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 21 - November 30, 2003
PSORIATIC ARTHRITIS MEDICAL NEWS

WOMAN WHO OPENED EYES ABOUT PSORIASIS DIES
Beverly Foster-Halprin raised awareness that the disorder isn't contagious

Written by PATRICK O'NEILL from the OREGONIAN dated 11/22/03

Because of severe psoriasis, Beverly Foster-Halprin, as a young woman, was chased out of grocery stores and told she couldn't swim in public pools.

At age 30, she founded an organization that would become the National Psoriasis Foundation, which works to educate the public about the disease and today has an annual budget of $6 million.

Foster-Halprin, of Salem, died Nov. 19 of pneumonia at age 67.

The foundation began after Foster-Halprin's then-husband, Larry Foster, placed a small classified advertisement in The Oregonian on her 30th birthday, Aug. 29, 1966. The ad asked readers with the skin disorder to call his wife to let her know she wasn't alone.

"The first week, she got more than 100 calls," said Gail Zimmerman, the charity's president and chief executive officer.

Foster-Halprin arranged meetings in the basement of the Multnomah County Library to let people with psoriasis exchange information.

"It took a lot of courage for Beverly to do this," Zimmerman said. "At the time she started, there was a lot of resistance from the leadership of the dermatology community. They felt it was inappropriate for a patient group to give information to the public."

Physicians at University of Oregon Medical School (now Oregon Health & Science University) helped recruit doctors nationwide to serve on the foundation board of directors, Zimmerman said.

Foster-Halprin also took the psoriasis message to Congress, testifying in favor of federal funding for research into the disease.

Kelley J. Foster, her daughter, said her mother worked tirelessly to spread the word that psoriasis, an autoimmune disorder that creates red, scaly lesions, is not contagious and to end the isolation and discrimination that often accompanies the disease. Foster-Halprin was born Aug. 29, 1936, in Riverton, Neb., but moved to Portland as a young girl. She attended Jefferson High School. She married Dr. Kenneth M. Halprin in 1989. He died in 1995. Survivors include her daughter, of Portland; son, Michael Warner of Estacada; and sister, Jacqueline Schaeffer of Brooks.

Editor's Note: It was with much shock and sadness that I learned of Beverly Foster's death, when a member of our group published the web site address for this article. Beverly Foster-Halprin was indeed a courageous woman with a generous spirit who advanced the understanding of Psoriasis in this country.

I first met Beverly in the early 1970's when several people in the metropolitan Detroit area decided to form The Michigan Chapter of the National Psoriasis Foundation. As part of that group for several years, I also wrote a monthly newsletter called the "Scratch Sheet". We were closely affiliated with the University of Michigan Medical School-Department of Dermatology, chaired by Dr. John Vorhees, MD.

Many, many of our members gave skin biopsies for research programs, and several of our people became the first individuals to try the new PUVA treatment. In June of 1976, I arranged to have my own Rheumatologist at that time, lecture on Psoriatic Arthritis to an audience of nearly 240 people from all over the State of Michigan. There was not much understanding or even basic patient knowledge about Psoriatic Arthritis in 1976.

While on business, I had the opportunity to spend time with Beverly and her small staff, in the Portland headquarters of the National Psoriasis Foundation, discussing our NPF Chapter growth and future plans. We had two of our Chapter members testify in Washington in an attempt to have Psoriasis classified as a permanent disability for Social Security purposes.

Her dedication to educate the world about this horrible disease will never be forgotten. We all owe Beverly Foster-Halprin a deep sense of gratitude for her years of boundless energy. Her devotion to all of us who know the pain of Psoriasis and Psoriatic Arthritis, was enormous.

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PSORIASIS MAY INCREASE RISK FOR CERTAIN CANCERS

CHICAGO - Patients with the skin disease psoriasis may be at an increased risk for developing lymphoma, according to an article in the November issue of The Archives of Dermatology, one of the JAMA/Archives journals.

Psoriasis is a common skin disease characterized by patches of thickened, red and scaly skin, usually on the torso or arms, and can be painful and disfiguring in some cases. According to the article, psoriasis affects about 1 percent to 2 percent of the population. Previous research has shown that people with psoriasis may be at an increased risk for developing lymphoma - a group of cancers affecting the lymph tissues found mainly in the lymph nodes and spleen.

Joel M. Gelfand, M.D., of the University of Pennsylvania, Philadelphia, and colleagues investigated whether the rate of lymphoma in patients with a history of psoriasis is different from the rate of lymphoma in patients without psoriasis.

