0 comments Monday, August 11, 2008

People who have gastrointestinal (GI) bleeding after a stroke are more likely to die or become severely disabled than stroke sufferers with no GI bleeding, according to a study published in the August 6, 2008, online issue of Neurology®, the medical journal of the American Academy of Neurology.

"This is an important finding since there are effective medications to reduce gastric acid that can lead to upper gastrointestinal bleeding," said study author Martin O'Donnell, MB, of McMaster University in Hamilton, Ontario. "More research will be needed to determine whether this is a viable strategy to improve outcomes after stroke in high-risk patients."

The study involved 6,853 people who had ischemic strokes. The most common type of stroke, ischemic strokes occur when blood flow to the brain is reduced or blocked. Of those, 829 people died during their hospital stay and 1,374 had died within six months after the stroke.

A total of 100 people, or 1.5 percent, had gastrointestinal bleeding, or bleeding in the stomach or intestines, while they were in the hospital from the stroke. In more than half of the cases, the GI bleeding occurred in people who had mild to moderate strokes.

The people with GI bleeding were more than three times more likely to die during their hospital stay or be severely dependent on others for their care at the time they left the hospital than people who did not have GI bleeding. A total of 81 percent of those with GI bleeding died in the hospital or were severely dependent, compared to 41 percent of those without GI bleeding.

Those with GI bleeding were also 1.5 times more likely to have died within six months after the stroke than those without GI bleeding. Of those with GI bleeding, 46 percent had died within six months, compared to 20 percent of those without GI bleeding. This relationship remained even after researchers adjusted for other factors, including other conditions such as pneumonia and heart attack.

The study was supported by the Canadian Stroke Network, the Ontario Ministry of Health and Long-term Care, the Canadian Institutes of Health Research, the Institute for Clinical Evaluative Sciences and the University Health Network Women's Health Program in Toronto.

The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, and multiple sclerosis.

For more information about the American Academy of Neurology, visit http://www.aan.com.

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Researchers at Duke University Medical Center appear to have solved at least a piece of a puzzle that has mystified physicians for years: why so many patients with asthma also suffer from GERD, or gastroesophageal reflux disease.

Clinicians first noted a relationship between the two diseases in the mid-1970s. Since then, studies have shown that anywhere from 50 to 90 percent of patients with asthma experience some aspect of GERD. But can GERD cause asthma, or, is it the other way around? Perhaps there is some shared mechanism at the root of both disorders causing them to arise together. Physicians could make a case for each scenario, but until now, the exact nature of the relationship was not clear.

Working in laboratory experiments with mice, Dr. Shu Lin, an assistant professor of surgery and immunology at Duke, discovered that inhaling tiny amounts of stomach fluid that back up into the esophagus - a hallmark of GERD - produces changes in the immune system that can drive the development of asthma.

In the experiments, researchers inserted miniscule amounts of gastric fluid into the lungs of mice (mimicking the human process of micro-aspiration, or breathing in tiny amounts) over a period of eight weeks. They compared these animals' immune systems with those of mice that were exposed to allergens but not the gastric fluid.

The immune systems of the two sets of mice responded very differently. Those that had the gastric fluid in their lungs developed what researchers call a T-helper type 2 response, a type of immune system reaction characteristic of asthma. The other mice responded in a more balanced manner, mounting an immune reaction consisting of both T-helper type 1 and T-helper type 2 responses.

"This is the first experimental evidence in a controlled, laboratory setting linking these two very common conditions in humans," says Lin, the senior author of the study published online in the European Journal of Clinical Investigation. "These data suggest that chronic micro-aspiration of gastric fluid can drive the immune system toward an asthmatic response."

"This does not mean that everyone with GERD is going to develop asthma, by any means," says William Parker, an assistant professor of surgery at Duke and a co-author of the study. "But it may mean that people with GERD may be more likely to develop asthma. If there is an upside to this, it is that developing GERD is something we can pretty much treat and control."

Parker says poor diet, a lack of exercise and obesity all contribute to the development of GERD, and that rising rates of reflux disease are part of a "perfect storm" of environmental and behavioral factors driving escalating rates of asthma, particularly in Western cultures. "People should avoid the risk factors for GERD. We strongly believe that the rise in asthma, particularly among adults in the country, is in large measure due to lifestyle choices that can be changed."

Lin and Parker agree that much more work needs to be done to fully understand the cellular and molecular mechanisms involved in the relationship between reflux disease and asthma, but both feel their study offers new directions for developing additional treatment options for both problems.

Lin says patients who already have GERD can minimize gastric reflux - and thereby lessen their chances of developing asthma - by following a few simple guidelines: Eat smaller meals and eat several hours before going to bed; raise the head of the bed a few inches; maintain a healthy weight; and limit fatty foods, coffee, tea, caffeine and alcohol - they can relax the esophageal sphincter and make reflux more likely.

