Cox-2 drugs may suppress immune function

[Guest guest]

Cox-2 drugs may suppress immune function

Study finds painkillers affect antibodies that attack germs

Reuters April 7, 2005

 

 

WASHINGTON - Analgesics called Cox-2 inhibitors, which U.S. health officials

restricted Thursday, can not only damage the heart and blood vessels but may

also suppress the immune system, researchers said.

A study published this week in the Journal of Immunology shows the drugs, used

by arthritis sufferers, might affect the antibodies that attack invading germs.

This could be both good news and bad news for the drugs, which have also

recently been shown to double or triple the risk of heart attacks and strokes,

the researchers at the University of Rochester in New York said.

Pfizer Inc. suspended sales of its Cox-2 inhibitor Bextra Thursday at the

request of U.S., European and Canadian regulators.

The Food and Drug Administration also asked Pfizer to include a strong " black

box " warning for its Cox-2 drug Celebrex. Merck & Co.'s Cox-2 Vioxx was

withdrawn last year.

The Cox-2 drugs were designed to be safer replacements for non-steroidal

anti-inflammatory drugs, or NSAIDS, such as aspirin, ibuprofen and naproxen.

NSAIDS can cause often deadly gastrointestinal bleeding and are blamed for

16,000 deaths a year in the United States.

NSAIDS affect two enzymes, Cox-1 and Cox-2, while the Cox-2 inhibitors were

meant to decrease side-effects by targeting only Cox-2, which is involved in

inflammation.

Richard Phipps, a professor of microbiology and immunology at Rochester, said

suppressing inflammation meant also suppressing immune function.

" We showed that B lymphocytes pulled right out of a person's blood and

appropriately activated expressed lots of the Cox-2 enzyme, " Phipps said in a

telephone interview.

" That tells us that they must be important for something. "

 

Not necessarily a bad thing

 

They gave Celebrex, as well as an NSAID called indomethacin, to mice and put it

onto human cells in the lab. This caused the immune cells to produce much less

antibody than usual.

" That could be good. There are situations where you may want to reduce antibody

production -- for example in people with autoimmune diseases such as rheumatoid

arthritis and lupus, " Phipps said.

In autoimmune disease the body mistakenly attacks healthy tissue. Non-Hodgkin's

lymphoma is a cancer involving B cells so the drugs have the potential to be

useful there, too.

" But if you are getting vaccinated and trying to generate an antibody response

to a virus or toxin, you want to have an optimal antibody response, " he said.

Long-term use of Cox-2s could have the potential to make people more vulnerable

to infections that the body fights using antibodies, Phipps said -- such as

pneumococcal bacteria, the Haemophilus influenzae bacteria that cause upper

respiratory infections and the influenza virus.

Aspirin has much weaker effects on immune function, Phipps said.

Last year Dr. Garret Fitzgerald of the University of Pennsylvania found that

Cox-2 inhibitors can damage the blood vessels in several ways.

FitzGerald's team found that a fatty acid made by the Cox-2 enzyme protects

female mice from hardening of the arteries. Shutting down Cox-2 long term may

actually kick-start atherosclerosis, FitzGerald said.

In mice, the hormone estrogen generates a fatty acid from Cox-2 called PGI2,

which limits activation of blood platelets that can cause clots and may damage

artery walls. PGI2 also reduces oxidative stress that damages the insides of

arteries.

 

URL: http://www.msnbc.msn.com/id/7421896/

 

 

 

 

Laura

 

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