Saturday, September 26, 2009
dementia bloeddruk
© 2009 American Academy of Neurology
Association of higher diastolic blood pressure levels with cognitive impairment
From the Comprehensive Stroke Center (G.T., A.V.A.), Department of Medicine (V.G.W.), Department of Epidemiology (R.C.P.G.), and Department of Biostatistics (G.H.), University of Alabama at Birmingham; Department of Neurology (G.T.), Democritus University of Thrace, University Hospital of Alexandroupolis, Greece; Department of Psychiatry (F.W.U.), Indiana University School of Medicine, Indianapolis; National Institute of Neurological Disorders and Stroke (C.S.M.), NIH, Bethesda, MD; and Department of Neurology (B.K.), University of Cincinnati, OH.
Address correspondence and reprint requests to Dr. Georgios Tsivgoulis, Comprehensive Stroke Center, University of Alabama at Birmingham, RWUH M226, 1530 3rd Avenue S, Birmingham, AL 35294-3280 tsivgoulisgiorg@yahoo.gr
Background: We evaluated the cross-sectional relationship of blood pressure (BP) components with cognitive impairment after adjusting for potential confounders.
Methods: Reasons for Geographic and Racial Differences in Stroke (REGARDS) is a national, longitudinal population cohort evaluating stroke risk in 30,228 black and white men and women 
45 years old. During the in-home visit, BP measurements were taken as the average of 2 measurements using a standard aneroid sphygmomanometer. Excluding participants with prior stroke or TIA, the present analysis included 19,836 participants (enrolled from December 2003 to March 2007) with complete baseline physical and cognitive evaluations. Incremental logistic models examined baseline relationships between BP components (systolic blood pressure [SBP], diastolic blood pressure [DBP], and pulse pressure [PP]) and impaired cognitive status (score of 
4 on 6-Item Screener) after adjusting for demographic and environmental characteristics, cardiovascular risk factors, depressive symptoms, and current use of any antihypertensive medication.
Results: Higher DBP levels were associated with impaired cognitive status after adjusting for demographic and environmental characteristics, risk factors, depressive symptoms, and antihypertensive medications. An increment of 10 mm Hg in DBP was associated with a 7% (95% confidence interval [CI] 1%–14%, p = 0.0275) higher odds of cognitive impairment. No independent association was identified between impaired cognitive status and SBP (odds ratio [OR] 1.02, 95% CI 0.99–1.06) or PP (OR 0.99, 95% CI 0.95–1.04). There was no evidence of nonlinear relationships between any of the BP components and impaired cognitive status. There was no interaction between age and the relationship of impaired cognitive status with SBP (p = 0.827), DBP (p = 0.133), or PP (p = 0.827) levels.
Conclusions: Higher diastolic blood pressure was cross-sectionally and independently associated with impaired cognitive status in this large, geographically dispersed, race- and sex-balanced sample of stroke-free individuals.
prostaat PSA
Prostate Cancer Screening; Is This a Teachable Moment?
Affiliations of author : American Cancer Society, Altanta, GA; Departments of Hematology and Oncology, Department of Medicine, and Department of Epidemiology, Emory University, Altanta, GA
Correspondence to: Otis W. Brawley, MD, American Cancer Society, 250 Williams St, Suite 600, Atlanta, GA 30303 (e-mail: otis.brawley@cancer.org ).
In this issue of the Journal, Welch and Albertsen (1) presented information that every man considering prostate cancer screening and treatment should know and understand. Prostate cancer screening has resulted in substantial overdiagnosis and in unnecessary treatment. It may have saved relatively few lives. Results from this article and recent results from prostate cancer screening and prevention trials demand reflection about what we as a society have done and are doing. Lessons to be learned have ethical and economic implications and involve our lack of respect for the scientific process and scientific evidence.
As I sat down to write this editorial, I heard a radio commercial that brings perspective to the issue. A local celebrity was promoting prostate cancer awareness. He said, "Prostate cancer is 100% curable when caught early." He encouraged all men to get screened and announced that a van was touring the area offering screening in supermarket parking lots. This was a community service project sponsored by the radio station, the supermarket chain, and a radiation oncology practice.
A commercial like this plays to our fears and prejudices. All of us have been taught from an early age that the best way to deal with cancer is to find it early. With the development of the prostate-specific antigen test, prostate cancer screening and early detection efforts surged in the United States in the late 1980s and continue to this day (2,3). By 1991, there were large prostate cancer awareness campaigns, health systems, and others who stood to profit from prostate cancer screening and treatment and encouraged it, implying benefit to those screened (4). Many were eager to push screening because of a financial incentive; some simply did not think too deeply due to the financial gain. Others truly thought they were doing a public service and felt urgency because prostate cancer is a leading cause of cancer death.
Although there was clear evidence of early detection, there was little evidence to show that screening decreased prostate cancer mortality or saved lives. There was strong vocal "expert opinion" that surrogate endpoints of earlier stage at diagnosis and increased survival indicated that screening saved lives. Some experts expressed legitimate concern that screening was unproven and premature (5). Collins and Barry (6) noted that screening advocates were using the same mistaken arguments that caused the advocacy of lung cancer screening with chest X-ray in the 1960s. This intervention was abandoned in the 1970s after trials showed it ineffective.
Many screening advocates (both physician and lay) have had difficulty accepting that some cancers are not going to progress and cause symptoms or death within the lifetime of the patient (7). The distinguished urologist Willet Whitmore recognized overdiagnosis as a problem in his famous quote, "The quandary in prostate cancer: Is cure necessary in those for whom it is possible, and is cure possible in those for whom it is necessary?"(8)
Truth be known, most of our pathological definitions of cancer were developed in the mid-1800s using light microscopy (9). Prostate cancer has not moved fully into the molecular and genetic age (10). We desperately need the ability to predict which patient has a localized cancer that is going to metastasize and cause suffering and death and which patient has a cancer that is destined to stay in the patient's prostate for the remainder of his life.
Because of overdiagnosis, the true effect of prostate cancer screening cannot be assessed by the increased proportion of low-stage tumors at diagnosis. Overdiagnosis also artificially prolongs survival statistics meaning survival statistics cannot be used to determine a positive screening effect. Indeed, the only trusted measure of screening success can be decreased cause-specific mortality as seen in a randomized clinical trial (7).
Lesson 1: Have respect for science and the scientific process. Understand and address the truly important questions.
"Does prostate cancer screening save lives?" is still a legitimate question. A recently published analysis of an American prospective randomized trial (11) showed no benefit to screening with up to 10 years of follow-up. A European study (12) showed a 20% decline in mortality after 9 years of follow-up with substantial overdiagnosis. More than 1400 men have to be screened and 48 additional men diagnosed and treated to avert one prostate cancer death after 9 years.
There has been a 40% decline in US prostate cancer mortality since 1993. The reasons are not known. It could be because of screening, more effective treatment of metastatic disease, changes in attribution of cause of death, or other factors (13). The American screening trial (hindered by our prejudice for screening) would suggest that screening attributed nothing to the statistic. The European study would estimate screening caused about half of the decline. It is of note that countries that do not have widespread screening as a policy have seen some declines in prostate mortality without the harm of frequent overdiagnosis (14).
