adiposity — not the cause of it, they speculate, a possibility supported by the findings of this study as well.

We should therefore treat the data from observational studies of vitamin D with caution.

Positive observational data have been proven wrong before after randomized trials in settings such as postmenopausal hormone therapy, they add. "We should therefore treat the data from observational studies of vitamin D with caution."

"It is now time to test the various hypotheses generated by observational studies of vitamin D, including that of Llewellyn et al, in adequately designed and conducted randomized controlled trials," they conclude. "Very importantly, such trials will also provide an opportunity to systematically assess potential harms of vitamin D supplementation, an issue that has been largely overlooked or dismissed.

"We should invest in trials that provide the best possible evidence on the benefits and risks of vitamin D before we invest in costly, difficult and potentially unrewarding interventional strategies."

NHANES III is funded by the Kaiser Permanente Division of Research. The InCHIANTI study is supported in part by the Italian Ministry of Health and by the United States National Institute on Aging. The authors have disclosed no relevant financial relationships.

Alzheimer's Association International Conference on Alzheimer's Disease 2010: Abstract 01-06-03. Presented July 11, 2010.

Arch Intern Med. 2010;170:1135-1141, 1099-1100.

Clinical Context

Vitamin D crosses the blood-brain barrier, and receptors to which it binds are located in the brain. Although its function in cognition and brain processes are not precisely known, it may be involved in vascular health, amyloid clearance from the brain, and other mechanisms involved in dementia risk.

Worldwide, approximately 1 billion people have vitamin D deficiency. In the northern hemisphere, risk factors include insufficient sun exposure, few dietary sources, and reduction in skin production of vitamin D with aging. A previous analysis from NHANES III showed no association between vitamin D levels and cognitive performance, but this may have been caused by choice of cognitive evaluation. No prospective study has previously studied the association between vitamin D levels and dementia or cognitive decline.

Study Highlights

  • The goal of the study was to examine whether low levels of serum 25-hydroxyvitamin D (25[OH]D) were associated with an increased risk for significant cognitive decline in an elderly population.
  • The InCHIANTI population–based study took place in Italy between 1998 and 2006.
  • The study cohort consisted of 858 adults at least 65 years old, of white European origin, who completed interviews, cognitive evaluations, physical examinations, and blood testing.
  • Severe serum 25(OH)D deficiency was defined as levels of less than 25 nmol/L, and sufficient levels of 25(OH)D were defined as 75 nmol/L or more.
  • Every 3 years, participants underwent follow-up evaluations.
  • Substantial cognitive decline was defined as a decrease of 3 points or more on the MMSE.
  • On Trail-Making Tests A and B, substantial decline was defined as the worst 10% of the distribution of decline or as discontinued testing.
  • Multivariate adjusted relative risk (RR) of substantial cognitive decline on the MMSE in participants with severe serum 25 (OH)D deficiency vs those with sufficient levels of 25(OH)D was 1.60 (95% CI, 1.19 - 2.00; P for trend = .02).
  • Compared with participants who had sufficient 25(OH)D levels, those who were severely 25(OH)D deficient had an additional decrease of 0.3 MMSE points per year, based on multivariate adjusted random-effects models.
  • The association remained significant when analyses were restricted to elderly subjects with no dementia at baseline.
  • Compared with participants who had sufficient 25(OH)D levels, those who were severely 25(OH)D deficient had an RR for substantial decline on the Trail-Making Test B of 1.31 (95% CI, 1.03 - 1.51; P for trend = .04).
  • There was no significant association of 25(OH)D levels with decline on Trail-Making Test A (RR, 1.16; 95% CI, 0.65 - 1.84; P for trend = .44).
  • On the basis of these findings, the investigators concluded that low levels of vitamin D were associated with substantial cognitive decline in the elderly population studied during a 6-year period.
  • They also suggest that this finding has important implications for treatment and prevention.
  • They note that low levels of 25(OH)D may be especially harmful to executive functions, whereas memory and other cognitive domains may be relatively preserved.
  • In future trials of vitamin D supplementation in the elderly population, it may be useful to include tests of cognitive function.
  • Limitations of this study include inability to determine whether these findings generalize to other regions or races, possible effect of attrition, and inability to determine the underlying cause of the observed cognitive changes.

Clinical Implications

  • In the InCHIANTI Italian population–based study, low levels of vitamin D were associated with substantial cognitive decline in the elderly population studied during a 6-year period.
  • This finding may have important implications for treatment and prevention. Low levels of 25(OH)D may be especially harmful to executive functions, whereas memory and other cognitive domains may be relatively preserved. Future trials of vitamin D supplementation in the elderly should include cognitive evaluation.

