Monday, March 29, 2010

How health system reform affects patients

The Patient Protection and Affordable Care Act (H.R. 3590)—health system reform legislation signed into law by President Obama on March 23—contains a number of key provisions for you and your patients. Some provisions may have an immediate impact on your practice and patients, while others will not take effect for some time.
Given the new direction for the nation's health system, the AMA has developed Health System Reform Insight to help you understand the new law and how it will affect you, when certain provisions are scheduled to take effect, how you can be ready when the regulations go into effect and what your patients need to know. The first issue of the series explained how health system reform will affect physician practices. Today we focus on information for your patients. We encourage you to visit the AMA's health system reform Web site (PDF) and print copies to share with them.
How health system reform affects patients
H.R. 3590 has many significant benefits for patients—those who already have health insurance and those who don't. While some benefits take effect in 2010, many others will be phased in over several years to allow the health care system to absorb the changes ahead. Here's a snapshot of those benefits.
Patient benefits that take effect in 2010
For patients with private health insurance:
  • Your insurer can no longer drop you from your plan if you get sick.
  • Children ages 18 and younger can no longer be denied private insurance coverage if they have a pre-existing medical condition.
  • For adults with pre-existing medical conditions who cannot obtain private insurance coverage, a temporary national "high-risk pool" will be established to provide coverage, with financial subsidies to make premiums more affordable, until all insurers are required to cover people with pre-existing conditions in 2014.
  • Young adults up to age 26 can remain as a dependent on their parents' private health insurance plan.
  • Your health insurance benefits can no longer run out because of a long or expensive illness because insurers can no longer impose lifetime financial limits on benefits.
  • Preventive services for women, such as mammograms, and immunizations for children must be covered by insurers, with no co-payments or deductibles required.
In addition, Medicare patients who will hit the coverage gap known as the "doughnut hole" this year under the prescription drug benefit will receive a $250 rebate from Medicare.
Patient benefits that take effect during the next four years
In the private health insurance market:
  • U.S. citizens and legal residents cannot be denied private health insurance coverage for any reason, beginning in 2014. All U.S. citizens and legal residents must obtain health insurance coverage or pay a minor tax penalty (although there are some exemptions). This is to ensure that everyone is in the insurance pool so no one can get a "free ride" by not having affordable coverage and then going to an emergency room for care.
  • State-based health insurance exchanges will begin operating in 2014, where people who do not have access to employer-based insurance can shop and compare the benefits and costs of private health insurance plans. These exchanges will create insurance pools that will allow people to choose among affordable coverage options. All insurance companies in the exchange must provide at least a minimum benefit package, as well as additional coverage options beyond a basic plan.
  • Federal subsidies through tax credits or vouchers will be provided in 2014 to people who cannot afford the full cost to help them purchase coverage through the exchanges.
  • Beginning in 2011, states can require insurance companies to submit justification for premium increases and can impose penalties for excessive increases.
For patients enrolled in Medicare or Medicaid:
  • You no longer will pay any cost-sharing for a number of preventive services, effective Jan. 1, 2011.
  • If you are subject to the "doughnut hole" for your Medicare drug coverage, you will receive a 50 percent discount on those prescription drugs beginning Jan. 1, 2011.
  • A series of pilot programs will be implemented during the next four years to help find new ways to improve quality and lower the cost of the care you receive from your doctors, hospitals and nursing homes in the Medicare and Medicaid programs.
  • Medicaid coverage will be expanded in 2014 to all eligible children, pregnant women, parents and childless adults under age 65 who have incomes at or below 133 percent of the federal poverty level.

Saturday, March 6, 2010

AAAAI: Test May Identify Asthma Patients Unresponsive to Steroids


By John Gever, Senior Editor, MedPage Today
Published: March 05, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit
for reading medical news

NEW ORLEANS -- Asthma patients who will be unlikely to gain control of symptoms with inhaled corticosteroids might be identified with a blood test, a researcher suggested here.

A plasma protein called uteroglobin appeared elevated enough in patients unresponsive to inhaled corticosteroids that a blood test might be feasible, reported Elena Goleva, PhD, of National Jewish Health in Denver.

By identifying such patients before starting on these drugs -- the standard of care for patients with persistent asthma -- they might instead be treated with alternative controller medications such as omalizumab (Xolair) or montelukast (Singulair), Goleva suggested in a featured poster presentation at the American Academy of Allergy, Asthma & Immunology meeting.