The early detection prejudice delegitimized the questions concerning screening and what are now clearly important scientific questions concerning disease prognostic factors and predictors of biological behavior. Indeed, over the past 20 years, many research dollars were spent addressing the question "how can men be encouraged to get screened?" when projects to better understand prostate cancer biology were not funded.
After we determine who needs treatment and who does not, we need to know how good the treatments are. Today there are nearly a dozen treatments for localized prostate cancer. Some of these treatments are very expensive and some have serious and long-lasting side effects (15,16). Little has been done to figure out which therapies are most effective. Every treatment looks good, when more than 90% of men getting it do not need it.
Lesson 2: In the past we have truly not appreciated the need for scientific evidence. In the future, will we accept scientific evidence?
Prostate cancer screening is not the only intervention we have adopted prematurely. Medicine and especially American medicine has often relied on the opinion of experts (often biased experts) rather than on the objective interpretation of scientific data. Too often, we have allowed opinion to undermine support for scientific study. Indeed, the list of medical interventions adopted and later withdrawn or substantially modified after initial assessment was determined incomplete is long. Among them are 1) the Halsted mastectomy for breast cancer (17), 2) bone barrow transplant for high-risk breast cancer (18), 3) neuroblastoma screening with a urine test (18,19), 4) lung cancer screening with chest X-ray (20), 5) erythropoetin therapy during chemotherapy (21), and 6) postmenopausal hormone replacement therapy (22).
The current political rhetoric supports "comparative effectiveness research." In principle, this is good. The strongest scientific supports for an intervention are findings from a prospective randomized controlled trial. In the case of prostate cancer screening, many screening advocates actually discouraged such trials even while the trials were under way.
Unfortunately, prospective randomized trials are not always practical because of expense or the needed duration. Some clinical decisions do need to be made through interpretation of results of lesser studies. These results need to be interpreted carefully and with an open mind. At times, the opinions of respected authorities based on clinical experience will need to be used. These authorities must remain objective.
Lesson 3: The rational use of medicine, not the rationing of medicine.
An important element of health-care reform is a reform of how we consume health care. The irrational tendency to adopt treatments and technologies without adequate assessment is a form of "medical gluttony" and a major reason that US per capita health-care costs are the highest in the world. We do not get what we pay for; our life expectancy is 29th among developed countries. Medical costs are approaching one-fifth of our gross domestic product (23). The economy cannot afford the continued growth of health-care costs seen over the past 30 years. Economic realities have already led to some restrictions or rationing. More will occur unless we begin the rational practice of medicine.
Lesson 4: Know what is known, know what is not known, and know what is believed. Label them accordingly.
The most important lesson of the prostate cancer screening saga is that we should appreciate the truth and clearly explain it as best as possible. Many men who thought their lives were saved by being screened, diagnosed, and treated for localized prostate cancer are perplexed to learn that so few benefit. They may be even more amazed that this is not a new finding. What is new is the fact that many health professionals are finally accepting it as true. They are accepting that there is overdiagnosis, unnecessary treatment and overtreatment, and questions regarding screening for this disease. They do this after several studies using varying methodologies have clearly shown that prostate cancer screening and treatment are very complicated (24–29).
I come from and have been supported by an African American community, where many are suspicious of physician motives and are convinced that doctors and those in medicine will take advantage of them and not tell them the truth. Distrust is actually a major reason for many disparities in health faced by black Americans (30). A closed-minded medical culture is a part of the problem. The well-meaning uninformed layman with a sound bite is also a part of the problem. Both can cause serious harm.
Given the estimates of Welch and Albertsen and the results of screening (11,12) and prevention (31) trials, we now know that prostate cancer is a highly complicated disease and prostate cancer screening is a complicated intervention. The benefits of prostate cancer screening are still open to question. This means that informed or shared decision making should be done using the data now available before screening is performed. Some of the confusion of prostate cancer screening can be avoided if we all clearly label what we know, as what we know; what we do not know, as what we do not know; and what we believe, as what we believe. Of course, one must not confuse what is believed with what is known to do this.
prostaat PSA
Affiliations of authors: VA Outcomes Group, Department of Veterans Affairs Medical Center, White River Junction, VT (HGW); Dartmouth Institute for Health Policy and Clinical Practice, Department of Medicine, Dartmouth Medical School, Hanover, NH (HGW); Department of Surgery, University of Connecticut School of Medicine, Farmington, CT (PCA)
Correspondence to: H. Gilbert Welch, MD, MPH, VA Outcomes Group (111B), Department of Veterans Affairs Medical Center, White River Junction, VT 05009 (e-mail: h.gilbert.welch@dartmouth.edu ).
Background: Although there is uncertainty about the effect of prostate-specific antigen (PSA) screening on the rate of prostate cancer death, there is little uncertainty about its effect on the rate of prostate cancer diagnosis. Systematic estimates of the number of men affected, however, to our knowledge, do not exist.
Methods: We obtained data on age-specific incidence and initial course of therapy from the National Cancer Institute’s Surveillance, Epidemiology, and End Results program. We then used age-specific male population estimates from the US Census to determine the excess (or deficit) in the number of men diagnosed and treated in each year after 1986—the year before PSA screening was introduced.
Results: Overall incidence of prostate cancer rose rapidly after 1986, peaked in 1992, and then declined, albeit to levels considerably higher than those in 1986. Overall incidence, however, obscured distinct age-specific patterns: The relative incidence rate (2005 relative to 1986) was 0.56 in men aged 80 years and older, 1.09 in men aged 70–79 years, 1.91 in men aged 60–69 years, 3.64 in men aged 50–59 years, and 7.23 in men younger than 50 years. Since 1986, an estimated additional 1 305 600 men were diagnosed with prostate cancer, 1 004 800 of whom were definitively treated for the disease. Using the most optimistic assumption about the benefit of screening—that the entire decline in prostate cancer mortality observed during this period is attributable to this additional diagnosis—we estimated that, for each man who experienced the presumed benefit, more than 20 had to be diagnosed with prostate cancer.
Conclusions: The introduction of PSA screening has resulted in more than 1 million additional men being diagnosed and treated for prostate cancer in the United States. The growth is particularly dramatic for younger men. Given the considerable time that has passed since PSA screening began, most of this excess incidence must represent overdiagnosis.
vitamine D bloeddruk
| Cardiovascular news provides daily news updates to help you stay informed. | |
Vitamin D deficiency exerts delayed effect on hypertension
25 September 2009
MedWire News: Premenopausal women who have a deficiency in vitamin D face a 3-fold increased risk for developing systolic hypertension in later life compared with their peers who have normal levels, study findings show.
The research was carried out by Flojaune Griffin (University of Michigan, Ann Arbor, USA) and colleagues who presented the findings at the recent American Heart Association 63rd High Blood Pressure Research Conference in Chicago, Illinois, USA.
For the study Griffen et al examined 559 Caucasian women aged an average of 38 years who in 1992 were enrolled on the Michigan Bone Health and Metabolism Study.
The women underwent annual systolic blood pressure assessments until the study endpoint in 2007. In addition, a single measurement of vitamin D status was taken from each participant in 1993 by way of the blood concentration of 25-hydroxyvitamin D (25(OH)D).
Griffen et al report that at the study onset in 1993, 2% of women had been diagnosed or were being treated for hypertension and an additional 4% of the women had undiagnosed systolic hypertension defined as 140 mmHg or greater.