The researchers studied a random sample of 10 percent of patients 65 years or older (2,718 patients with psoriasis; 105,203 without) who were registered with a general practitioner who contributed to the General Practice Research Database (GPRD) between 1988 and 1996. The GPRD was established in the United Kingdom in 1987 and is a medical record database that holds data on more than 8 million patients including information on diagnoses and medications. The median follow-up time for the patients was 46 months (the median is the middle value; half the patients follow-up times were longer than 46 months, half were shorter than 46 months).

During the study period, the authors identified 276 lymphomas. "Patients with psoriasis had an almost 3-fold increased rate of lymphoma compared with patients without psoriasis," the authors write. "Patients 65 years or older who had psoriasis developed an additional 122 lymphomas per 100,000 patients annually."

After reviewing the medical records of patients with psoriasis who had lymphoma, the researchers found that "all patients with psoriasis who developed systemic lymphoma were treated with medications consistent with psoriasis and had outcomes consistent with the diagnosis of lymphoma (e.g. referral to an oncology service)"

"Additional studies are necessary to determine if the increased rate of lymphoma is related to psoriasis severity, psoriasis treatment, or an interaction between these risk factors," conclude the authors. Date:11-18-03 Journal of The American Medical Association. Thanks again Micky (Michael Szczygiel) from London.

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Editor's Note: Additional comments regarding the previous article from another news source, are as follows:

PSORIASIS MAY INCREASE CANCER RISK By Sid Kirchheimer WebMD Medical News Nov. 17, 2003

Three-Fold Rate of Lymphoma Noted in Those with Skin Condition

Having psoriasis could triple the risk of developing a group of cancers that affect the lymph nodes, a new study shows.

In reviewing medical records of nearly 108,000 people living in England, researchers from the University of Pennsylvania note that those with the itchy, scaly skin condition called psoriasis developed lymphoma cancers three times more often than their similarly aged peers without psoriasis. All the patients studied were at least age 65, and included 2,700 with psoriasis.

Still, the three-fold increased rate of lymphoma translates to only 12 additional cases for every 10,000 people with psoriasis. The skin condition affects about 5 million Americans.

"While 12 cases per 10,000 patients is an important number when you're talking about cancer, people shouldn't think they will get lymphoma just because

they have psoriasis," says researcher David J. Margolis, MD, PhD. "The risk is still relatively low."

But his new research backs previous studies, including at least one other by Margolis, that suggest people with psoriasis -- among the so-called autoimmune diseases that also include rheumatoid arthritis, lupus and multiple sclerosis -- face a measurably higher risk of lymphomas, which are grouped together as non-Hodgkin's and Hodgkin's lymphomas. They are cancers of the lymphatic system, part of the body's immune system.

"In past studies I've done, we saw maybe a two-fold increased risk for anyone with psoriasis compared to the general population -- even in younger patients," says Margolis, a longtime investigator on the link between cancer and psoriasis. "But the rates were three to four times higher in those getting psoriasis medications."

His new study, published in the November issue of Archives of Dermatology, is the latest to help scientists better understand whether the increased risk of lymphoma stems from the psoriasis itself or from use of some medications employed to treat severe cases.

"The problem is that it is hard to know if people with immunological disease -- and that's what psoriasis is -- are predisposed to an immunological cancer like lymphoma," Margolis tells WebMD. "We know that people with rheumatoid arthritis are, so it makes sense that people with psoriasis also are."

With psoriasis, the immune system sends faulty signals to speed up the growth cycle in skin cells, resulting in new skin cells developing over existing ones and causing the telltale patches of thickened, red and scaly plaques that typically develop on the torso, arms or legs.

Drugs used to treat severe psoriasis such as methotrexate, Neoral, and Sandimmune suppress the immune system and thus increase the risk of infection as well as cancer.

But Margolis found that the risk of lymphoma was the same in psoriasis patients whether or not they were receiving the immune suppressing drug methotrexate.

"Often it's a trade-off: Many patients getting these psoriasis medications know there's an increased risk of cancer," Margolis tells WebMD. "But even so, they're willing to take that risk because they have been incapacitated by the disease. These are usually patients with severe psoriasis over most of their body, sometimes to the point where they can't use their hands or feet. It's not a minor thing."

Gerald Krueger, MD, spokesman for the National Psoriasis Foundation, tells WebMD, "I personally have three patients of the 400 or so I treat who have psoriasis that currently have lymphoma, so I know they are out there. Still, the risk is very low, and psoriasis patients shouldn't obsess over whether they will develop lymphoma." Krueger is also professor of dermatology at the University of Utah Health Sciences Center.