Goleva said about 15% to 20% of patients seen at her institution show poor responses to inhaled steroids. However, National Jewish Health is a national referral center, she pointed out, and the percentage would likely be smaller in an ordinary community practice.
Action Points  
  • Explain to interested patients that inhaled corticosteroids are the standard of care for long-term control of asthma symptoms and that most patients respond to them when used as directed.
  • Explain that other medications are available for patients who fail to respond to these drugs after a fair trial.
  • Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered preliminary until published in a peer-reviewed journal.
She and her colleagues conducted a study in a total of 89 patients, 24 of whom were determined to be steroid-resistant.
These 24 patients continued to show asthma symptoms despite treatment with inhaled corticosteroids. They also showed essentially no improvement in lung function (as measured by FEV1) following oral treatment with prednisone.
In contrast, symptomatic patients believed to be responsive to steroids had a mean 39% increase in FEV1 with the prednisone burst.
Previous research had suggested that uteroglobin, which is produced by Clara cells in the lung, was increased in patients with steroid-resistant asthma, but with insufficient detail to confirm that the protein could be a useful biomarker.
Goleva and colleagues initially performed bronchoalveolar lavage in 20 patients, including 13 with steroid-resistant asthma and seven with asthma responding to the drugs.
Mean levels of uteroglobin expression, as measured by mRNA for the uteroglobin gene in BAL fluid, was elevated about six-fold in the resistant patients (P<0.05).
Actual levels of uteroglobin protein in the lavage fluid were roughly twice as high on average in the resistant patients (P<0.01), the researchers found.
Moreover, they discovered that mean uteroglobin levels in plasma were about 50% higher in the resistant patients, prompting the researchers to perform blood tests on an additional 25 patients, including 11 with steroid-resistant disease.
The findings were initially somewhat disappointing, Goleva explained.
The means were still significantly different -- about 65 ng per μg of plasma protein in the resistant patients, compared with about 45 in the steroid-sensitive group, but there was considerable overlap between the individual results.
For example, setting the cutoff at the lowest value in the steroid-resistant group would leave about three-quarters of the steroid-sensitive group above it as well.
But Goleva said her team hypothesized that airway disease might allow uteroglobin in the lungs to "leak" into circulation in the steroid-sensitive group, inflating their plasma levels of the protein.
If that were the case, they believed, lung proteins such as surfactant protein D and mucin-1 would also be elevated in the patients' plasma.
When they tested for those proteins, they found that four patients with elevated plasma levels of those lung proteins also had high plasma levels of uteroglobin.
With those four patients removed, there was clearer separation among the groups in their uteroglobin levels, although some overlap still remained, Goleva reported.
Finally, the researchers performed an in vitro experiment on peripheral blood mononuclear cells from 44 asthmatic patients, without regard to whether they were steroid-resistant, to correlate plasma uteroglobin with steroid responsiveness.
The latter was measured by the quantity of dexamethasone required to suppress lymphocyte proliferation and tumor necrosis factor production, both of which are associated with inflammatory activity.
The researchers found strong correlations -- r coefficients of 0.35 and 0.46, respectively, both with P<0.05 -- between uteroglobin and steroid responsiveness in these cells.
In sum, she said, it appears that uteroglobin could be a useful biomarker in guiding treatment selection.
Stanley Szefler, MD, also of National Jewish Health, although not involved with the study, said the research held some promise but cautioned that most cases of "steroid resistance" seen in routine practice have nonbiologic causes -- especially lack of treatment compliance or inadequate dosing.

Saturday, February 27, 2010

ASA: Coffee Drinkers Have Lower Stroke Risk

By Todd Neale, Staff Writer, MedPage Today
Published: February 26, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner   
Earn CME/CE credit
for reading medical news


SAN ANTONIO -- Drinking just one cup of coffee a day -- either regular or decaffeinated -- was associated with a 30% reduced risk of stroke, a large, prospective study showed.

Greater consumption did not heighten the apparent protective effect, according to Yangmei Li, MPhil, of the University of Cambridge in England.

The results, gathered over a mean 12-year follow-up, were not affected by adjusting for several known stroke risk factors, Li reported at the American Stroke Association meeting here.

Coffee drinking has been linked to lower risks of several other conditions, including type 2 diabetes and impaired cognition. (See Tea, Coffee Seem to Protect Against Diabetes and Caffeine May Slow Cognitive Decline in Women)Action Points 
Explain to interested patients that this study could not establish a causal relationship between coffee drinking and stroke risk.


Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered preliminary until published in a peer-reviewed journal.
Studies examining the association with stroke, however, have been mixed, with some showing no relationship and others echoing the lower risk in the current analysis. (See High Coffee Consumption Linked to Lower Stroke Risk for Women)

Li and her colleagues explored the issue using data on 9,978 men and 12,254 women from the U.K. general population who were taking part in the European Prospective Investigation into Cancer (EPIC)-Norfolk.