Regression analysis revealed that women with a vitamin D deficiency had a modest and non-significantly increased risk for concurrent systolic hypertension relative to women in the normal range, with an odds ratio of 1.1.
Meanwhile, 15 years later in 2007, 19% of the women had been diagnosed or were being treated for hypertension and an additional 6% had undiagnosed systolic hypertension, a significant increase from baseline.
Notably, women who had a vitamin D deficiency in 1993 had a significantly increased risk for systolic hypertension in 2007 relative to women with normal levels in 1993, with a risk ratio of 3.0 after adjusting for age, fat mass, anti-hypertensive medication use, and smoking.
“Our study highlights the importance of vitamin D in the risk for high blood pressure later in life, a major health problem in the USA,” Griffin said at the conference.
However, she added that there is currently no general agreement about the optimal intake of vitamin D. Some researchers recommended intake of 400–600 IU daily is inadequate and suggest a much higher daily intake, from 1000–5000 IU.
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009
American Heart Association 63rd High Blood Pressure Research Conference; Chicago, Illinois, USA: 23–26 September 2009
Friday, September 25, 2009
prostaat hormonen
Medscape Conference Coverage, based on selected sessions at the:
This coverage is not sanctioned by, nor a part of either the European CanCer Organisation nor the European Society for Medical Oncology (ECCO 15 - 34th ESMO Multidisciplinary Congress).
September 24, 2009 (Berlin, Germany) — The risk for heart disease is increased with all hormonal therapies used as primary treatment for prostate cancer, but the risk is increased more by gonadotrophin-releasing hormone (GnRH) agonist therapy than by antiandrogens. These results come from a huge new Swedish study, which also showed that the risk is increased for all types of cardiovascular disease, including ischemic heart disease, myocardial infarction, heart failure, and cardiac arrhythmias.
The findings were presented here at a presidential session at the 15th Congress of the European CanCer Organization and the 34th European Society for Medical Oncology Multidisciplinary Congress, and highlighted at a congress press briefing.
The finding that the risk for cardiovascular disease is increased across the board is "very relevant to daily clinical practice," said Fortunato Ciardiello, MD, from the Cattedra di Oncologia Medica at Naples University in Italy, who moderated the press briefing. "When we prescribe these drugs, we have to explain to our patients that this testosterone deprivation can affect other aspects of their lives."
"It is important to take heart disease into account before starting endocrine treatment, especially as these drugs are prescribed not only for metastatic prostate cancer but also for less severe disease," said presenter Mieke van Hemelrijck, a PhD student and cancer epidemiologist at King's College in London, United Kingdom.
Largest Study to Date; Focus on Primary Treatment
Although there have been reports of an increased risk for heart disease, mainly from the United States, overall the previous findings have been inconsistent, Ms. van Hemelrijck explained to Medscape Oncology.
"This is the largest and most comprehensive study to date," she said. It is also the first to show a difference in risk between the different types of hormonal therapies, and to examine the effect on different types of cardiovascular disease, she added.
The researchers analysed data from the Swedish National Prostate Cancer Registry, which includes data on more than 80,000 men, accounting for more than 96% of all cases of prostate cancer in Sweden. They found 30,642 men who had received hormonal therapy as the primary treatment for their prostate cancer between 1997 and 2006.
About 10% of these men received antiandrogens, 30% received GnRH agonists, and 38% received a combination of the 2 therapies, Ms. van Hemelrijck told Medscape Oncology. In addition, some men underwent orchidectomy. They were followed for an average of 3 years.
The team compared national statistics for hospitalization and mortality for these men with those in the general population, taking into account age and history of heart disease.
"We found that prostate cancer patients treated with hormone therapy had an elevated risk of developing all of the individual types of heart problems, and that they were more likely than normal to die from those causes," Ms. Van Hemelrijck reported.
The increase in risk was seen within a few months of initiating hormone therapy, she added.
Compared with the general population, men taking hormonal therapy for prostate cancer showed an increased risk of developing cardiovascular disease that required hospitalization, and of dying from this. Specifically, their risk was increased:
- by 24% for a nonfatal myocardial infarction and by 28% for a fatal myocardial infarction
- by 19% for developing cardiac arrhythmias and by 5% for dying from this
- by 31% for developing ischemic heart disease and by 21% for dying from this
- by 26% for heart failure (for both incidence and mortality).
About 10 extra ischemic heart disease events a year will appear for every 1000 prostate cancer patients treated with such drugs.
"If we have observed a causative effect, then for all hormone therapies put together, we estimate that, compared with what is normal in the general population, about 10 extra ischemic heart disease events a year will appear for every 1000 prostate cancer patients treated with such drugs," Ms. van Hemelrijck noted.
However, the therapies differed from one another in the amount by which they increased the risk for cardiovascular disease.
Differences Between Hormonal Treatments
Patients who were taking GnRH agonist therapy were at the highest risk, and those taking antiandrogens alone were at the lowest risk, although the risk was still elevated in these patients for all of the cardiovascular problems except for death from ischemic heart disease, Ms. Van Hemelrijck explained.
For example, the risk for heart failure was increased by 5% with antiandrogens and by 34% with GnRH agonists, and the risk for ischemic heart disease was increased by 13% with antiandrogens and 30% with GnRH agonists.
The increase in risk seen in men who had undergone orchidectomy was similar to the increase in those treated with GnRH agonists. Both approaches dramatically reduce the amount of circulating testosterone; however, antiandrogens do not reduce the amount of testosterone in the body, they inhibit it from reaching the prostate cells, the researcher explained.
"The finding that antiandrogens carry the least heart risk supports the view that circulating testosterone may protect the heart," she noted.
In addition, the increase in the risk for cardiovascular disease seen with hormonal therapy for prostate cancer was less pronounced in men who had a history of such problems. For instance, men who had a history of ischemic heart disease had a 17% increased risk of developing a new event, compared with an increase of 41% in men with no history. The explanation might be that the men with a history of heart disease were already taking medication, which protected them from the further risk imposed by the hormone treatment, Ms. Van Hemelrijck suggested.
"We now need studies verifying the association and exploring plausible biological mechanisms," she said.
In the meantime, the main message from this study for doctors who prescribe hormonal therapies for prostate cancer is to be aware that they might increase the risk for cardiovascular disease, to take this into account when considering all potential treatment options, and to "be on the look out for it" in men taking these therapies, she said.
The study was funded by the Swedish Research Council, the Stockholm Cancer Society, and Cancer Research UK.
15th Congress of the European CanCer Organization (ECCO 15) and the 34th European Society for Medical Oncology (34th ESMO) Multidisciplinary Congress: Abstract 0272. Presented September 22, 2009.
Authors and Disclosures
Journalist
Zosia Chustecka
Zosia Chustecka is news editor for Medscape Hematology-Oncology and prior news editor of jointandbone.org, a Web site acquired by WebMD. A veteran medical journalist based in London, UK, she has won a prize from the British Medical Journalists Association and is a pharmacology graduate. She has written for a wide variety of publications aimed at the medical and related health professions. She can be contacted at ZChustecka@webmd.net.
Zosia Chustecka has disclosed no relevant financial relationships.