He says the study is useful to doctors by alerting them to check for and more closely consider the early "vague" and other dismissed symptoms of lymphoma in their patients with psoriasis. These include fever, sweating, chills, unexplained weight loss, itching, and fatigue.

Hodgkin's disease is a highly curable type of cancer, with a five-year survival rate of 84%, reports the American Cancer Society. But non-Hodgkin's lymphoma, which killed Jacqueline Kennedy Onassis, is the fifth most common cancer in the U.S. and the third-fastest growing after lung cancer and melanoma. Unfortunately, it is more difficult to treat, with a five-year survival rate of about 50%.

SOURCES: Gelfand, J, Archives of Dermatology; vol 139; pp 1425-1429. National Psoriasis Foundation. American Cancer Society. Nature Genetics Advance Online Publication. David J. Margolis, MD, PhD, associate professor of dermatology and epidemiology, University of Pennsylvania Health System, Philadelphia. Gerald Krueger, MD, professor of dermatology, University of Utah Health Sciences Center, Salt Lake City; spokesman, National Psoriasis Foundation.

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BLOCKING ENZYMES COULD HALT ARTHRITIS
Written by Gabe Romain from the Betterhumans Staff

November 13, 2003-The discovery of a molecule's function in blocking enzymes that play a pivotal role in the onset of arthritis could lead to the creation of new anti-arthritic drugs.

Researchers from Cardiff University in Wales, UK found that inhibiting the molecule PKR prevents two processes central to the onset of arthritis: The production and activation of enzymes that break down connective tissue and cartilage.

"Collectively these results support our hypothesis that PKR is implicated in the cartilage degradation that occurs in arthritic disease," say the researchers.

Leading cause of disability
Arthritis is a chronic disease characterized by inflammation and swelling of cartilage and the lining of joints, generally accompanied by increased fluids in joints.

One of the most pervasive diseases in the US, arthritis is the leading cause of disability, affecting one out of every three Americans.

Osteoarthritis and rheumatoid arthritis are the two most common types of the disease. Osteoarthritis is primarily the result of wear and tear on cartilage whereas rheumatoid arthritis is an autoimmune disease in which the body attacks its own joint lining.

Despite the differences between the two types of arthritis, researchers think that similar molecular pathways are involved.

PKR inhibition
Increased activation of two enzymes, MMP-2 and MMP-9, has been implicated in cartilage degradation associated with arthritis.

Researchers led by Sophie Gilbert found that when they stimulated cartilage cells with two particular molecules but inhibited PKR, the release of the MMP enzymes was significantly reduced, implying that PKR is a significant player in the progression of arthritis.

The researchers hope that through understanding the molecular pathway mediated by PKR, they will be able to discover new drug treatments for arthritis.

The research is reported in the journal Arthritis Research. British researchers say they have discovered a way to block a molecular mechanism that triggers arthritis, and they claim their finding could lead to new drugs for the joint disease.

Working with cultured cartilage cells, the scientists found blocking the enzyme protein kinase R (PKR) stopped the production of enzymes that break down connective tissue and allow proteoglycan, a basic component of cartilage, to be lost.

"We found that treating cartilage cells with tumor necrosis factor-alpha (TNF-alpha) and C2-ceramide simulated the arthritic processes by a number of mechanisms," says lead researcher Dr. Sophie Gilbert, a connective tissue expert from the School of Biosciences at Cardiff University. Specifically, Gilbert and her colleagues saw an increase in the release of matrix metalloproteinase (MMP-2 and -9), two enzymes involved in arthritis.

Treatment of the cartilage cells with TNF-alpha and C2-ceramide also led to an increased loss of proteoglycans, and "we also saw increased cartilage cell death," Gilbert adds.

"Our results suggest that ceramide may help TNF-alpha signaling in cartilage. These effects were blocked by treatment of cartilage with 2-aminopurine, an inhibitor of the PKR, which has not previously been linked to ceramide signaling in cartilage," she says.

"This study confirms that a new intracellular signaling pathway involving PKR is important in cartilage degradation," she says. Through understanding these basic mechanisms underlying arthritis, studies such as this may lead to the discovery of new arthritis drugs, Gilbert adds.

The study appears in the current online issue of Arthritis Research and Therapy. "Since arthritis is a significant cost to health care, financially and in human suffering, it is essential to identify mechanisms of disease onset so that intervention and diagnosis can be achieved before debilitating cartilage loss. This study goes some way to achieving this goal," she says.