The participants' mean age was 59 (range 39 to 79).

All were free of known heart disease, stroke, and cancer at the baseline period from 1993 to 1997.

Overall, 17,807 reported drinking some amount of coffee -- 3.1 cups a day on average -- and 4,425 said they never drank any coffee.

Through March 2008, 855 strokes occurred, with a lower risk among those who reported drinking any amount of coffee.

Adjusting for smoking, social class, educational level, body mass index, alcohol intake, physical activity, tea drinking, urinary sodium:creatinine, urinary potassium:creatinine, plasma vitamin C, systolic blood pressure, diabetes, and serum cholesterol did not affect the results.

Although men appeared to derive more of a benefit from drinking coffee than women -- HR 0.62 versus 0.84 -- the confidence intervals overlapped, and it was not clear that they were actually different.

Among current smokers, coffee drinkers had a 61% reduced risk of stroke (HR 0.59, 95% 0.38 to 0.94).

Li noted that the subgroup analyses may have lacked statistical power.

Commenting on the study, Daniel Lackland, DrPH, of the Medical University of South Carolina in Charleston, said the main weakness of the study was the use of self-reported data, which makes it difficult to determine the actual quantity of coffee consumed.

He said that even if the association is confirmed, it would be hard to identify the mechanism underlying it, which would be the next challenge.

Compounds in the coffee itself, something linked to the act of coffee drinking, or social behaviors surrounding coffee drinking could all be involved, he said.

Li could not identify a mechanism either, but suggested that compounds in coffee might benefit by improving insulin sensitivity, inhibiting platelet aggregation, and decreasing endothelial dysfunction. Coffee has also been shown to have some antioxidant properties.

Until a mechanism is established, probably in a large clinical trial, Lackland said, it is unlikely the medical community will be telling patients to drink more coffee to prevent stroke.

"Are you going to see this in the recommendations? I don't think right now," Lackland said.

Wednesday, February 3, 2010

Blocking Enzyme in Mice Reduces Fat

By Michael Smith, North American Correspondent, MedPage Today
Published: February 02, 2010
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit
for reading medical news

Action Points  
  • Note that this study, in animals, suggests that interfering with a single enzyme might lead to substantial changes in energy expenditure and body fat.
  • Caution that more research is needed to find a compound that can block the enzyme safely in humans.
Blocking a single enzyme leads to increased energy expenditure and loss of body fat -- at least in mice, researchers said. Mice treated with a compound that blocks the so-called Fyn kinase expended 14% more energy than animals treated with an inert compound, according to Claire Bastie, PhD, and colleagues at Albert Einstein College of Medicine in New York City.
They also displayed a significant weight loss within 12 hours of receiving the compound, compared with animals given the inert substance, Bastie and colleagues reported in the Feb. 3 issue of Cell Metabolism.
"This is a new mechanism to help the body to burn extra energy," Bastie said in a statement.
The Fyn kinase has previously been linked to energy use: animals with the enzyme blocked burn more fatty acids and are leaner than their normal littermates, Bastie and colleagues noted.
Those animals also had increased insulin sensitivity, the researchers said, but the absence of the enzyme did not block the normal anabolic processes of protein synthesis and muscle growth during the feeding cycle.
The findings suggested that drugs blocking the enzyme might have a significant effect on energy balance and weight, they theorized.
To test the idea, they turned to wild-type mice and a compound called SU6656, a known inhibitor of the Src family of tyrosine kinases, of which Fyn is a member.
The mice spent spent 48 hours getting used to a so-called metabolic chamber, which allows researchers to monitor energy intake and expenditure. Then the compound was administered via intraperitoneal injection.
Control animals got injections of an inert substance, the researchers said. The shots were given at the beginning of the light cycle, when the animals are least active.
Both groups showed identical carbohydrate use during the dark cycle (when they are most active) that preceded the injection.
After the injection, the control animals reduced energy use as their bodies switched to the normal lipid production seen during the light cycle.
The treated animals, on the other hand, continued to expend energy at a rate that was significantly greater (P<0.0098) than the controls, although there was no significant difference in physical activity.
Because mice eat 80% of their calories during the dark cycle, they have a daily pattern of weight loss and gain, Bastie and colleagues noted, so that 12 hours after the start of the light cycle -- when they had been given the shots -- their weight was lowest.
But the SU6656-treated mice had a 40% greater weight loss than the control group, a difference that was significant at P<0.003.
Lean mass was slightly reduced in all the animals, Bastie and colleagues said, but without significant differences between groups. On the other hand, fat mass was significantly reduced (P<0.05) in the SU6656-treated mice, they found.
The metabolic effect of the inhibitor appears to be specific to Fyn, because it had no effect on mice lacking the enzyme, the researchers noted.
Unfortunately, SU6656 itself isn't a good choice for clinical trials of the idea in humans, Bastie said, because the Fyn kinase affects the brain, as well as muscle and fat tissue.
"Our next goal," she said, "is to design something extremely specific to muscle and adipose."