Medscape Medical News © 2009 Medscape, LLC
Send press releases and comments to news@medscape.net.
statins
NEW YORK (Reuters Health) Sep 21 - The impact of statin therapy on mortality in patients with decompensated heart failure is limited to those who have ischemic heart disease, say researchers from Israel.
Dr. Roman Nevzorov and colleagues from Ben-Gurion University of the Negev in Beer-Sheva analyzed 1-year mortality rates in 887 patients hospitalized for acute decompensated heart failure.
According to the researchers' report in the European Journal of Internal Medicine for September, their cohort included 656 (74%) patients with ischemic heart disease and 231 without. Overall, 281 patients (31.7%) had been treated with statins in the 3 months preceding admission.
One-year mortality reached 21% in the patients who were treated with statins and 31.8% in the no-statins group, the authors report.
Differences in rates of fatal events were significant among patients with ischemic heart disease (20.1% in the statin group versus 30.6% in the no-statin group, p=0.006), but not among patients with non-ischemic heart disease (25.6% with statin treatment versus 34.6% without, p=0.24).
Statin therapy and implantable cardioverter-defibrillator placement were independent predictors of improved survival in a multivariate analysis of patients with ischemic heart failure. In patients with non-ischemic heart failure, the only predictors of 1-year mortality were hyponatremia, hypoalbuminemia, and Charlson's comorbidity index.
"The clinical question is whether a statin should be prescribed to every patient with heart failure," the investigators say. "Based on the recent randomized trials and results of our analysis the answer is probably no in the case of heart failure of non-ischemic origin."
"On the other hand," the researchers say, patients with active coronary artery disease and heart failure should receive statins as "secondary and tertiary prevention" unless they have contraindications.
Eur J Intern Med 2009;20:494-498.
Tuesday, September 22, 2009
kwakzalver altenative medicin
Medscape gastro-enterology
published: 9-8-09
What is the attraction of alternative medicin?
Therapeutic modalities once considered outside the realm of conventional medicine are gradually being integrated into medical practice, partly because evidence shows that they provide benefit and partly because of their growing popularity.
The National Center for Complementary and Alternative Medicine (NCCAM) estimates that in the United States about 38% of adults and 12% of children use some form of complementary and alternative medicine (CAM).[1] According to the 2007 National Health Interview Survey, which polled over 12,000 persons, CAM use among adults in the United States is greater among women and those who have higher levels of education and higher incomes.
The growing popularity of CAM therapies has prompted contributors to Medscape's Physician Connect (MPC), an all-physician discussion board, to ask why so many persons are attracted to these treatments.
"People are trying different solutions because the official treatment does not work or because they are opponents of the chemical way of thinking," says a general practice doctor. "Western medicine has become a technical and chemical factory. We forget that the psyche of the patient plays a very important part."
"I see it as a sign that the disease in question is probably not one that responds well to traditional Western medicine," says an internist. "For many of the symptoms people seek relief from, we have little to offer, and while I don't think colon cleanse will cure fatigue, I'm not terribly confident in my SSRI [selective serotonin reuptake inhibitor]/CPAP [continuous positive airway pressure]/B12/weight loss prescriptions either."
Another contributor considers the interest in CAM therapies to be an indication of the public's ignorance of the scientific method. "Many people believe something is true because their cleaning lady's neighbor's aunt heard it. Progress in medicine in the last 50 years has been based on controlled studies that replaced the often erroneous opinion of some respected authority." The contributor finds it ironic that "the public accepts claims for untested herbal therapies, colonic cleansing, magnets, etc, but worries about the safety of extensively tested drugs."
The NCCAM defines CAM as a group of diverse medical and healthcare systems, practices, and products that are not generally considered part of conventional medicine.[1] Complementary medicine is used together with conventional medicine, whereas alternative medicine is used in place of conventional medicine -- although the NCCAM Website does not generally distinguish between the 2 types. Among the CAM therapies included in the 2007 National Health Interview Survey were acupuncture, ayurveda, biofeedback, chiropractic, diet-based therapies (eg, vegetarian diet), energy healing (eg, Reiki), guided imagery, homeopathic treatments, natural products (eg, herbs and enzymes), tradition healers (eg, shaman), and yoga.[1]
Nonvitamin and nonmineral natural products are the most commonly used CAM therapies among adults,[1] and this gives MPC contributors cause for concern. "Who knows what impurities lurk in the preparations now available?" posits a psychiatrist. "My mom was poisoned by eating bone meal tablets. The cow bones they were made from had accumulated arsenic. She developed a neuropathy from it."
The Website www.ConsumerLab.com provides information about the contents of unregulated supplements, such as echinacea, glucosamine, and vitamins. An internist familiar with the Website says, "This not-for-profit group of chemists analyze[d] OTC [over-the-counter] alternative products to determine if the brand actually contains the substance they claim. No surprise that many brands do not."
In addition to issues of product content, most MPC contributors are concerned that there is little evidence to suggest that many CAM therapies provide any benefit whatsoever.
"Anecdotal evidence of relief from one type of alternative approach or another is worthless without controls and without greater understanding of the process that allegedly results in improvement or cure," says an orthopaedic surgeon.
"The difference between evidence-based medicine and alternative medicine is that evidence-based medicine is willing to examine a therapeutic modality and determine if it is more valuable than a placebo," a pediatrician comments.
"On the other hand," comments another MPC contributor, "try to look at all this from the alternative healer's viewpoint, who would say we docs are relatively new to evidence-based medicine, and much of what we offer our patients is pretty much based on faith, just as his stuff is."
The anecdotal claims are gradually being subjected to a growing number of clinical trials. In addition, organizations, such as the Cochrane Library, evaluate the quality of evidence provided by these trials addressing CAM efficacy.[2] A recent noteworthy addition to the evidence-based literature is the ACP Evidence-Based Guide to Complementary and Alternative Medicine, published by the American College of Physicians.[3]
In the forward to the ACP Guide, Ralph Snyderman, MD, Chancellor Emeritus of Duke University, Durham, North Carolina, states a case for an integrated medicine that combines the best approaches of CAM and conventional medicine. "The conventional healthcare system focuses on powerful therapies designed to specifically deal with established disease using approaches that frequently have significant side effects. CAM, on the other hand, offers choices that are designed to enhance or restore wellness and often involve hands-on and ongoing relationships with the caregiver. Integrating the best of scientific medicine with CAM strategies is termed integrative medicine and is, in my view, a more effective as well as compassionate approach to healthcare."
Several MPC contributors see value in combining conventional and CAM approaches into integrative medicine. "The question is not whether Western medicine is better than alternative medicine, but how those systems could work together to improve health," comments a pulmonologist.
A psychiatrist remarks, "The point of alternative medicine is that it is helpful for chronic illnesses where conventional medicine shines in the treatment of acute illnesses. There are many very well-trained physicians who have a foot in each camp."
An internist, who has written a book on acupuncture, says that he uses the modality daily in his practice: "It works great -- for pain, especially."
"A friend of mine is a physical medicine and rehabilitation guy, and he strongly advocates alternative medicine -- especially acupuncture -- instead of narcotics for chronic pain," comments a general medicine physician. "The reason for this is clear enough -- as [a way of] preventing narcotic dependence. Who is more of a sucker? The narcotic-dependent patient or the acupuncture user? Maybe the former."
An MPC contributor agrees, "Having a patient who says acupuncture helps is more satisfying than writing yet another Percocet® script."
