Psoriatic Arthritis List NEWSLETTER

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News & Views Newletter
edited by Jack Nicholas, cornishpro@aol.com

PSORIATIC ARTHRITIS NEWS AND VIEWS
VOL. 3 ISSUE 20 - November 15, 2003
PSORIATIC ARTHRITIS MEDICAL NEWS

NEW DRUG SHOWS PROMISE AGAINST ARTHRITIS
By JANET McCONNAUGHEY .c The Associated Press 11/13/03

An experimental new drug designed to shut down the body's misguided assault on its own joints is showing promise against rheumatoid arthritis, relieving its crippling effects with few if any side effects.

The drug, still in testing, neutralizes the immune system T cells that help direct the assault.

It could give doctors another weapon in their arsenal of drugs against rheumatoid arthritis, which afflicts 2.1 million Americans.

Other drugs target some of the processes that underlie rheumatoid arthritis, but this is the first to attack the disease in precisely this way.

In a study of 339 patients, CTLA4Ig was added to methotrexate - the standard drug - in arthritis sufferers who had not gotten enough relief from methotrexate and still had many swollen and painful joints.

After six months, 60 percent of these patients were feeling better - some of them dramatically so. Only 35 percent of the patients on methotrexate alone reported some relief.

``I'm very excited about it. But there's still a considerable amount of work to be done,'' said Dr. Gary Firestein, chief of rheumatology, allergy and immunology at the University of California at San Diego and chairman of the Food

and Drug Administration's arthritis advisory committee.

Bristol-Myers Squibb Co. said it expects to apply to the FDA some time next year for approval to sell the drug.

More than 2,000 patients are taking part in the final round of tests needed to win FDA approval.

The findings were published in Thursday's New England Journal of Medicine. The study was led by Dr. Joel M. Kremer, director of research at the Center for Rheumatology in Albany, N.Y., and clinical professor of medicine at Albany Medical College.

The drug cannot be taken by mouth; it must be given by an intravenous infusion. In the study, it was given three times in one month, then once every month after that for five months. People who received it with methotrexate had no more side effects than those who got only methotrexate.

CTLA4Ig is one of many drugs on the market or in development that take advantage of scientists' clearer understanding of the complicated processes of inflammation and autoimmune diseases. Different drugs take aim at different parts of the process.

TNF inhibitors, for example, target an inflammation-causing protein called tumor necrosis factor, or TNF.

Methotrexate, originally developed to fight cancer, replaced gold salts - which helped less than one-third of all patients - as the standard drug against rheumatoid arthritis in the late 1980s. However, two-thirds of all patients still hurt. TNF inhibitors have helped some of them.

Firestein said there is a good chance that people who do not respond to TNF inhibitors will respond to the new drug.

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PSORIASIS DRUG HELPS RHEUMATOID ARTHRITIS Amevive Significantly Improves Pain in Combination with Methotrexate

By Laszlo Dosa WebMD Medical News Nov. 7, 2003 (Orlando)

Patients with rheumatoid arthritis may look forward to relief from a drug that is already on pharmacy shelves.

Researchers tested Amevive in combination with methotrexate to ease the pain of rheumatoid arthritis. Currently, there is no other rheumatoid arthritis drug that soothes inflammation in the same way as Amevive.

Amevive is a commonly prescribed drug to treat psoriasis. It controls inflammation by targeting a special kind of immune cell, so-called memory T-cells. Since both psoriasis and rheumatoid arthritis stem from a specific overactivity of the immune system, researchers tested Amevive in combination with the common rheumatoid arthritis drug methotrexate. Methotrexate eases inflammation by reducing formation of white blood cells.

Just as methotrexate is commonly used with other powerful inflammation fighters to treat rheumatoid arthritis, such as Enbrel and Remicade, researchers wanted to see if the combination of Amevive and methotrexate could also pack a powerful one-two punch. Matthias Schneider, MD, professor of medicine at Heinrich Heine University in Duesseldorf, Germany, presented his study at the 67th annual scientific meeting of the American College of Rheumatology.

In his study, 36 patients were given methotrexate along with either Amevive or placebo. The 28 women and 8 men had been afflicted with severe rheumatoid arthritis for an average of 10 years. In order to help determine the true effect of Amevive, neither the researchers nor the patients knew if they were receiving Amevive or the placebo.

Over a 12-week period, each person received methotrexate along with Amevive -- given as a weekly injection -- or placebo injections. Treatment with Amevive or placebo was stopped after 12 weeks and the patients were then evaluated several times over the following 24 weeks.