CME Test

Questions answered incorrectly will be highlighted.

According to the InCHIANTI Italian population-based study by Llewellyn and colleagues, which of the following statements about the association of vitamin D levels with cognitive decline in the elderly population is not correct?
Compared with participants who had sufficient 25(OH)D levels, those with severe 25(OH)D deficiency had an additional decrease of 0.3 MMSE points per year
The association was not significant when analyses were restricted to elderly subjects with no dementia at baseline
Compared with participants who had sufficient 25(OH)D levels, those with severe 25(OH)D deficiency had an RR for substantial decline on the Trail-Making Test B of 1.31
There was no significant association of 25(OH)D levels with decline on the Trail-Making Test A
According to the study by Llewellyn and colleagues, which of the following statements about clinical implications of the association between vitamin D levels and cognitive function is correct?
The mechanism underlying the association is well understood
Low levels of 25(OH)D may be especially harmful to memory
Executive functions may be relatively preserved in patients with vitamin D deficiency
Future trials of vitamin D supplementation in the elderly population should include cognitive evaluation

Authors and Disclosures

As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.

Author(s)

Susan Jeffrey

Susan Jeffrey is the news editor for Medscape Neurology & Neurosurgery. Susan has been writing principally for physician audiences for nearly 20 years. Most recently, she was news editor for thekidney.org and also wrote for theheart.org; both of these Web sites have been acquired by WebMD. Prior to that, she spent 10 years covering neurology topics for a Canadian newspaper for physicians. She can be contacted at SJeffrey@webmd.net.

Disclosure: Susan Jeffrey has disclosed no relevant financial relationships.

Editor(s)

Brande Nicole Martin

CME Clinical Editor, Medscape, LLC

Disclosure: Brande Nicole Martin has disclosed no relevant financial relationships.

CME Author(s)

Laurie Barclay, MD

Freelance writer and reviewer, Medscape, LLC

Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

Sarah Fleischman

CME Program Manager, Medscape, LLC

Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

CME Information

CME Released: 07/19/2010; Valid for credit through 07/19/2011

Target Audience

This article is intended for primary care clinicians, geriatricians, neurologists, psychiatrists, nutritionists, and other specialists caring for elderly persons at risk for dementia and vitamin D deficiency.

Goal

The goal of this activity is to provide medical news to primary care clinicians and other healthcare professionals in order to enhance patient care.

Learning Objectives

Upon completion of this activity, participants will be able to:

  1. Describe the association of low levels of vitamin D with cognitive decline in an elderly population studied during a 6-year period in the InCHIANTI Italian population-based study.
  2. Describe the implications of low levels of vitamin D with cognitive decline in the elderly population from the InCHIANTI study for treatment and prevention of cognitive decline.

Credits Available

Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™

Family Physicians - maximum of 0.25 AAFP Prescribed credit(s)

All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation.

Physicians should only claim credit commensurate with the extent of their participation in the activity.

Accreditation Statements

For Physicians

Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

Medscape, LLC designates this educational activity for a maximum of 0.25 AMA PRA Category 1 Credit(s)™ . Physicians should only claim credit commensurate with the extent of their participation in the activity. Medscape News CME has been reviewed and is acceptable for up to 300 Prescribed credits by the American Academy of Family Physicians. AAFP accreditation begins September 1, 2009. Term of approval is for 1 year from this date. Each issue is approved for .25 Prescribed credits. Credit may be claimed for 1 year from the date of this issue.

Note: Total credit is subject to change based on topic selection and article length.

Medscape, LLC staff have disclosed that they have no relevant financial relationships.

AAFP Accreditation Questions

Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact CME@medscape.net

Instructions for Participation and Credit

There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page.

Follow these steps to earn CME/CE credit*:

  1. Read the target audience, learning objectives, and author disclosures.
  2. Study the educational content online or printed out.
  3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. MedscapeCME encourages you to complete the Activity Evaluation to provide feedback for future programming.

You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates by accessing "Edit Your Profile" at the top of your Medscape homepage.

*The credit that you receive is based on your user profile.

Hardware/Software Requirements

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MedscapeCME Clinical Briefs © 2010 Medscape, LLC

Disclaimer

The material presented here does not necessarily reflect the views of Medscape, LLC or companies that support educational programming on www.medscapecme.com. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity.

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Saturday, July 24, 2010

 

bisphosphanates Calcium fosamax phosamax

Effect Also Seen in Breast Cancer Patients

Dr. Gnant points out that the potential anticancer effects of bisphosphonates have also been reported in several studies of women who already have breast cancer, including one by his team. In that study, the Austrian Breast and Colorectal Cancer Study Group trial (n = 1803), and in ZO-FAST (Zometa-Femara Adjuvant Synergy Trial; n = 1065), the intravenous bisphosphonate zolendronic acid reduced cancer recurrence in bone and nonbone sites, including contralateral breast cancer, he notes.