The full discussion about alternative medicine is available at: http://boards.medscape.com/forums/.29f3846e.
View this and other discussions in Physician Connect (physicians only; click here to learn more)Saturday, September 19, 2009
From International Journal of Clinical Practice
Homocysteine, Vitamin B12, Folate and Cognitive Functions: A Systematic and Critical Review of the Literature
CM
Summary and Introduction
Summary
Elevated serum homocysteine, decreased folate and low vitamin B12 serum levels are associated with poor cognitive function, cognitive decline and dementia. Despite evidence of an epidemiological association, randomised controlled trials did not provide any clear evidence so far that supplementation with vitamin B12 and/or folate improves dementia or slows cognitive decline, even though it might normalise homocysteine levels. In this report, we review the current knowledge on the relationship between homocysteine, folate and vitamin B12 levels and the way their disruption influences cognitive function in adults.
Introduction
The prevalence of cognitive impairment increases with advancing age, making it a major public health concern in ageing populations. Dementia represents the main cause of cognitive problems among the elderly people and is characterised by a progressive deterioration of cognitive skills, leading ultimately to difficulties performing daily activities. The number of people suffering from dementia might triple over the next 50 years, for reasons of an increase in the proportion of the oldest-old segment of the population[1]. Alzheimer disease (AD) accounts for about two-thirds of dementia. The prevalence of AD rises exponentially with age, affecting 50% of adults aged 95 years. Other causes of dementia are Lewy body dementia, vascular dementia, Parkinson's disease-associated dementia, fronto-temporal dementia and reversible dementias. Measures for prevention of cognitive impairment are crucial for many reasons, most notably the lack of efficient therapies, the high prevalence of dementia and the devastating consequences of dementia for patients' caregivers and healthcare system.
The most relevant risk factors for AD are advancing age, female gender and low level of education. Other non-genetic risk factors for AD include cardiovascular disease, stroke, hypertension, diabetes and traumatic head injury. Biomarkers associated with the risk of late-life cognitive impairment or dementia are not well-described and poorly understood. Despite this, it is interesting from a physiopathological perspective to take into account the nutritional component and diet.
An association between neuropsychiatric or neurological disorders (e.g. 'subacute combined degeneration of the cord') and vitamin B12 (cobalamin) deficiency has been recognised since pernicious anaemia was first described in 1849[2]. Inappropriate levels of vitamin B are a common cause of the reversible type of dementia. The association between vitamin B abnormalities and impaired cognitive function or dementia remains questionable as studies and interventional trials have reported conflicting results.
Several human studies have demonstrated a link between vitamin B deficiency (or hyperhomocysteinemia) and cognition. However, these studies were very heterogeneous in terms of the populations studied, cut-offs used to define vitamin B deficiency, definitions of vitamin B deficiency (serum levels, dietary intakes), assessments of cognitive impairment, definitions of cognitive impairment [incident dementia, prevalent dementia, type of dementia, mild cognitive impairment (MCI)] and study designs. Thus, comparing studies is difficult and caution is necessary when analysing and interpreting the results.
In this article, we distinguished three types of studies: cross-sectional studies, longitudinal studies, featuring a generally more adequate nutrient exposure and intervention studies with vitamin B supplementation.
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References
- Ziegler-Graham K, Brookmeyer R, Johnson E, Arrighi HM. Worldwide variation in the doubling time of Alzheimer's disease incidence rates. Alzheimers Dement 2008; 4: 316-23.
- Addison T. Anemia: disease of the suprarenal capsules. Lond Med Gaz 1849; 43: 517.
- Andrès E, Loukili NH, Noel E et al. Vitamin B12 (cobalamin) deficiency in elderly patients. CMAJ 2004; 171: 251-9.
- Clarke R. B-vitamins and prevention of dementia. Proc Nutr Soc 2008; 67: 75-81.
- Malaguarnera M, Ferri R, Bella R, Alagona G, Carnemolla A, Pennisi G. Homocysteine, vitamin B12 and folate in vascular dementia and in Alzheimer disease. Clin Chem Lab Med 2004; 42: 1032-5.
- Köseoglu E, Karaman Y. Relations between homocysteine, folate and vitamin B12 in vascular dementia and in Alzheimer disease. Clin Biochem 2007; 40: 859-63.
- Quadri P, Fragiacomo C, Pezzati R et al. Homocysteine, folate, and vitamin B-12 in mild cognitive impairment, Alzheimer disease, and vascular dementia. Am J Clin Nutr 2004; 80: 114-22.
- Feng L, Ng TP, Chuah L, Niti M, Kua EH. Homocysteine, folate, and vitamin B-12 and cognitive performance in older Chinese adults: findings from the Singapore Longitudinal Ageing Study. Am J Clin Nutr 2006; 84: 1506-12.
- Miller JW, Green R, Ramos MI et al. Homocysteine and cognitive function in the Sacramento Area Latino Study on Aging. Am J Clin Nutr 2003; 78: 441-7.
- Arioğul S, Cankurtaran M, Dağli N, Khalil M, Yavuz B. Vitamin B12, folate, homocysteine and dementia: are they really related? Arch Gerontol Geriatr 2005; 40: 139-46.
- Ravaglia G, Forti P, Maioli F et al. Elevated plasma homocysteine levels in centenarians are not associated with cognitive impairment. Mech Ageing Dev 2000; 121: 251-61.
- Seshadri S, Beiser A, Selhub J et al. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med 2002; 346: 476-83.
- Luchsinger JA, Tang MX, Shea S, Miller J, Green R, Mayeux R. Plasma homocysteine levels and risk of Alzheimer disease. Neurology 2004; 62: 1972-6.
- Mooijaart SP, Gussekloo J, Frölich M et al. Homocysteine, vitamin B-12, and folic acid and the risk of cognitive decline in old age: the Leiden 85-Plus study. Am J Clin Nutr 2005; 82: 866-71.
- Tucker KL, Qiao N, Scott T, Rosenberg I, Spiro A 3rd. High homocysteine and low B vitamins predict cognitive decline in aging men: the Veterans Affairs Normative Aging Study. Am J Clin Nutr 2005; 82: 627-35.
- Fioravanti M, Ferrario E, Massaia M et al. Low folate levels in the cognitive decline of elderly patients and the efficacy of folate as a treatment for improving memory deficits. Arch Gerontol Geriatr 1998; 26: 1-13.
- Bryan J, Calvaresi E, Hughes D. Short-term folate, vitamin B-12 or vitamin B-6 supplementation slightly affects memory performance but not mood in women of various ages. J Nutr 2002; 132: 1345-56.
- Sommer BR, Hoff AL, Costa M. Folic acid supplementation in dementia: a preliminary report. J Geriatr Psychiatry Neurol 2003; 16: 156-9.
- Durga J, van Boxtel MP, Schouten EG et al. Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial. Lancet 2007; 369: 208-16.
- Rapin JR, LePoncin M, Grebyl J. Blood folates deficiencies and cognitive functions in aging. Trends Biomed Gerontol 1988; 1: 315-23.
- Eussen SJ, de Groot LC, Joosten LW et al. Effect of oral vitamin B-12 with or without folic acid on cognitive function in older people with mild vitamin B-12 deficiency: a randomized, placebo-controlled trial. Am J Clin Nutr 2006; 84: 361-70.