Overall, 67% of the patients on methotrexate and Amevive had an improvement in their arthritis at any point during the course of the trial, compared with only 17% on methotrexate and placebo. Schneider called the responses to Amevive "superior."

"What I see as most important is that even when we stopped the medication after a 12-week trial, we still had response in more than 40% after the initial 12 weeks, without giving any further medication," he tells WebMD. "We don't see major side effects and, what's great, no opportunistic infection, which is a great risk with these medications."

Opportunistic infections are those that occur when the immune system's ability to fight infection has been impaired -- either by medication or disease.

Stanley Cohen, MD, of the University of Texas Southwestern Medical School in Dallas, is involved in his own research on rheumatoid arthritis treatments. He says that the initial findings on Amevive look very good for improving symptoms of rheumatoid arthritis.

But he is still concerned about Amevive's potential effects on the immune system. He says time will tell if blocking T-cells significantly impairs the body's ability to fight infection in rheumatoid arthritis patients.

"It seems to be relatively safe. However, we are concerned about the issue of T-cell depletion; it's something that needs to be closely monitored in those patients. It remains to be seen what that would mean long term for the patients. But at this point, it would be certainly indicated for patients who are treatment failures -- patients who have not done well with other medication or conventional therapy,"

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RAPTIVA APPROVED FOR PSORIASIS TREATMENT High-Tech Drug Blocks Immune Cells That Cause Psoriasis - Daniel DeNoonWebMD Medical News Oct. 28, 2003

Raptiva is the newest drug to gain FDA approval for chronic moderate to severe psoriasis.

It's the second so-called biologic agent to treat the autoimmune problems at the heart of psoriasis. Raptiva -- generic name, efalizumab -- is a designer antibody. It's designed to throw a monkey wrench into the mechanisms by which immune cells cause psoriasis.

"I've been treating psoriasis for over 15 years and have always been frustrated by the limited options available to treat patients with this chronic disease," Craig Leonardi, MD, clinical associate professor of dermatology of Saint Louis University in St. Louis, Mo., and a Raptiva clinical investigator, says in a news release. "Raptiva has the potential to break the cycle of intermittent therapy by offering patients and their doctors a convenient treatment regimen that can be used continuously."

"This is not just a victory for psoriasis patients, it is a victory for biom edical research," Gail Zimmerman, president and CEO of the Psoriasis Foundation, says in a news release. "In just 20 years we have gone from having little understanding of the roots of psoriasis to seeing the FDA approve drugs, like Raptiva, that improve a patient's symptoms by targeting specific cells in the immune system. The biologic revolution is generating valuable new choices for those living with this incurable disease."

Raptiva is administered by a once-weekly injection under the skin. Patients give themselves the simple injections at home.

Other biologic drugs that can or could potentially be used to treat psoriasis include: Amevive, the first systemic biologic agent approved specifically for psoriasis treatment. It's given by intravenous feed or intramuscular injection. Enbrel is approved for psoriatic rheumatoid arthritis. It's given twice weekly by skin injection. The FDA is reviewing it for treatment of psoriasis. Remicade is approved for rheumatoid arthritis and Crohn's disease. It's given by intravenous infusion every several weeks. It is also in advanced clinical trials for treatment of psoriasis.

Side Effects - In clinical trials, common adverse events that occurred at least 2% more frequently in patients treated with Raptiva than in patients treated with placebo include: Headache, chills, fever, nausea, and muscle pain. These symptoms usually followed the first two Raptiva injections. Subsequent injections were no more likely to cause these symptoms than placebo.

Infection (mostly upper respiratory infections)

Precautions - Raptiva suppresses the immune system. It therefore can increase risk of infection and reactivate existing latent infections. It's not known whether Raptiva affects cancer risk, although some immune-suppressing drugs do increase the risk of some cancers.

When It Will Be Available - Raptiva is expected to be available by the end of 2003. Invented by the small biotech firm XOMA, Raptiva is manufactured by Genentech Inc

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THREE GENES LINKED TO PSORIASIS SUSCEPTIBILITY ON CHROMOSOME 17 Major Advance Marks the Beginning, Not the End, of Understanding Complex Role of Genetics in Psoriasis PORTLAND, Ore -Nov. 9, 2003

Researchers using data gleaned from a tissue bank created by the National Psoriasis Foundation have identified three of the first genes associated with psoriasis. The finding, published in the December 2003 issue of the prestigious journal Nature Genetics, marks a significant advance in the understanding of psoriasis, an immune-mediated disease with both genetic and environmental triggers, and may lead to new treatments for the disease.