Tuesday, February 2, 2010

Metformin Cuts Obese Teens' Weight

By Michael Smith, North American Correspondent, MedPage Today
Published: February 01, 2010
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit
for reading medical news




The diabetes drug metformin can help obese teenagers lose weight even if they don't have the disease, researchers said.


In a randomized, placebo-controlled study that combined nearly two years of treatment and follow-up, the drug was associated with a statistically significant drop in body mass index, according to Darrell Wilson, MD, of Stanford University, and colleagues.


But the drug appeared to have no effect on many other aspects of obesity, including fat distribution and insulin resistance, Wilson and colleagues reported in the February Archives of Pediatrics & Adolescent Medicine.


The study is the longest and largest to test the effect of the drug, Wilson told MedPage Today. Treatment lasted 48 weeks, with another 48 weeks of follow-up, for 77 randomized volunteers.


The researchers enrolled the teens (ages 13 to 17) at six pediatric centers in the U.S. After a one-month run-in, they were randomized to 2,000 milligrams of extended-release metformin or to a placebo.
Action Points  

  • Explain to interested patients that this study found that, for obese teens without diabetes, the diabetes drug metformin can help them lose weight.
All participants also took part in a lifestyle modification program that included diet and exercise.
To be eligible, the participants had to be in the 95th percentile or higher for their age and sex and could not have diabetes, Wilson said.
The primary goal was to see if the drug had any effect on body mass index, but Wilson and colleagues also measured body fat using dual-emission X-ray absorptiometry and computer tomography (CT) scanning, and measured insulin resistance using an oral glucose tolerance test.
After 48 weeks, they found, those in the metformin group had experienced on average a 0.9-point drop in body mass index, compared with a 0.2-point gain in the control group. The difference was significant at P=0.03.
The weight loss is roughly equivalent to three kilograms (6.6 pounds) for a 5' 5" adolescent, Wilson and colleagues said.
"It's not a 20-pound weight loss, it's not what the world is looking for in a weight-loss drug," he said. "It was a meaningful weight loss, just not a spectacular one."
On the other hand, the researcher reported significant differences in body composition, abdominal fat, or insulin indices.
The loss of weight lasted between 12 and 24 weeks after stopping the drug, the researchers reported. After that, the BMI of participants in the active group trended back toward levels of the placebo group.
There were no significant differences between the groups in adverse events, which were mostly mild or moderate. Two cases of nausea in metformin-treated volunteers were considered probably related to the study drug. One participant stopped the drug because of the nausea.
For clinicians, the study suggests that the drug might be useful in treating some obese adolescents, Wilson said.
"We've certainly started some of our patients on it, but it has not unleashed us on a campaign of getting everybody on it," he said.

Wednesday, January 20, 2010

Fish Oils May Slow Genetic Aging

By Kristina Fiore, Staff Writer, MedPage Today
Published: January 19, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner   
Earn CME/CE credit
for reading medical news








For heart disease patients, omega-3 fatty acids may protect against morbidity and mortality by slowing biological aging, researchers say.

Patients who had the highest omega-3 fatty acid blood levels also had telomeres that shortened at a significantly slower rate than patients with lower intake, Ramin Farzaneh-Far, MD, of the University of California San Francisco, and colleagues reported in the Jan. 20 JAMA.

Patients in the lowest quartile of omega-3 fatty acid blood levels had the fastest rate of telomere shortening over five years: 0.13 telomere-to-single-copy gene ratio (95% CI 0.09 to 0.17).

Those who had the highest omega-3 fatty acid blood levels had the slowest rate of telomere shortening: 0.05 telomere-to-single copy ratio (95% CI 0.02 to 0.08, P<0.001).
Action Points 
Explain that patients who had the highest intake of omega-3 fatty acids had the slowest decrease in telomere length. On the other hand, patients with the lowest levels of omega-3s in their blood had the fastest rate of telomere shortening.
Telomeres are the protective caps at the end of chromosomes that reveal how biological stress ages a person.
"Patients with the highest levels of omega-3 fish oils were found to display the slowest decrease in telomere length, whereas those with the lowest levels of omega-3 fish oils in the blood had the fastest rate of telomere shortening," Farzaneh-Far said. "This suggests that these patients were aging faster than those with higher fish oil levels."