- Hvas AM, Juul S, Lauritzen L, Nexø E, Ellegaard J. No effect of vitamin B-12 treatment on cognitive function and depression: a randomized placebo controlled study. J Affect Disord 2004; 81: 269-73.
- McMahon JA, Green TJ, Skeaff CM, Knight RG, Mann JI, Williams SM. A controlled trial of homocysteine lowering and cognitive performance. N Engl J Med 2006; 354: 2764-72.
- Aisen PS, Schneider LS, Sano M et al. High dose B vitamin supplementation and cognitive decline in Alzheimer disease. A randomized Controlled trial. JAMA 2008; 300: 1774-83.
- Lewerin C, Matousek M, Steen G, Johansson B, Steen B, Nilsson-Ehle H. Significant correlations of plasma homocysteine and serum methylmalonic acid with movement and cognitive performance in elderly subjects but no improvement from short-term vitamin therapy: a placebo-controlled randomized study. Am J Clin Nutr 2005; 81: 1155-62.
- Dali-Youcef N, Andrès E. An update on cobalamin deficiency in adults. QJM 2009; 102: 17-28.
- Malouf R, Grimley Evans J. Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people. Cochrane Database Syst Rev 2008; 8: CD004514.
Authors and Disclosures
As an organization accredited by the ACCME, MedscapeCME 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.
MedscapeCME 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)
Thomas Vogel, MD
Pôle de Gériatrie, Hôpitaux Universitaires de Strasbourg, Hôpital de la Robertsau, Pavillon Schutzenberger, Strasbourg Cedex, France
Disclosure: Thomas Vogel, MD, has disclosed no relevant financial relationships.
Nassim Dali-Youcef, PhD
Pôle de Biologie, Nouvel Hôpital Civil, Hôpitaux Universitaires de Strasbourg, Strasbourg Cedex, France
Disclosure: Nassim Dali-Youcef, PhD, has disclosed no relevant financial relationships.
Georges Kaltenbach, MD
Pôle de Gériatrie, Hôpitaux Universitaires de Strasbourg, Hôpital de la Robertsau, Pavillon Schutzenberger, Strasbourg Cedex, France
Disclosure: Georges Kaltenbach, MD, has disclosed no relevant financial relationships.
Emmanuel Andrès, MD
Service de Médecine Interne, Clinique Médicale B, Hôpital Civil, Hôpitaux Universitaires de Strasbourg, Strasbourg Cedex, France
Disclosure: Emmanuel Andrès, MD, has disclosed no relevant financial relationships.
CME Author(s)
Désirée Lie, MD, MSEd
Clinical Professor, Family Medicine, University of California, Orange; Director, Division of Faculty Development, UCI Medical Center, Orange, California
Disclosure: Désirée Lie, MD, MSEd, has disclosed no relevant financial relationships.
Editor(s)
Graham Jackson, MD, FESC, FRCP, FACC
Honorary Consultant Cardiologist, Cardiothoracic Centre, Guy's and St. Thomas' Hospital, London, United Kingdom
Disclosure: Graham Jackson, MD, FESC, FRCP, FACC, has disclosed that he has served as an academic advisor for Pfizer Inc.; Eli Lilly & Co., Inc.; Plethora Solutions Limited; Shire; and SERVIER, and has served as chairman of the Sexual Dysfunction Association. Dr. Jackson regularly gives sponsored lectures that are rigorously noncommercial.
Leslie Citrome, MD, MPH
Director, Clinical Research and Evaluation Facility, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York; Professor of Psychiatry, New York University School of Medicine, New York, NY
Disclosure: Leslie Citrome, MD, MPH, has disclosed that he is a consultant for, has received honoraria from, or has conducted clinical research supported by Abbott Laboratories; AstraZeneca Pharmaceuticals LP; Avanir Pharmaceuticals; Azur Pharma Ltd.; Barr Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; Eli Lilly & Co., Inc.; Forest Research Institute; GlaxoSmithKline; Janssen; Jazz Pharmaceuticals, Inc.; Pfizer Inc.; and Vanda Pharmaceuticals Inc.
Karen Costenbader, MD, MPH
Rheumatology and Immunology, Brigham and Women's Hospital, Boston, Massachusetts
Disclosure: Karen Costenbader, MD, MPH, has disclosed no relevant financial relationships.
Serge Jabbour, MD
Associate Professor of Clinical Medicine, Division of Endocrinology, Diabetes, and Metabolic Diseases, Department of Medicine, Jefferson Medical College/Thomas Jefferson University, Philadelphia, Pennsylvania
Disclosure: Serge Jabbour, MD, has disclosed that he has served on the speaker's bureau for Amylin Pharmaceuticals, Inc. and Eli Lilly & Co., Inc.
Rubin Minhas
General Practitioner; Honorary Senior Lecturer, Faculty of Science, Technology, and Medical Studies, University of Kent, Kent, United Kingdom
Disclosure: Rubin Minhas, has disclosed no relevant financial relationships.
Matt Rosenberg, MD, BA
Medical Director, Mid-Michigan Health Centers, Jackson, Michigan
Disclosure: Matt Rosenberg, MD, BA, has disclosed that he has served as a consultant for Abbott Laboratories; Allergan, Inc.; Astellas Pharma, Inc.; GlaxoSmithKline; Novartis Pharmaceuticals Corporation; Ortho-McNeil-Janssen Pharmaceuticals, Inc.; Pfizer Inc.; Roche Laboratories Inc.; sanofi-aventis; and Verathon Inc. Dr. Rosenberg has also disclosed that he has received fees for non-CME services from Abbott Laboratories; Allergan, Inc.; Astellas Pharma, Inc.; GlaxoSmithKline; Esprit Pharma; Ortho-McNeil-Janssen Pharmaceuticals, Inc.; and Roche Laboratories Inc., and conducted research funded by sanofi-aventis.
Jagdish Sharma, FRCP, FESO
Sherwood Forest NHS Trust, Nottinghamshire, United Kingdom
Disclosure: Jagdish Sharma, FRCP, FESO, has disclosed no relevant financial relationships.
Anthony Wierzbicki, FACA, FACB
Senior Lecturer in Chemical Pathology, St. Thomas' Hospital, London, United Kingdom
Disclosure: Anthony Wierzbicki, FACA, FACB, has disclosed that he has received support for travel from Abbott Laboratories; AstraZeneca Pharmaceuticals LP; Merck KGaA; and Merck Sharp & Dohme, and received lecture honoraria from Abbott Laboratories; AstraZeneca Pharmaceuticals LP; Bristol-Myers Squibb Company; Genzyme Corporation; Gilead Sciences, Inc.; Merck KGaA; Merck Sharp & Dohme; Pfizer Inc.; Roche Laboratories Inc.; Schering-Plough Corporation; and Solvay/Fournier. Dr. Wierzbicki is an advisory board member for Abbott Laboratories; AstraZeneca Pharmaceuticals LP; Bristol-Myers Squibb Company; Genzyme Corporation; Gilead Sciences, Inc.; Kowa Company Ltd.; LifeCycle Pharma; Merck KGaA; Merck Sharp & Dohme; Pfizer Inc.; Roche Laboratories Inc.; Schering-Plough Corporation; Solvay/Fournier; Surface Logix, Inc.; and Takeda Pharmaceuticals North America, Inc.