"This is an exciting breakthrough that opens a new chapter in our quest to unlock the secrets of psoriasis," said Gail Zimmerman, president and CEO of the National Psoriasis Foundation. "We are clearly making great progress in understanding the complex genetic underpinnings of this often debilitating disease."

Anne M. Bowcock, Ph.D., of Washington University in St. Louis, and her colleagues identified three genes on chromosome 17 in which the "on and off" switches are impaired in statistically significant numbers of psoriasis patients.

Several other psoriasis susceptibility genes are expected to be identified in the months and years ahead, including one on chromosome 6. In all, it is suspected that more than a dozen genes are involved in psoriasis.

"Over the next few years, researchers are going to identify a large number of psoriasis susceptibility genes," Dr. Bowcock said. "These will be important building blocks toward finding a cure in the future. In the meantime, the findings could help pharmaceutical and biotechnology companies craft the next generation of medications to treat the disease, and ultimately lead to more successful management of psoriasis."

This scientific research was made possible by the efforts of the Psoriasis Foundation, which created the National Psoriasis Tissue Bank and opened it in 1994 with money donated by Foundation members. This tissue bank, built with blood samples from hundreds of families with psoriasis, provided the raw material that the Bowcock team analyzed in its ground-breaking discovery.

"The financial and physical contributions of psoriasis patients a decade ago are now bearing fruit," said Gerald G. Krueger, M.D., a professor of dermatology at the University of Utah Medical School in Salt Lake City and a member of the Psoriasis Foundation's Medical Board. "This advance in our scientific knowledge is part of an intricate web of factors that seems to determine who gets psoriasis and who does not."

The Psoriasis Foundation recently funded follow-up research that the Bowcock team is doing to investigate the precise role in psoriasis played by the genes on chromosome 17. Other teams are also working on identifying the other genes thought to play a role in the disease. The National Institutes of Health (NIH) also contributed significantly to the National Psoriasis Tissue Bank and the Bowcock team.

"Supporting cutting-edge research is a key commitment of the Psoriasis Foundation," added Zimmerman. "We will continue to work with NIH and interested scientists to promote research that will lead to new treatments and ultimately a cure for psoriasis."

Editors note: My thanks to Michael Szczygiel from England for forwarding this information.

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RESEARCHERS FIND CHEMISTRY BEHIND SKIN'S BARRIER
By Mary Beth Gardiner - September. 12, 2002

A group of researchers at Vanderbilt has discovered unusual chemical activity behind an inherited skin disorder that causes fish-like scaling and flaking. The findings give life to an enzyme thought to be inactive, and link its function to a second enzyme, both of which appear to be essential to creating the normal permeability barrier of the skin.

The group found that the two enzymes, both lipoxygenases, work together in a coordinated and unexpected way that provides a logical explanation for why disruption of one or other of the genes encoding the enzymes leads to skin disease. A description of the work appears in the Aug. 5 issue of Proceedings of the National Academy of Sciences.

There are six lipoxygenase (LOX) enzymes known to occur in people and mice, according to Alan R. Brash, Ph.D., professor of Pharmacology and principal investigator of the study. One of them - 5-LOX - is particularly well understood, because it's involved in inflammation, activating substances called leukotrienes. The enzyme works in a similar manner to the way cyclooxygenase, or COX, enzymes activate prostaglandins.

"In the same way that you take aspirin and Celebrex, which are COX inhibitors, to knock down prostaglandins for an anti-inflammatory effect, you can take medications to combat these leukotrienes," said Brash. "The drug Singular, for example, is an asthma treatment that blocks the receptor for products of 5-LOX."

The function of the other LOX enzymes is less certain, but they are known to be specific to certain cell types and to produce distinct products.

"The two that are essential to this study - 12R-LOX and eLOX3 - are mainly confined to the skin," Brash said.

The 12R-LOX enzyme, which Brash's lab discovered in 1998, is highly expressed in psoriasis. "The thinking was that this enzyme might have an inflammatory role in psoriasis in the same way that 5-LOX has a role in inflammation of the lungs in asthma," he said. "But when Diane Keeney, Ph.D., assistant professor of Biochemistry, looked to see where the enzyme was expressed, it wasn't deep down in the skin where all the trouble was arising. It was expressed out near the edge, just where the cells are changing from the last living cells to the ones that help form a barrier."