They said omega-3s may protect against oxidative stress, or increase the activity of the telomerase enzyme, which would decrease telomere shortening by creating more accurate telomere copies.

But some cardiologists were quick to point out that the results are preliminary and need to be replicated before physicians can use them in practice.

Since the study was observational and couldn't prove cause-and-effect, "we don't really know whether ingestion of omega-3 fatty acids resulted in this 'benefit,'" Steven E. Nissen, MD, of the Cleveland Clinic, noted in an e-mail. "It remains entirely possible that individuals who consume more fish also have other favorable healthy habits."

Nissen also pointed out that the study was not randomized to compare fish oil directly with a placebo treatment, and cautioned that "the relationship between telomere shortening and cardiovascular health is not well established."

Studies have shown that omega-3s appear to be effective for patients with coronary artery disease. Yet the underlying mechanisms are not well understood. Some researchers think it may have something to do with anti-inflammatory, triglyceride-lowering, antihypertensive, antiplatelet, or antiarrhythimic effects.

Research has shown that the length of telomeres -- chromosome caps that have long been compared to the plastic ends of shoelaces -- may be a marker of biological age. Biological age is independent of chronological age, and takes into account genetic and environmental stressors that may wreak havoc on cells.

Since there's been increasing evidence that omega-3s exert direct effects on aging and age-related diseases, the researchers decided to investigate them as a potential mechanism for protective effects in heart patients.

So they conducted a prospective cohort study of 608 patients in California with stable coronary artery disease. Patients were recruited from the Heart and Soul Study between September 2000 and December 2002.

They were followed for five years, and the researchers assessed telomere length of their leukocytes at baseline and again at the end of follow-up.

"By measuring telomere length at two different times," Farzaneh-Far said, "we were able to see the speed at which the telomers are shortening and that gives us some indication of how rapidly the biological aging process is taking place in these patients."

The researchers found that baseline omega-3 fatty acid levels were positively correlated with changes in telomere length over five years (P=0.001).

The relationships remained after controlling for potential confounders including demographics, blood pressure, serum lipids, and inflammatory biomarkers.

The researchers noted that each standard-deviation increase in fatty acid levels was associated with a 32% reduction in the odds of telomere shortening (95% CI 0.47 to 0.98).

So how do omega-3s stop telomeres from getting smaller?

They may protect against oxidative stress, which is a major driver of telomere shortening and aging. Or, fatty acids may increase the activity of the enzyme telomerase, which can result in more accurate copying and hence, longer telomeres, the researchers suggested.

The researchers agreed that the study was limited by its observational nature, which leaves no room for definitive conclusions about causality. Also, they only measured telomere length in leukocytes, which means the findings may not translate to other cell types, including myocardial or endothelial cells.

Researchers who were not involved in the study noted that omega-3s have been shown to have effects on other factors that contribute to heart disease risk.

"Omega-3 fatty acids have a potent positive impact on lipids that circulate in the blood stream and damage the heart," said Cam Patterson, MD, of the University of North Carolina Chapel Hill McAllister Heart Institute. "The effects of omega-3 fatty acids on lipids are still the best advertisement for their use to prevent heart disease."

Merle Myerson, MD, of Columbia University, agreed. "[The researchers] don't mention that omega-3 fatty acids lower triglycerides and non-HDL cholesterol, and stabilize cell membranes -- all of which may reduce risk for coronary artery disease and sudden cardiac death."

Myerson said the findings need to be replicated in future studies.

While their study may not have implications for intake of omega-3s among the general population, the researchers said it upholds recommendations for patients with heart disease.

"The results of our study underscore the recommendations of the American Heart Association, that patients with known coronary artery disease should be getting at least one gram a day of omega-3 fish oil," Farzaneh-Far said.

Tuesday, January 19, 2010

Gastric Bypass Extends Life for Most Patients

By John Gever, Senior Editor, MedPage Today
Published: January 18, 2010
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit
for reading medical news