There were also 2 previous studies of the oral bisphosphonate clodronate in women with breast cancer (total n = 1371) that showed a delay in the development of bone metastases and an improvement in disease-free and overall survival.

In addition, laboratory studies suggest that bisphosphonates have both direct and indirect anticancer effects, including effects on cancer cell apoptosis, inhibition of cancer cell adhesion and extravasation, inhibition of angiogenesis, and activation of immune cells with anticancer activity.

It is possible that these are a class effect of the bisphosphonates, Dr. Gnant writes.

All of these researchers and the editorialist urge further study in this field, because, as Dr. Gnant writes, "the potential implications would be far-reaching."

Dr. Gnant reports acting as a consultant/advisor, and/or receiving honoraria and/or research funding from AstraZeneca, Novartis, Pfizer, Roche, and Sanofi-Aventis. Dr. Chlebowski reports acting as a consultant/advisor for AstraZeneca, Novartis, Pfizer, Amgen, and Eli Lilly, and receiving honoraria from AstraZeneca, Novartis, and Amgen. Several coauthors report links with Novartis and Merck, and one coauthor holds stock in Merck. Dr. Rennert, Dr. Newcomb, and their colleagues have disclosed no relevant financial relationships.

J Clin Oncol. Published online June 21, 2010. Abstract, Abstract, Abstract


Saturday, July 17, 2010

 

vitamine D cognition

n.

From Medscape Medical News

Low Vitamin D Levels Associated With Increased Risk for Cognitive Impairment

Susan Jeffrey

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July 13, 2010 (Honolulu, Hawaii) — Results of a new analysis using data from the Third National Health and Nutrition Survey (NHANES III) show that vitamin D deficiency is associated with an increased risk for cognitive impairment in older Americans.

The findings echo those from a second report from the same group in a different cohort showing that low levels of vitamin D were associated with subsequent cognitive decline during 6 years of follow-up.

Taken together, it appears that, "low levels of vitamin D are just genuinely bad for the brain," lead author David J. Llewellyn, PhD, from the University of Exeter Peninsula Medical School in the United Kingdom, told Medscape Medical News. "That's why we're so excited, because vitamin D supplements are such an obvious thing that we can do something about now."

Dr. David J. Llewellyn

The expected epidemic of dementia with the aging population is already starting to appear, he said, and although long-term strategies are needed, trials that may have a short- to medium-term payoff are urgently required immediately. In that setting, trials of vitamin D for prevention may be a promising strategy, he said.

The results from NHANES III were presented here at the Alzheimer's Association International Conference on Alzheimer's Disease 2010. The results from the Invecchiare in Chianti (InCHIANTI) study appear in the July 12 issue of the Archives of Internal Medicine.

NHANES Findings

Vitamin D was once just of interest in bone health, but recent work has suggested low vitamin D levels may be a risk factor for a wide range of age-associated diseases, Dr. Llewellyn said, including cancer, hypertension, stroke, and more recently, cognitive decline.

It is known that vitamin D crosses the blood–brain barrier and that receptors for vitamin D are found across the brain, but its precise role is still not known, Dr. Llewellyn noted. It does seem to play a role in processes that may be important for dementia risk, including vascular health and amyloid clearance from the brain. Given these associations, he noted, it seems "biologically plausible" that there might be an association of low vitamin D levels with dementia risk and cognitive performance in the general population.

It is estimated that about a billion people worldwide have vitamin D levels considered insufficient (<75>

A previous paper using data from NHANES III did not find an association between vitamin D levels and cognitive performance (McGrath J, et al. Neuroepidemiol. 2007;29:49-54), but the researchers speculated this may have related to methodology — specifically, the choice of cognitive tests included.

The previous paper used only delayed verbal memory from the Mini-Mental State Examination (MMSE) and the East Boston Memory Test, Dr. Llewellyn said. "I threw everything in, because I was interested in whether this would be a more stable representation of these individuals' cognitive status."

The researchers also adjusted for a wide range of variables, including vitamin E levels, family income, more extensive measures of physical activity, and obesity.

A total of 3325 adults aged 65 years or older had complete cognitive assessments and blood samples available; cognitive impairment was defined as the worst 10% of the distribution of combined scores. Vitamin D levels were divided by cut points previously established for bone health, from severely deficient (<25>

Compared with those patients with sufficient levels of vitamin D, those participants who were very vitamin D deficient had a 6-fold higher risk for cognitive impairment, with a doubling of risk still for those who were considered deficient (≥25 to <50>

"We see some attenuation in the fully adjusted model, but this is still a relatively large effect size, I think it's fair to say," Dr. Llewellyn noted. "People [with severe vitamin D deficiency] have about 4 times higher odds of cognitive impairment, and again the trend across groups remains significant."