The other enzyme, eLOX3, was discovered at the German Cancer Institute in Heidelberg. The enzyme is expressed in the epidermis, but until this latest study, Brash said, no one knew what it did.

"We tried the human eLOX3, the mouse eLOX3, and we tried them under lots of different conditions to get the enzyme to make products," he said, "and nothing. It didn't do anything. So it sat in the freezer waiting for a better idea."

A better idea came along, Brash said, when a paper came out linking mutations in these two LOX enzymes with a rare type of ichthyosis, or scaly skin disease. "The funny thing was, some of the families had mutations in 12R-LOX and some of them had mutations in eLOX3, which we thought had no function, yet both had the same skin problems."

Up to this point, all LOX genes were considered to work independently, but these results suggested that the enzymes might be in the same pathway. "It was an enlightening thought," said Brash. "Neither we nor anybody else had thought about that possibility, but it makes sense because you could block the pathway by one way or the other."

Zheyong Yu, a third year graduate student in Brash's lab, took on the task of exploring this idea. Yu added eLOX3 to every lipoxygenase product available to test for activity.

"It turned out that the products from 12R-LOX were the best substrate by far," said Brash. "And they were being converted by eLOX3 by a previously undescribed enzymatic activity that appears to be unique.

"The reason this is such a nice finding is that the enzyme that seemed to be dead really did have activity when the right substrate was provided," he said. "And it pointed to a very rational explanation for what was wrong in these patients with the inherited skin disease. Furthermore, it suggests that in normal people these two enzymes are helping in the final stages of sealing off the barrier of the skin."

Brash theorizes that in the disease, the skin is making a lot of extra cells in an attempt to compensate for the imperfect process. The result is the scaling and flaking that gives ichthyosis its name, which stems from a Greek root meaning fish.

The lab's next steps will include testing the product of eLOX3 in cultured skin cells to determine its biological activity; determining if the product is being made in normal skin or in normal cultured skin cells; and looking at where eLOX3 is expressed in skin and if it is expressed in the same cells as 12R-LOX.

Other Vanderbilt researchers listed as authors on the PNAS paper include Claus Schneider, Ph.D., William E. Boeglin, and Lawrence J. Marnett, Ph.D. The work was supported by grants from the National Institutes of Health and the Core

Laboratories of the Vanderbilt Skin Disease Research Center Grant.

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COMPANY DEVELOPING ABUSE-PROOF OXYCONTIN
By PAUL ELIAS - The Associated Press 11/06/03

SAN FRANCISCO - Biotechnology company Pain Therapeutics is developing an abuse-resistant version of the painkiller OxyContin.

The South San Francisco-based company said Wednesday its experimental gel capsule resists the easy tampering that turns the approved pill from a legally prescribed painkiller for long-suffering patients into a potent and sometimes fatal high for drug abusers.

OxyContin was hailed as a breakthrough in the treatment of severe chronic pain when it was introduced in 1996. But the drug has become a problem in recent years after users discovered that crushing the time-release tablets and snorting or injecting the powder yields an immediate, heroin-like high.

Pain Therapeutics chief executive Remi Barbier said the company's Remoxy is a sticky gel cap, which makes it hard to ground into powder and that the active ingredient - oxycodone - is difficult to extract when submerged in alcohol and water, two popular ways to refine OxyContin for abuse.

``We have caged it in a number of molecules and chemicals that makes it very difficult, if not impossible, to separate the formula,'' Barbier said.

Hundreds of overdose deaths have been attributed to OxyContin abuse and have overshadowed the drug's legitimate use by cancer patients and others who suffer from chronic pain.

Drug counselors, lawmakers and others have been advocating for a harder-to-abuse version of OxyContin, which remains popular despite its negative publicity, highlighted recently by radio commentator Rush Limbaugh's admission he has misused OxyContin.

Last year, about 7 million OxyContin prescriptions were written for about $1.27 billion in sales, its manufacturer Purdue Pharma of Stamford, Conn., has said.

The gel technology used to create Remoxy was developed by Cupertino-based Durect Corp., which will share with Pain Therapeutics in any future profits the drug may garner.

``Given a choice between prescribing abuse-resistant Remoxy or easily abusable controlled-release oxycodone, we believe physicians will choose the less abusable alternative,'' said Dr. Nadav Friedmann, Pain Therapeutics' chief operating and medical officer.