For most patients in most categories, bariatric surgery increases life expectancy, according to a new mathematical model. Only when short-term mortality following bariatric surgery is expected to be high or the likelihood of success is low will the procedure fail to improve life expectancy, researchers reported in the January Archives of Surgery.
Computer modeling predicted that a hypothetical "base case" patient -- a 42-year-old woman with a body mass index of 45 -- would gain 2.95 years of additional survival following bariatric surgery, according to Daniel P. Schauer, MD, of the University of Cincinnati, and colleagues.
Surgery failed to be beneficial in the model only when 30-day mortality reached 9.5% or the likelihood that surgery would not add life-years was 2% or less, they found.
Baseline 30-day mortality in the model was 0.2%, and the baseline efficacy of surgery in extending life expectancy was 53%.
"While not all patients are guaranteed a good outcome, our model indicates that gastric bypass increases life expectancy for most patient subgroups," they concluded.
Their analysis was based on a Markov decision model using published data to estimate 30-day mortality following bariatric surgery and the efficacy of surgery in reducing long-term death rates.
The latter had two components: reduction in excess mortality associated with obesity, and research data on long-term mortality following bariatric surgery.
Excess mortality estimates came from National Health Interview Survey data on some 400,000 participants from 1991 to 1996 linked to the National Death Index. Inputs on surgery efficacy were derived from a 2007 study of nearly 8,000 patients who had undergone gastric bypass and the same number of medically treated or untreated obese controls.
That study found that the procedure cut death rates by half during about seven years of follow-up. (See Missing Link Found: Bariatric Surgery Reduces Mortality)
Schauer and colleagues obtained rates of inhospital mortality following bariatric surgery from the 2005 National Inpatient Survey, then multiplied them by three to estimate 30-day mortality.
The researchers explained that according to earlier research, inhospital death rates typically underestimate 30-day mortality by a factor of two to three.
Their threefold correction factor represents "a conservative estimate that biases the model against gastric bypass surgery," they wrote.
Schauer and colleagues tested this correction factor and other aspects of the model in sensitivity analyses.
The biggest gains in life expectancy occurred in younger women with relatively high BMI values, the model showed.
The age effect was less important than BMI at the time of surgery. A 35-year-old woman with BMI of 45 would gain about 3.2 years of extra life, whereas at 55, a similarly obese woman would gain about 2.5 extra years.
But a 35-year-old woman with BMI of 55 could expect to live five more years with surgery, the model indicated.
Men in general derived less survival benefit from bariatric surgery, particularly with advancing age at the time of the procedure.
At 35, the difference in life expectancy gained was roughly 10%, but by age 75 it had grown to about 50%.
The sensitivity analyses found that relatively large changes in most parameters used in the model did not affect the overall results substantially.
The effect of 30-day mortality on whether or not surgery was beneficial for long-term survival was related to BMI and gender.
For women with a BMI of 40, 30-day mortality of more than 5% would mean surgery was not helpful, but short-term mortality had to exceed 15% for surgery not to be preferable for those with BMI of 55 or more. These thresholds were about 10% higher for men.
The efficacy of surgery in reducing mortality was less important for older men, the analysis also showed. A 75-year-man with a BMI of 35 could expect only a very slight gain in life span -- perhaps one or two months.
"Younger patients have lower surgical risk and more time over which to realize the benefits of surgery. For older patients, the gain is smaller, and for some, gastric bypass surgery will decrease life expectancy," Schauer and colleagues wrote.
However, they identified several potentially serious limitations to the analysis.
The study of long-term mortality following bariatric surgery was conducted at a single center and was not randomized. Additionally, long-term complications, such as need for repeat surgery, were not addressed in the model. Certain other risks that might be heightened after bariatric surgery were excluded as well, and quality of life was not modeled.
"The decision analysis presented here is a step forward in understanding optimal patient selection but also highlights some of the areas for which better data are needed," the researchers wrote.

Wednesday, January 13, 2010

Exercise May Aid Cognitive Function

By Charles Bankhead, Staff Writer, MedPage Today
Published: January 12, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit
for reading medical news