Thursday, July 15, 2010

 

suicide antidepressants

Antidepressants and Suicide Reexamined

Nassir Ghaemi, MD, Psychiatry/Mental Health, 12:39PM Jun 27, 2010

In the recent NCDEU meeting, Thomas Laughren, the head of the FDA neuropsychopharmacology branch, once again reviewed the question of antidepressants and suicide. In reviewing the published FDA meta-analysis of the randomized clinical trials (RCTs) of antidepressants, he summarized the rather clear finding that antidepressants seemed to have an age-dependent effect on suicide risk: In children and young adults below age 25, they increased the risk (relative risk 2.22 in children and adolescents, 1,55 age 18-24), in later adult years they were neutral (risk 1.00 for age 25-30), and in middle age and in the elderly they were protective (risk 0.77 age 31-64, risk 0.39 above age 65). When all these age groups are summarized, antidepressants have a small protective benefit for suicide (relative risk 0.84, confidence intervals 0.69 to 1.02). In all these analyses, suicidality (defined as actual suicide, suicide attempts, or notable increase in suicidal ideation) is being assessed, one should say, rather than completed suicide. There were only 8 suicides in 77382 subjects, though 2 were on placebo and 6 on antidepressant. Predictors of antidepressant-related suicidality with antidepressants were interesting: Suicide attempts (i.e., actual behavior) were more associated with antidepressants rather than increase in suicidal ideation (thoughts without behavior). Also, non-depressed persons (e.g., studies of antidepressants in other conditions such as anxiety disorders or PTSD) were more likely to be suicidal with antidepressants than those diagnosed with clinical depression (major depressive disorder).

Dr. Laughren also addressed the common critique that adolescent suicides increased after the FDA warning, which led to a decrease in antidepressant prescriptions in children. He reviewed data showing that suicides per 100,000 population for adolescents occurred at rate of 7.3 in 2003, 8.2 in 2004, 7.6 in 2005, and 7.2 in 2006. The FDA warning came out in 2004, but that increase in suicide rates occurred before the decline in antidepressant prescription rates for adolescents, which happened more in 2005 and 2006, corresponding to a decrease in adolescent suicide rates.

It is a not entirely appealing aspect of our profession that we wish to criticize, but not be criticized: Many of us are critical of the pharmaceutical industry, or of diagnosing mental illnesses like bipolar disorder in children, and yet we react angrily when asked to restrain our use of drugs. Instead, we should think seriously about the clear question arising from these data: Why are antidepressants preventive of suicide in later adulthood, and causative of it in younger age?


 

statins

Do Statins Slow Progression of Rheumatic Mitral Stenosis?

Findings from a retrospective study suggest that they do.

The pleiotropic anti-inflammatory properties of statins are believed to bring about the slowing in progression of calcific aortic stenosis seen in some previous studies (but not in all; see JW Cardiol Jul 15 2005). In this observational study, investigators examined the effect of statin therapy on the progression of rheumatic mitral stenosis (MS).

The study population consisted of 315 patients with rheumatic MS (mean age, 61 years; 71% women), of whom 35 (11%) were taking statins, and 280 (89%) were not. Baseline echocardiographic characteristics, including mitral valve area (MVA) and degree of mitral regurgitation, were similar in both groups. After a mean follow-up of 6.1 years, the annualized decrease in mean MVA was significantly smaller in statin-treated patients than in non–statin-treated patients (0.027 vs. 0.067 cm2; P=0.005). In a multivariable analysis, statin treatment independently predicted slower MS progression.

Comment: This is the first study to examine the effect of statin therapy on progression of rheumatic MS. Given the high prevalence of rheumatic disease in many parts of the world, even the small decrease in disease progression that was demonstrated in this study could have important public health implications. These findings support the need for a randomized trial of statin therapy for the prevention of valvular stenosis in patients with rheumatic heart disease.

Howard C. Herrmann, MD

Published in Journal Watch Cardiology July 14, 2010


 

statins

Statins and Primary Prevention for Patients at High Risk for Heart Disease

July 15, 2010 | Thomas L. Schwenk, MD

The benefit, if any, is very small.

Reviewing: Ray KK et al. Arch Intern Med 2010 Jun 28; 170:1024

de Lorgeril M et al. Arch Intern Med 2010 Jun 28; 170:1032

Kaul S et al. Arch Intern Med 2010 Jun 28; 170:1073

Green LA. Arch Intern Med 2010 Jun 28; 170:1007


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