However, Remoxy has yet to be tested in people and the company is at least two years from applying for Food and Drug Administration approval.

Pain Therapeutics has asked the FDA for permission to begin initial human experiments by March and a larger study by the end of 2004, the company said Wednesday. The company said it hopes to present Remoxy to the FDA for marketing approval by the middle of 2005.

``That's a very aggressive timeline,'' said Ken Trbovitch, an analyst with C.E. Unterberg, Towbin. ``Could they do it? Sure. But it's highly unlikely.''

The privately held Purdue Pharma's Web site said the company ``has committed hundreds of millions of dollars'' attempting to create its own tamper-resistant drug. Company spokesman James Heins said Purdue doesn't expect to file for approval of that drug, which is currently being tested in human experiments, for another four to five years.

``This is difficult science,'' he said.

Heins wouldn't comment on Pain Therapeutics' project, but said the FDA is expected to give higher scrutiny to any new oxycodone-based painkillers because of the abuse issue. Further, any new technology can't completely eradicate misuse of painkillers, he said.

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FIBROMYALGIA ISN'T DEPRESSION - But Depression May Add to Patients' Woes

Depression doesn't cause the pain of fibromyalgia, a new study shows. But clinical depression can deepen a fibromyalgia patient's experience of pain.

The findings come in a report by Thorsten Giesecke, MD, during the annual scientific meeting of the American College of Rheumatology. Giesecke is a member of the University of Michigan research team, led by Daniel J. Clauw, MD, using state-of-the-art technology to study fibromyalgia.

"People still doubt fibromyalgia is a disease," Giesecke tells WebMD. "Previously, we found that fibromyalgia patients really do have increased central pain processing. Now we can show this is not affected by depression. Something is wrong here, and it is not at all connected with depression."

The pain of fibromyalgia is one thing. But patients also face the pain of not being taken seriously, notes Roland Staud, MD, director of the musculoskeletal pain research center at the University of Florida, Gainesville. Staud reviewed the study for the ACR program committee.

"Due to the fact that very few physical abnormalities are present in these patients, bias has occurred. Many people think mood abnormalities play a major role," Staud tells WebMD. "Giesecke's group looked at brain responses to painful stimuli, and then checked to see if there was any difference between depressed and nondepressed fibromyalgia patients. They showed the activation of areas of the brain related to pain were not different in patients with and without depression." But there is a difference between people with and without fibromyalgia, he says.

SEEING PAIN IN THE BRAIN - The researchers use an imaging device called functional magnetic resonance imaging, or fMRI, to look at how the brain responds to pain. Study participants get a mildly painful pressure on their thumb, which makes the brain's pain centers "light up" on the image. Thumb pressure -- at a level healthy people hardly feel -- sets off a firestorm in the pain centers of fibromyalgia patients' brains.

This showed that fibromyalgia pain is real. But some researchers still think this heightened sensitivity to pain is the result of a psychological process -- depression, perhaps. To check this out, Giesecke and colleagues rated 30 fibromyalgia patients on a scale of depression symptoms, then gave them the fMRI thumb-pain test.

The result: Depression -- even clinical depression -- had no relation to how the pain centers of the patients' brains reacted to experimental pain.

"All you can say here is the depressed and nondepressed fibromyalgia patients processed the stimulus in an identical way," Staud says. "Depressed fibromyalgia patients do have more clinical pain, we know this."

A LINK BETWEEN DEPRESSION AND PAIN - Seven of the 30 fibromyalgia patients turned out to be suffering from true clinical depression, as well as fibromyalgia. And while their pain centers responded just like those of other fibromyalgia patients, these depressed patients did indeed have something else going on in their brains.

Depressed fibromyalgia patients responded to pain in two extra brain areas not involved in pain sensation. These parts of the brain -- the anterior insula and the amygdala -- are involved in emotional responses. While they don't appear to affect the sensation of a particular pain, they can deepen the experience of pain.

"The anterior insula is involved in a lot of emotional things that tell you how you feel," Giesecke says. "It is not usually associated with depression, but with the experience of adverse stimuli like bad smells and pictures of faces with fearful expressions. This seems to be a key area that responds to a pain stimulus but also responds to depression."

Depression, it seems, doesn't make fibromyalgia pain more intense. But it may add something unpleasant to the experience of pain. "Pain is mostly determined by the intensity of the pain stimulus and the unpleasantness occurring along with the stimulus," Staud says. "The imaging showed that most of the unpleasantness of the sensation is in these areas that contribute to these feelings. That is very important to the experience of pain."