Dr. John Klippel, president and chief executive officer of the Arthritis Foundation, comments that "cartilage destruction occurs in both rheumatoid and osteoarthritis, and this study shows that PKR has an important role in activating enzymes that are known to cause joint damage in both diseases."

"So PKR appears to be a target for developing drugs that can prevent cartilage damage and limit the risk of disability from arthritis," he adds

Thanks, Micky from London, for adding vital information to our newsletter.

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PSORIASIS, LUPUS, RHEUMATOID ARTHRITIS SHARE ONE GENE Medical Author: Frederick Hecht, M.D. Medical Editor: Barbara Hecht, Ph.D.

Nov. 11, 2000 -- Changes in one gene have been discovered that are shared by three common autoimmune diseases -- the skin condition psoriasis as well as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The genetic changes involve a gene called Runx-1.

What is Runx-1?
Runx-1 is a protein that acts as a transcription factor. It controls when genes are switched on or off. Runx-1 does so by binding to regulatory sequences -- specific sequences of DNA -- that are close to the genes they regulate. These DNA sequences, called Runx-1 binding sites, are scattered throughout the human genome, wherever there is a gene under the control of Runx-1.

Runx-1 stands for runt-related transcription factor 1. Runx-1 is also called AML1 because it is also altered in a form of acute myeloid leukemia, but that is a very different story, one to be told another time.

The Tie-in with Autoimmunity
Changes in Runx-1 appear to contribute to autoimmune diseases. A Runx-1 binding site on chromosome 2 is altered in many patients with systemic lupus erythematosus. Many psoriasis patients have a changed Runx-1 binding site on chromosome 17. And a Runx-1 binding site on chromosome 17 is changed in patients with rheumatoid arthritis. Thus, there are genetic connections, some involving Runx-1, between diverse autoimmune diseases.

The Tie-in with Lupus
The tie-in between Runx-1 and lupus is not new. It was reported back in 2002 by Ludmila Prokunina and her colleagues from Sweden. They found that a polymorphism (a normal variation) in the programmed cell death 1 gene dubbed PDCD1 was associated with susceptibility to systemic lupus erythematosus. They traced this down and found that it reflected an altered binding site for Runx-1.

The Tie-ins with Psoriasis and Rheumatoid Arthritis
The reports linking Runx-1 to psoriasis and to rheumatoid arthritis are very new. They were just published back-to-back online in the journal Nature Genetics on November 9. The work on psoriasis was from a multicenter American research effort while that on rheumatoid arthritis emanated from Japan.

Perspective
The fact that Runx-1 is involved in at least three common autoimmune diseases is clearly remarkable and noteworthy. It is also clear that the changes in Runx-1 do not cause these diseases. Runx-1 is a susceptibility gene locus, or loci, since there are Runx-1 binding sites strewn about the genome. Changes in these different Runx-1 sites make a person vulnerable to these different autoimmune diseases.

Runx-1 appears to be one piece in the autoimmune disease puzzle.

Original Sources:
1. Prokunina, L. et al.,
2. Helms, C. et al.,
3. Tokuhiro, S.

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LIFE WITH AN AUTOIMMUNE DISEASE
By Star Lawrence WebMD Feature November 10, 2003

If you have general, lingering symptoms, you may be suffering from an autoimmune disease -- which means your immune system is attacking healthy tissue.

Your first symptoms of an autoimmune disease may be general, such as fatigue, low-grade fever, and difficulty concentrating, making autoimmune diseases difficult to diagnose at first. You also may feel depressed and consult a doctor for that.

According to Mary J. Shomon, author of the book Living Well With Autoimmune Disease: What Your Doctor Doesn't Tell You ... That You Need to Know, what ensues after registering these complaints may be an odyssey to pinpoint which of the almost 60 different autoimmune disorders you might have, all of which affect the body differently.

About 50 million Americans -- the vast majority of them women, especially women of working and childbearing age -- suffer from autoimmune ailments. Rheumatoid arthritis, type I diabetes, psoriasis, alopecia, lupus, thyroid disease, Addison's disease, pernicious anemia, celiac disease, multiple sclerosis, myasthenia gravis, Guillain-Barre syndrome -- these are just a few of the ailments that scientists now think stem from a common phenomenon: the activation of the body's immune system against the body itself. Also suspected of having this as a component are chronic fatigue syndrome and fibromyalgia.