Source: Michelle Gailiun
Duke University Medical Center

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Researchers at The Evergreen State College in collaboration with the U.S. Department of Agriculture at Texas A&M have been working to increase food safety by reducing the populations of E. coli in the guts of sheep and cattle. The goal of the research is to increase understanding of the complex predator-prey relationship between bacteria (the prey) and bacteriophages (the viral predator). The research could lead to safer food.

E. coli O157:H7 is a dangerous bacterial food pathogen that occurs naturally in the guts of livestock without making them sick. E. coli is easily passed from farm animals to humans. The bacterium causes food poisoning, sickness, and sometimes death in people who eat tainted meat or contaminated produce or water.

Andrew Brabban and Betty Kutter, microbiologists at Evergreen State College in Olympia, Washington, have been studying tiny E. coli predators known as bacteriophages, which attack E. coli bacteria. The Evergreen State phage biology lab was established in 1973 and together Kutter and Brabban have more than six decades of research experience on phages.

Brabban, Kutter, and colleagues have uncovered bacteriophages that attack various strains of E. coli naturally in cattle or sheep's stomach. Recent results appeared under the title "Prevalence of Escherichia coli O157 and O157:H7-infecting bacteriophages in feedlot cattle feces" in the October issue of Letters in Applied Microbiology. The research is funded by the U.S. National Institutes of Health, Phage Biotics, the National Cattlemen's Beef Association and the U.S. Department of Agriculture.

By using phage as a natural predator, it may be possible to better target and tame E. coli and increase the safety of food. Using bacteriophages provides a potentially cheap and broadly applicable way to treat cattle that offers advantages over traditional antibiotics.

Phage treatment is more specific to E. coli, which means it is less likely to encourage resistance in other harmful bacteria and less likely to kill useful bacteria. Also, much like the bacteria, the bacteriophage is easily transferred from one infected individual to another, resulting in a more robust solution to E. coli infections.

Economic impacts could also be significant. "E. coli contamination results in waste of meat, and ultimately wasted meat costs consumers," says Brabban. "Hundreds of millions are also spent to treat E. coli infections," he adds.

But while economics are important, healthier food is the top priority of the research. "It would be very rewarding if we could come up with an increased understanding or an application that leads to safer food down the line," says Brabban. "We all would like food to be safer."

The Evergreen State College
http://www.evergreen.edu

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A pre-cancerous condition linked to chronic acid reflux often gets overlooked. Can the medical community do a better job intervening? Researchers from the Hutchinson-MRC Research Centre in Cambridge think so.

In a review published in the inaugural issue of Disease Models & Mechanisms (DMM), experts on a disease known as "Barrett's oesophagus" discuss how "Barrett's" presents unique challenges in diagnosis and treatment. They cite key factors which make this illness difficult to detect, and suggest how scientists and doctors can team up to improve the odds of intervention.

Doctors want to understand more about this condition because patients with Barrett's have 30 to 125 times increased risk of an often fatal cancer of the oesophagus. One of the most common indicators of Barrett's is severe and chronic acid reflux. The authors of the review article discuss several reasons why most Barrett's cases are undiagnosed. The wide-spread availability of over-the-counter antacid medications may contribute by suppressing symptoms such that only the most severe and persistent cases of acid reflux are recommended for screening. Additionally, in order to screen for Barrett's, the oesophagus must be examined with a small light and camera (endoscope) which is not a routine procedure.

The biological basis of Barrett's is an abnormal change, or dysplasia, in the oesophagus. Normally, the oesophagus is lined with flat-shaped cells known as squamous cells. However, in patients with Barrett's, the cell lining consists of rectangular-shaped columnar cells. This process of normal cells morphing into abnormal cells is common to several types of cancer, not just oesophageal cancer. Thus, a greater understanding of Barrett's can also lead to potential therapies for similar pre-cancerous conditions.

In order to advance the diagnosis of Barrett's oesophagus, researchers recommend identifying standardized indicators which can be used to identify the presence of Barrett's as well as predict the likelihood that it will progress into cancer. Additionally, they recommend developing less costly screening methods to allow routine checks for Barrett's in patients with acid reflux. They point out the need for developing laboratory animal models of this disease in order to study the underlying molecular mechanisms of Barrett's, as well as to test potential novel therapies.

The review was written by Massimilian di Pietro, Christopher J. Peters and Rebecca C. Fitzgerald of the Hutchinson-MRC Research Centre in Cambridge, UK. The report was published in the inaugural July/August issue of a new research journal, Disease Models & Mechanisms (DMM), published by The Company of Biologists, a non-profit based in Cambridge, UK.

The DMM website is located at: http://dmm.biologists.org