The findings, Giesecke suggests, may partially explain why some antidepressants are effective in the treatment of pain. And they take researchers a step closer to understanding the mysterious ailment known as fibromyalgia.

"I think the most important point is that fibromyalgia is really a disease," Giesecke says. "I am pretty sure we are on the right track to find the pathophysiology of fibromyalgia. We are getting closer." SOURCES: Proceedings, American College of Rheumatology Annual Scientific Meeting. © 2003 WebMD Inc.

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EVER HAD A BOUT OF METAPNEUMOVIRUS? - ASSOCIATED PRESS

The answer is almost certainly yes, scientists say

Something called the metapneumovirus, discovered just two years ago, is turning out to be an exceedingly common cause of human misery, responsible for garden-variety colds in grown-ups and more severe coughing, wheezing and congestion in children. Researchers are beginning to piece together the scope of this ubiquitous but overlooked bug, which now appears to afflict just about everybody, probably over and over.

Even though the virus seems to be rarely serious, its vast presence intrigues microbiologists, and it is one of the most talked-about topics at this week's meeting in Chicago of the American Society for Microbiology.

Experts say the metapneumovirus is almost certainly not a new bug but something that has been around for eons.

Like many other respiratory bugs, this one is most likely to cause severe illness in infants encountering it for the first time. Although repeat infections are thought to be common, they result in much less intense illness, often just an ordinary cold or perhaps no symptoms at all. However, the bug may cause more serious problems in the elderly and people with other medical conditions.

Although new microbes, such as the ones that cause AIDS and SARS, are occasionally recognized, it is unusual to discover a virus as omnipresent as this.

"Thousands of hospitalizations occur every year due to this virus in infants," said Dr. James Crowe Jr. of Vanderbilt University. His research suggests that the metapneumovirus is second only to respiratory syncytial virus as a cause of severe lower respiratory infections in the young, occurring about two-thirds as often. Both viruses are members of the paramyxovirus family.

Crowe's team looked at nasal specimens taken from 2,000 children after they were treated for lower respiratory infections since 1976.

The newly discovered virus turned out to cause about 12 percent of these severe illnesses. They also caused 15 percent of common colds in children, including one-third of the colds complicated by middle-ear infections. "When we put this in perspective, it appears to be the second most common cause of respiratory illnesses in children," he said.

The virus went undiscovered because it does not grow well in cell cultures, a standard tool for sorting out the viruses that cause human disease. It was identified in 2001 by researchers from Erasmus Medical Center in Rotterdam. They calculated that every child catches the virus by age 5.

As with many respiratory viruses, such as the rhinoviruses and coronaviruses that cause many colds, the body does not remember the metapneumovirus clearly and so contracts it over and over, even though repeat bouts seem to be milder.

Now that scientists know what to look for, they can seek out the virus' genetic footprints in nasal secretions. This way, they are trying to assess how often - and how severely - it makes people sick through life.

A SOURCE OF RECURRING COLDS? - "At least in adults, we are figuring out whether it is a big deal. It is a little too early to say," said Dr. Ann Falsey of the University of Rochester. Nevertheless, she said, it is probably a source of recurring colds, although they may be less common than ones caused by the rhinoviruses, long considered the classic cold bug.

Without testing, victims cannot tell what sort of virus is causing their sniffles. However, Falsey said it appears that hoarseness is more often a symptom of metapneumovirus colds.

In other studies at the conference: Researchers from McGill University looked at elderly patients hospitalized with pneumonia or chronic obstructive pulmonary disease. The metapneumovirus was found in 2 percent, which was the same as influenza A.

A team from Hadassah University in Jerusalem looked for signs of metapneumovirus infection in children. They found that one-third had been infected by their first birthday, and half had it by age 2.

Researchers from Oxford University tested children up to age 12 being seen for coughs and fever and found that 8 percent had metapneumovirus. In these youngsters, flu was the most common cause of illness.

Whether the metapneumovirus plays some role in SARS is also a matter of debate. The primary cause of SARS is a newly discovered coronavirus. However, a recent study from Hong Kong found that half of the SARS patients tested during last spring's outbreak were also infected with the metapneumovirus. © 2003 Associated Press.

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Good Health to all,

Jack Nicholas
Newsletter Editor
Cornishpro@aol.com
Issue 2003 11/15/03-20