Action Points  
  • Explain to patients that two different studies showed that physical activity in midlife or late in life may improve certain aspects of cognitive function.
  • The studies differed in that one showed benefits only in women and with vigorous activity whereas the other study demonstrated benefits in men and women but was limited to moderately intense exercise.
Almost any amount of moderate physical activity in mid- or late life reduced the odds of mild cognitive impairment by 30% to 40% in an ongoing cohort study, researchers reported. Men and women derived similar benefit, which was limited to moderate exercise -- not light or vigorous physical activity, investigators wrote in the January Archives of Neurology.
"Our findings contribute to the growing body of literature that indicates the potentially beneficial relationship between physical exercise and cognition," Yonas E. Geda, MD, of the Mayo Clinic in Rochester, Minn., and colleagues concluded. "A future population-based cohort study is needed to confirm whether physical exercise is associated with decreased risk of incident mild cognitive impairment."
Meanwhile, a small, separate interventional study described in the same journal showed that six months of high-intensity aerobic exercise was associated with significant improvement in executive function in older women at increased risk of cognitive decline, but not in older men.
Mild cognitive impairment confers a five- to 10-fold increased risk of dementia compared with normal cognition. Observational studies have shown that physical activity may protect against dementia and Alzheimer's disease, and some evidence suggests that exercise for individuals with mild cognitive impairment offers some protection, too, the authors wrote.
Geda and colleagues continued exploration of the association between physical activity and cognitive impairment with an evaluation of the effect of physical activity in midlife, approximately the age of onset for mild cognitive impairment. Data for the study came from the Mayo Clinic Study of Aging.
The study included 1,324 participants who completed a standardized questionnaire about physical activity. Their median age was about 80, and none of the participants exhibited signs of dementia at baseline.
Investigators assessed the frequency and intensity of physical activity as reported by each participant.
  • Light exercise: bowling, leisurely walking, stretching, slow dancing, and golfing using a cart.
  • Moderate exercise: brisk walking, hiking, aerobics, strength training, swimming, tennis doubles, yoga, martial arts, weight lifting, moderate use of exercise machines, and golfing without use of a cart.
  • Vigorous exercise: jogging, backpacking, bicycling uphill, tennis singles, racquetball, skiing, and intense or extended use of exercise machines.
The neuropsychologic evaluation consisted of nine tests that assessed memory, executive function, language, and visuospatial skills.
A consensus panel classified each participant as having normal cognition (N=1,126) or mild cognitive impairment (N=198). The two groups differed significantly in several respects. Participants with mild cognitive impairment were more likely to be men, older, less educated, more likely to be depressed, and had more comorbidity (P<0.001 to P=0.02).
Any frequency of moderately intense activity in midlife (ages 50 to 65) was associated with an odds ratio of 0.61 for mild cognitive impairment (95% CI 0.43 to 0.88, P=0.008). Moderate activity in later life was associated with an odds ratio of 0.68 (95% CI 0.49 to 0.93, P=0.02).
More or less intense activity of any frequency or duration did not significantly affect the odds ratio for mild cognitive impairment.
The authors noted several limitations of the study, including a cross-sectional design than could not assess causality, self-reported physical exercise data and relatively few subjects engaged in vigorous exercise in late life, which limited statistical power for that analysis.
A prospective evaluation of high-intensity aerobic exercise for patients with existing mild cognitive impairment showed that women had improved executive function, but men did not.
The study involved 17 women and 16 men ages 55 to 85. All had mild cognitive impairment by standardized assessment criteria, and all reported sedentary lifestyles at enrollment, Laura D. Baker, PhD, of the Veterans Affairs Puget Sound Health Care System in Seattle, and colleagues reported.
Participants were randomized 2:1 to aerobic exercise or stretching activity (control) and followed for six months. Both groups engaged in their assigned, supervised activities four times a week for 45 to 60 minutes at each session.
After two weeks, activity was supervised once a week. Participants assigned to aerobic exercise increased the duration and intensity of exercise over the first six weeks until they reached 75% to 85% of heart rate reserve, a level maintained for the remainder of the study.
Cognitive function was assessed at baseline and after three and six months of follow-up, as were physical status and laboratory values.
The results showed overall improvement in executive function among aerobic exercisers (P=0.04). Including gender as a predictive variable in the statistical model revealed significant interaction, reflecting a difference in response to the intervention for men and women (P=0.04).
Aerobic exercise increased glucose disposal, and reduced fasting plasma levels of insulin, cortisol, and brain-derived neurotrophic factor in women, the researchers reported. Among men, aerobic exercise increased plasma levels of insulin-like growth factor I.
Women on aerobic exercise demonstrated improvement in all four assessments of executive function, while men showed improvement in only one test.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits," the authors concluded. "The results of this study suggest that exercise also provides a cognitive benefit from some adults with mild cognitive impairment."
They also noted several limitations, including small sample size, exclusion of a number of subjects for medical reasons, and the fact that "the demands of the aerobic intervention are suited for a controlled trial, but may not be well-tolerated in less structured, less supervised population-based studies."