Traits in Common
That such different-seeming diseases as psoriasis and diabetes could stem from a common cause actually is a relatively new notion, according to Noel R. Rose, MD, PhD, professor of molecular microbiology and immunology and pathology at the Johns Hopkins University in Baltimore. Back in the early days of the last century, he says, the idea took hold that if the immune system were to benefit us, it would have to be warding off foreign invaders from outside the body.

Now, scientists know that the immune system is a set of actions and reactions that can be triggered by a number of things besides an invading germ, virus, or bacteria. One thing that puts you at risk for being attacked by your own immune system is your genetics, says Rose. In other words, if your parents have a predisposition to autoimmune disease, you may, too. "And it's an overlapping inheritance," Rose says. "If you have one autoimmune disease, you may have more -- and you may have different ones than your parent did (or your siblings do)."

Another common characteristic of all autoimmune diseases is that it is thought that an outside agent is required to start the process. Even with a genetic tendency, a person may not develop an autoimmune disease without an environmental influence to set it off. Examples of these are infections, certain foods (iodine or gluten products), and toxins (some drugs, smoking, certain hair dyes, chemicals in the workplace).

Dozens of culprits have been identified. Shomon reels off a list of possible suspects in the more common autoimmune ailments: hair dye and certain drugs for lupus, silica exposure for scleroderma; gluten for diabetes; mycoplasmas for rheumatoid arthritis; measles virus for Epstein-Barr; Coxsackie's virus for diabetes; smoking for thyroid, lupus, and arthritis; hepatitis B infection for multiple sclerosis. She says physical trauma can also touch off the immune response.

As the disease develops -- or more than one, as Rose points out -- vague symptoms start to appear, such as joint and muscle pain (very common), general muscle weakness, possible rashes or low-grade fever, trouble concentrating, or weight loss. More specific signs can point toward something being wrong: numbness and tingling in hands and feet (also common), dry eyes (common), hair loss, shortness of breath, heart palpitations, or repeated miscarriages can also be caused by an autoimmune response.

Research Continues
Although autoimmune disorders can make life miserable, they usually are chronic and not fatal, Shomon says. Most are handled by a range of doctors from internist to rheumatologist to dermatologist. "There is no such thing as an auto immunologist," she says. Usually, the researchers are seeking to attack the disorders as a common group.

According to Rose, some approaches being tried include a complete "reboot" of the immune system -- the famous bone marrow transplant. "This is only tried if other treatments have failed," he says. "The idea is that if the entire immune system is erased, it might to a better job the second time around." Doctors at Johns Hopkins use a chemotherapy drug called cyclophosphamide to "reboot" the immune system. This has showed promise in a number of lupus patients.

If the causative agent of the disease is known, a vaccine can be developed. Immunoglobulin or antibodies are being used in children with the heart disease called Kawasaki disease, as well as Guillain-Barre and multiple sclerosis.

What You Can Do Now
If you suspect you may have an autoimmune problem, it's very important to identify and deal with any food allergies, according to Shomon. The main offenders are wheat, diary, corn, soy, fish (especially shellfish), nuts, and fruits. High sugar, she contends, stresses the immune system. Make sure you eliminate trans fats and other bad fats and get enough good fats such as olive oil, fish oil, and avocado.

You also want to minimize infections -- wash your hands frequently. Take care of your teeth for the same reason: Gum diseases leak triggers into the body. Some people even lavage their noses with warm salt water to remove possible troublemakers.

Each autoimmune disorder also will have separate dietary and therapeutic recommendations. It's important to follow your doctor's orders. This is not a quick fix -- it's a lifestyle.

For more information, check out the web site of the American Autoimmune-Related Diseases Association, www.aarda.org.

Star Lawrence is a medical journalist based in the Phoenix area. SOURCES: Mary J. Shomon, author, Living Well With Autoimmune Disease. Noel R. Rose, MD, PhD, professor of molecular microbiology, immunology, and pathology, Johns Hopkins University, Baltimore.

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ASPIRIN WITHDRAWAL RISKY FOR HEART PATIENTS
By Megan Rauscher (Reuters Health)

NEW YORK (Reuters Health) - In patients with coronary artery disease, withdrawal of aspirin therapy can precipitate coronary events, according to a study presented during CHEST 2003, the 69th annual meeting of the American College of Chest Physicians.

"Stopping aspirin is not harmless - it can be very dangerous," Dr. Emile Ferrari, who led the study, said in an interview with Reuters Health.