Mark Harries, MA, PhD, FRCP
Consultant in Medical Oncology, Guy's and St. Thomas' Hospital, London, United Kingdom
Disclosure: Mark Harries, MA, PhD, FRCP, has disclosed no relevant financial relationships.
Gabrielle Cremer, MD
Cremer Consulting, Strasbourg, France
Disclosure: Gabrielle Cremer, MD, has disclosed no relevant financial relationships.
Carol Peckham
Site Editorial Director, MedscapeCME
Disclosure: Carol Peckham has disclosed no relevant financial relationships.
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CME Information
CME Released: 08/31/2009; Valid for credit through 08/31/2010
Target Audience
This activity is intended for primary care clinicians, geriatricians, neurologists, psychiatrists, and other specialists who care for older adults.
Goal
The goal of this activity is to review the association between vitamin B12 and folic acid deficiency, homocysteinemia, and cognitive decline in adults.
Learning Objectives
Upon completion of this activity, participants will be able to:
- Describe tests and their limitations for the diagnosis of vitamin B deficiencies
- Describe types of studies linking vitamin B with cognitive function
- Advise patients on use of folic acid and vitamin B12 for preventing cognitive decline
Credits Available
Physicians - maximum of 0.50 AMA PRA Category 1 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
MedscapeCME is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
MedscapeCME designates this educational activity for a maximum of 0.5 AMA PRA Category 1 Credit(s)™ . Physicians should only claim credit commensurate with the extent of their participation in the activity.
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*:
- Read the target audience, learning objectives, and author disclosures.
- Study the educational content online or printed out.
- 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
MedscapeCME is accessible using the following browsers: Internet Explorer 6.x or higher, Firefox 2.x or higher, Safari 2.x or higher. Certain educational activities may require additional software to view multimedia, presentation or printable versions of their content. These activities will be marked as such and will provide links to the required software. That software may be: Macromedia Flash, Adobe Acrobat, or Microsoft PowerPoint.
E Released: 08/31/2009; Valid for credit through 08/31/2010
AF warfarin anticoagulation
From Heartwire CME
Net Clinical Benefit of Warfarin in AF Is Highest in Prior Stroke Victims and the Very Old
CME Released: 09/11/2009; Valid for credit through 09/11/2010
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CME Information
Target Audience
This article is intended for primary care clinicians, cardiologists, neurologists, and other specialists who care for patients with atrial fibrillation who are at risk for stroke.
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
Lisa Nainggolan
Lisa Nainggolan is a journalist for theheart.org, part of the WebMD Professional Network. She has been with theheart.org since 2000. Previously, she was science editor of Scrip World Pharmaceutical News, covering news about research and development in the pharmaceutical industry, and a consultant editor of Scrip Magazine. Graduating in physiology from Sheffield University, UK, she began her career as a poisons information specialist at Guy's Hospital before becoming a medical journalist in 1995. She can be reached at LNainggolan@webmd.net.
Disclosure: Lisa Nainggolan has disclosed no relevant financial relationships.
Brande Nicole Martin
is the News CME editor for Medscape Medical News.
Disclosure: Brande Nicole Martin has disclosed no relevant financial information.
Désirée Lie, MD, MSEd
Clinical Professor, Family Medicine, University of California, Orange; Director, Division of Faculty Development, UCI Medical Center, Orange, California
Disclosure: Désirée Lie, MD, MSEd, has disclosed no relevant financial relationships.
Learning Objectives
Upon completion of this activity, participants will be able to:
- Describe the net clinical benefit of warfarin for preventing stroke in patients with atrial fibrillation.
- Identify patients with atrial fibrillation most likely to benefit from warfarin therapy.
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
MedscapeCME is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
MedscapeCME 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.
AAFP Accreditation Questions
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: 09/11/2009; Valid for credit through 09/11/2010
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*:
- Read the target audience, learning objectives, and author disclosures.
- Study the educational content online or printed out.
- 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
MedscapeCME is accessible using the following browsers: Internet Explorer 6.x or higher, Firefox 2.x or higher, Safari 2.x or higher. Certain educational activities may require additional software to view multimedia, presentation or printable versions of their content. These activities will be marked as such and will provide links to the required software. That software may be: Macromedia Flash, Adobe Acrobat, or Microsoft PowerPoint.
September 11, 2009 — A contemporary assessment of the real-world clinical care of patients with atrial fibrillation (AF) has identified those who will gain the most benefit from taking warfarin therapy [1]. Dr Daniel E Singer (Massachusetts General Hospital, Boston, MA) and colleagues report their findings, taken from the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) cohort, in the September 1, 2009, issue of the Annals of Internal Medicine.
Existing guidelines for warfarin therapy are based on "old data—randomized clinical trials completed in the 1990s, for the most part," Singer explained to heartwire , "and they don't completely take into consideration the risk of intracranial hemorrhage [ICH]. We were looking to see, 'What is the net benefit of warfarin?'—the good things, ie, a reduction in clot strokes—vs the bad things, ie, increased bleeding into and around the brain."
They found that the net benefit of warfarin was highest among patients with the highest untreated risk for stroke, because the absolute increase in risk for ICH due to warfarin remains fairly stable across thromboembolic risk categories. These included those with a history of ischemic stroke and those in the highest CHADS2 category (where patients score 1 point each for congestive heart failure, hypertension, age, and diabetes and 2 points for stroke). Those with a CHADS2 score of 0 or 1 gained no benefit from warfarin, with net benefit being seen in those with a CHADS2 score of 2 or greater.
Notably, the benefit was greater the older the patient, Singer said, so one of the important messages of this study is that age should not be a barrier to warfarin treatment, as long as the patient "is not falling and is not terribly demented. We can't go out and anticoagulate everyone over 85, but if you think they are reasonable candidates, the data suggest they will benefit."
In an accompanying editorial [2], Drs Robert G Hart (University of Texas Health Science Center, San Antonio) and Jonathan L Halperin (Mount Sinai Medical Center, New York) say: "These new observations underscore the importance of risk stratification to identify patients who are likely to benefit most from long-term anticoagulation. These results challenge us to reconsider the benefit of warfarin for a substantial proportion of patients with AF."
ATRIA: A Large, Contemporary Cohort
One of the strengths of this observational analysis, said Singer, is that the ATRIA database is large, with six years and more than 66 000 person-years of follow-up from a large cohort of 13 000 patients with AF. "We accumulated 1000 ischemic strokes and multiple hundreds of ICHs, so we had enough events to look at both sides of the equation."
Singer said they found that, in general, the background rates of ischemic stroke in this population were "much lower than had previously been reported, by as much as a half," and that this is in line with findings from other recent studies of those with AF.
The net clinical benefit of warfarin was defined in the study as the reduction in ischemic stroke and systemic embolism balanced against the increase in ICH (the latter weighted by a factor of 1.5 because of the severity of the health consequences of intracranial bleeding).
The researchers did not include extracranial bleeding, because 90% of deaths attributed to warfarin involve ICH, but the editorialists say they believe this to be an oversight that may have led to an overestimation of the net clinical benefit of anticoagulation.
Those with a history of stroke, the very elderly, benefit most
The patient groups with the largest net benefit from warfarin were those with a history of ischemic stroke (number needed to treat for one year to prevent one ischemic stroke equivalent=40) and those older than 85 (number needed to treat for one year to prevent one ischemic stroke equivalent=43).