Tuesday, January 12, 2010

Nursing Homes Overuse Antipsychotics

By Nancy Walsh, Contributing Writer, MedPage Today
Published: January 11, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner 


In 2006, a year after the FDA issued mortality warnings about prescribing antipsychotic drugs for the elderly, nearly 30% of nursing home residents received the medication -- despite the fact that a third of them had no indication for the drugs, a study revealed. In nursing homes where rates of antipsychotic drug use were highest, residents had a risk ratio of 1.37 (95% CI 1.24 to 1.51) for receiving at least one of them, compared with facilities where rates of prescribing were low, according to Yong Chen, MD, of the University of Massachusetts Medical School in Worcester, and colleagues.
This elevated risk associated with facility-level prescribing was seen for patients with dementia but no psychosis (RR 1.40, 95% CI 1.23 to 1.59), and in residents with neither psychosis nor dementia (RR 1.54, 95% CI 1.24 to 1.91), the researchers reported in the Jan. 11 Archives of Internal Medicine.
An unrelated study, also released today, indicated that office-based physicians were in fact cutting back on prescription of antipsychotics for dementia as a result of FDA warnings.
Recent research suggest that there's wide variation in use of antipsychotics among facilities, reflecting what the authors of the current study called "an institutional prescribing culture."
Previous work had suggested that facility-level factors contributed to this effect in Canada, but the extent to which these factors exist in the U.S. has been unclear.
So Chen and colleagues assessed a nationwide, cross-sectional sample of 16,586 U.S. residents newly admitted to 1,257 nursing homes.
The nursing homes were categorized into quintiles according to their rates of antipsychotic use, with prescribing rates in the previous year ranging from zero to 24.4% in quintile one to 43.8% to 100% in quintile five.
The sample included 972 patients with psychosis, 6,188 patients with dementia but no psychosis, and 9,426 with neither dementia nor psychosis.
Among residents with psychosis, 74.8% received at least one antipsychotic, as did 41.1% of those with dementia but no psychosis, and 16.4% of those with neither condition.
Compared with residents in quintile five facilities, those in quintile one were more likely to be:
  • Older (>75 years, 75% versus 59%, P<0.001)
  • Women (69.4% versus 60.9%, P<0.001)
  • White (85% versus 71.9%, P<0.001)
Residents in quintile one also were more likely to be frail, as determined by the Changes in Health, End-stage disease and Symptoms and Signs (CHESS) score of 3 or higher (24.7% versus 14%, P<0.001), than those in quintile five.
They also had better Cognitive Performance Scale scores of 0 or 1 (39.2% versus 31.4%, P<0.001).
Conversely, compared with patients in quintile one nursing homes, those in quintile five facilities were more likely to have:
  • Moderate or severe behavioral problems (23.5% versus 12.6%, P<0.001)
  • Dementia (52.3% versus 41.4%, P<0.001)
  • Psychosis (10.3% versus 4%, P<0.001)
Residents in quintile five had twice the unadjusted risk ratio of receiving antipsychotics compared with those in quintile one (RR 2, 95% CI 1.78 to 2.24), although this was reduced to 1.37 after adjusting for demographics, health status, and potential indication for antipsychotics.
When the investigators looked at individual patient characteristics, they found that antipsychotic medication users were:
  • Younger (≤65, 13.7% versus 10.2%, P<0.001)
  • Male (37.6% versus 34.1%, P<0.001)
  • Less frail (CHESS score 0, 24.9% versus 17.6%, P<0.001)
Antipsychotic users also tended to have:
  • Moderate and severe behavioral problems (32.3% versus 8.9%, P<0.001)
  • Dementia (68.8% versus 36.9%, P<0.001)
  • Psychosis (15.1% versus 2.1%, P<0.001)
The study confirms the existence of facility-level variation in prescribing, with the likelihood of a new resident being given an antipsychotic medication being "strongly and independently related to the facility-level antipsychotic prescribing rate, even after adjustment for clinical and sociodemographic characteristics," the investigators wrote.
Only a small proportion of residents receiving the drugs had diagnoses of schizophrenia, bipolar disorder, or aggressive behavioral symptoms of dementia, which suggests that managing behavioral problems is an important component of facility-level decisions regarding antipsychotic medication use.
The study also suggests that organizational culture plays an important role in medication prescribing in nursing homes, because in these settings, prescribing decisions often are made without direct contact between the prescriber and the patient.
Among the limitations of the study were its cross-sectional design, which precludes conclusions about causality, and the use of a sole data source: a single long-term-care pharmacy provider. They also pointed out that "we have excluded NHs with fewer than five residents. . . . and we further excluded short-stay residents because of their distinct characteristics from long-stay residents. Limiting our study sample therefore prevents us from extending the interpretation of our findings to smaller facilities."
They further pointed out that the "prevalence of psychoses in our sample was lower compared with that found in another study using medical records. Thus, we may have underestimated the prevalence of psychoses in this sample."
The investigators concluded that "safety concerns continue to persist in the use of antipsychotic medications in [nursing home] residents whose benefits from these agents are unclear."
They called for further research to clarify why this prescribing culture exists and to determine whether there are adverse health consequences for patients.