Ferrari, from University Hospital Pasteur in Nice, France, and colleagues reviewed the cases of 1,236 patients with coronary artery disease who were hospitalized for an acute coronary syndrome, such as chest pain (unstable angina), clot formation in an implanted heart stent, or heart attack, between September 1999 and April 2002.

They discovered that 51 had stopped taking aspirin less than one week prior to the event. This accounted for 4.1 percent of all the hospitalizations for coronary events. Prior to hospitalization, all patients had been taking aspirin for at least three months.

"However, if you consider only patients who had a recurrent coronary event, 10 percent of those patients had stopped aspirin on average seven days before the event," Ferrari said. "I think it is a very important percentage," he added.

The coronary history of the 51 patients is also noteworthy, Ferrari said. While 15 had a previous heart attack and 36 had stable angina, none had unstable angina prior to aspirin withdrawal.

Reasons for aspirin withdrawal included minor surgery, fibroscopy, dental treatment, bleeding and noncompliance with recommended treatment.

"Coronary patients preparing for dental work or surgery are often advised to stop taking aspirin in order to avoid increased bleeding," Ferrari said in a statement. "Our study serves as a reminder for all medical professionals who treat coronary patients that aspirin withdrawal should not be advised, and that alternative recommendations should be considered." Copyright © 2003 Reuters Limited. All rights reserved.

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CAN C REACTIVE PROTEIN MAKE YOU OLDER?
By Daniel DeNoon WebMD Medical News Reviewed By Brunilda Nazario, MD

As Heart Risk Marker Rises, Physical Fitness Drops

Nov. 13, 2003 -- C-reactive protein is a marker for heart disease. It may also be a marker for poor physical fitness.

Being fit protects against heart disease. Fitness improves all conventional markers of heart disease risk -- and then some. Where does the extra benefit come from? Part of it may be in reducing inflammation of blood vessels.

Inflammation starts as a protective process. Inflamed tissues swell, redden, and leak fluids. They also attract and activate cells of the immune system, which attack whatever they recognize as harmful. The process fights infection -- but causes tissue damage, too. Inflammation is a key factor leading to heart disease and stroke.

C-reactive protein is a chemical messenger that tissues give off when they get inflamed. People with heart disease have abnormally high levels of C-reactive protein -- 8.0 mg/L or higher. Does fitness have anything to do with C-reactive protein levels? Yes, finds Johns Hopkins researcher Samia Mora, MD.

In studies reported at this week's Scientific Sessions meeting of the American Heart Association, Mora measured C-reactive protein in patients with premature heart disease and in 500 of their apparently healthy siblings. She found that as C-reactive protein levels went up, fitness went down.

"Every 1 mg/L increase in C-reactive protein was equivalent to the effect [on exercise duration] of being approximately two years older," Mora writes in her presentation abstract.

However, it's not yet clear whether C-reactive protein is the cause or the effect of poor fitness.

"At this point, we're not sure if poor fitness level causes the increase in C-reactive protein or vice versa," Mora says in a news release. SOURCES: Mora, S. Circulation: Journal of the American Heart Association, Oct. 28, 2003; vol 108: pp IV-760, abstract 3432. News release, American Heart Association. © 2003 WebMD Inc. All rights reserved.

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NO DIFFERENCE FOUND IN CLOTTING AND STENTS
By LAWRENCE K. ALTMAN

The Food and Drug Administration said yesterday that the rate of blood clots found after implantation of a new drug-coated heart stent was no higher than with other stents.

Less than a month ago, the agency issued a second advisory to doctors, cautioning that as many as 60 deaths had been associated with implants of the drug-coated stent, the Cypher, made by Cordis, a unit of Johnson & Johnson.

Yesterday, the agency sought to play down the links between the deaths and other complications from the stents, tiny metal scaffolds, restating its earlier position that the Cypher stent was a "safe and effective product when used according to the labeling, particularly the sections of the labeling that deal with the selection of patients and the appropriate use of medication" in Cypher recipients.

Some leading cardiologists have said some doctors had implanted mismatched sizes of the stent when one particular Cypher stent of the largest diameter was in short supply in the weeks after it first became available in April. They also suspected that some recipients had not taken their medications properly.

Yesterday, the agency did not address all of those issues. It did say some patients experienced allergic reactions to the treatment, but it said those side effects could be associated with the procedure.

As of Nov. 21, the agency said, it had received reports of 360 cases of clotting, including 70 deaths, since the stent was marketed.

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Good Health to all,

Jack Nicholas
Newsletter Editor
Cornishpro@aol.com
Issue 2003 11/30/03-21