Singer stressed to heartwire , however, that patients must be compliant with warfarin therapy to achieve these benefits: "Anticoagulation is highly dependent on the quality of warfarin management. Patients should be in the INR [international normalized ratio] range of 2 to 3 for 60% or more of the time. We had 65% of our patients in INR 2 to 3, which is good-quality anticoagulation."
Despite their findings, Singer says, "What we really need going forward is better ways to stratify patients. The things we are using are fairly crude risk predictors. What we'd really like to get to is those at the very highest risk: if your risk is 10% per year of having an ischemic stroke and we can get you on anticoagulation, focused very carefully, then we can spare some of the people at lower risk."
He also noted that the whole field is likely to be shaken up by a host of new oral anticoagulants that don't need monitoring in the way that warfarin does, such as dabigatran etexilate (Boehringer-Ingelheim). RE-LY, a landmark study showing that this new agent prevents strokes and peripheral embolic events in patients with AF at least as well as warfarin, with better safety, was reported at the European Society of Cardiology 2009 Congress, in Barcelona, Spain.
The editorialists agree: "New oral anticoagulants are on the horizon, and the net clinical benefit at different levels of intrinsic stroke risk will need to be assessed for these agents."
Singer reports being a consultant for Boehringer-Ingelheim, Bayer, AstraZeneca, Sanofi-Aventis, Daiichi Sankyo, and Johnson & Johnson and receiving honoraria from Bristol-Myers Squibb and Pfizer and grants from Daiichi Sankyo. The editorialists have disclosed no relevant financial relationships.
References
- Singer DE, Chang Y, Fang MC, et al. The net clinical benefit of warfarin anticoagulation in atrial fibrillation. Ann Intern Med 2009; 151: 297-305.
- Hart RG and Halperin JL. Do current guidelines result in atrial fibrillation? Ann Intern Med 2009; 151: 355-356.
microcephaly
September 15, 2009 — A new Practice Parameter counsels neurologists on how to evaluate the child with microcephaly for the presence of neurologic and cognitive conditions. The document, prepared jointly by the American Academy of Neurology (AAN) and the Child Neurology Society, is published in the September 15 issue of Neurology.
"For physicians, this parameter is helpful because it has some terrific appendices that are on the AAN Website, and they have lots of succinct information about many of the different neuroimaging abnormalities that are seen with microcephaly, as well as metabolic diseases and genetic conditions," corresponding author Stephen Ashwal, MD, from the Loma Linda University School of Medicine, California, told Medscape Neurology.
The problem that a neurologist or pediatrician faces after they have made a diagnosis of microcephaly is how much testing to undertake to screen for causes and associated conditions, Dr. Ashwal said.
"That's where these appendices are very helpful, because in this document we have algorithms to help physicians with a clinical pathway to figure out whether they should do — or not do — certain tests, and then also provide guidance, based on history or physical features, [on] what genetic testing should be done," he added.
Common Problem
Microcephaly is common, affecting more than 25,000 infants in the United States each year, a release from the AAN notes. It is generally defined as a head circumference of more than 2 standard deviations below the mean for age and sex, and if not present at birth, it usually develops before 2 years of age.
Microcephaly can arise from any insult that disturbs early brain growth and is seen in association with hundreds of genetic conditions, the guideline authors write. Although it is an important neurological sign, there is no uniformity at this time in how it is defined or evaluated, although it can be associated with serious comorbid conditions, they note.
For this guideline, authors reviewed and classified the current literature and made recommendations based on a 4-tiered system. They found that few data are available at this time to make evidence-based recommendations about diagnostic testing in these children. The yield of neuroimaging ranges from 43% to 80%, they note.
Microcephaly arises from genetic etiologies in 15.5% to 53.3% of cases, the researchers report. The prevalence of metabolic disorders is unknown, they add, but is estimated to be 1%.
Children with severe microcephaly, defined as more than 3 standard deviations below the mean for age and sex, are more likely to have imaging abnormalities and more severe developmental impairments than those with milder microcephaly, the researchers report, with these conditions occurring in about 80% of those with severe microcephaly and about 40% of those affected more mildly.
About 40% of children with microcephaly also have epilepsy, 20% have cerebral palsy, 50% have mental retardation, and 20% to 50% have ophthalmologic and audiologic disorders, the authors write.
Based on their findings, their recommendations include the following.
- Level A recommendations:
- Because children with cerebral palsy are at risk of developing acquired microcephaly, serial head circumference measurements should be followed.
- Because children with microcephaly are at risk for developmental disability, physicians should periodically assess development and academic achievement to determine whether further testing and rehabilitative efforts are warranted.
- Level C recommendations:
- Neuroimaging may be considered useful in identifying structural causes of microcephaly.
- Targeted genetic testing may be considered to determine a specific etiology.
- Because children with microcephaly are at risk for epilepsy, physicians may consider educating caregivers of these children on how to recognize clinical seizures.
- Because these children are at risk for cerebral palsy, physicians and other care providers may consider monitoring them for early signs so that supportive treatments can be initiated.
- Screening for ophthalmological abnormalities may be considered.
- Level U (insufficient evidence):
- There is insufficient evidence to support or refute obtaining metabolic testing on a routine basis for the evaluation of the newborn or infant with microcephaly.
- There are insufficient data to support or refute obtaining a routine electroencephalogram in a child with microcephaly.
Dr. Ashwal has disclosed that he serves on the scientific advisory board of the Tuberous Sclerosis Association and the International Pediatric Stroke Society. He also serves as an editor of Pediatric Neurology and receives research support from the National Institutes of Health. Disclosures for coauthors appear in the Practice Parameter document.
Neurology. 2009;73:887–897.
Authors and Disclosures
Journalist
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.
Friday, September 11, 2009
glaucoom H2 antagonist bepotastine (Talion)
September 9, 2009 — The FDA has approved bepotastine besilate 1.5% ophthalmic solution (Bepreve, ISTA Pharmaceuticals, Inc) for the twice-daily treatment of ocular itching associated with allergic conjunctivitis in patients aged 2 years and older.
Approval of the histamine H1 receptor antagonist was based primarily on data from 2 phase 3 double-blind, conjunctival allergen challenge studies (n = 237) showing that bepotastine significantly decreased ocular itching relative to use of the vehicle alone at 15 minutes and 8 hours postdose.
Adverse events reported in 2% to 5% of treated patients included eye irritation, headache, and nasopharyngitis.
"Patients who experience ocular itching due to allergies want comfortable, quick and long-lasting relief for their eyes. Bepreve is the first truly new treatment for allergic conjunctivitis approved in several years.... I am excited patients will have this new treatment option," noted Gregg J. Berdy, MD, assistant professor of clinical ophthalmology, Washington University School of Medicine, St. Louis, Missouri, in a company news release.
To minimize the risk for contamination, patients should be advised to avoid touching the eyelids or surrounding areas with the dropper tip of the medication bottle.
Because soft contact lenses can absorb benzalkonium chloride (used as a preservative), they should be removed before instillation of bepotastine drops. Lenses may be reinserted 10 minutes after dosing.
Oral bepotastine previously was approved in Japan for the systemic treatment of allergic rhinitis and urticaria/pruritis.
