Now, how meaningful is this? If COX-2 inhibitors (or NSAIDs, as also suggested) really caused big jumps in inflammation, people would know about it (ouch!) Also, everyone knows NSAIDs and Cox-2s don't cure problems with joints. Are they reporting this clearly, or is it just me?
Headline: Study questions how well new "super-aspirins" work
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WASHINGTON, June 1 (Reuters) - British researchers on
Tuesday questioned how well new "super-aspirins" called COX-2
inhibitors work, saying they may, in some cases, worsen
conditions that cause pain and inflammation.
Experiments on rats may explain why drugs, including the
new COX-2 inhibitors, may help relieve the initial symptomatic
pain of diseases such as arthritis but do not ever help the
underlying damage, Paul Colville-Nash and colleagues at the
William Harvey Research Institute in London said.
Two COX-2 inhibitors have been approved by the U.S. Food
and Drug Administration (FDA) -- Monsanto (NYSE:MTC) unit GD
Searle & Co's Celecoxib (Celebrex) and Merck's (NYSE:MRK) Vioxx,
known generically as rofecoxib.
Many others are in the works. The drugs are designed to be
an improvement on old-fashioned aspirin and related drugs,
known as non-steroidal anti-inflammatory drugs (NSAIDs).
Such drugs, which include ibuprofen and other popular
analgesics, act on a compound known as cyclooxygenase, or COX.
But there are two forms of COX, COX-1 and COX-2.
Studies indicate that it is COX-2 that causes pain and
inflammation, while COX-1 has a broader role. The studies
suggest that suppressing COX-1 causes the stomach damage that
aspirin and other NSAIDS are blamed for and which kills 16,000
people in the United States every year.
But writing in the journal Nature Medicine, Colville-Nash
and colleagues said COX-2 may not be all bad.
They tested rats with pleurisy, an inflammation of the
membranes that cover the lungs.
Writing in the journal Nature Medicine, they said when they
caused pleurisy by injecting a substance into the rats' chests,
there was immediate inflammation marked by a spike in levels of
COX-2.
"However, at 48 hours there was a second increase in COX-2
expression, 350 percent greater than that at two hours," they
wrote. At this point, the inflammation started to die down,
they added.
Then they did the same experiment and also gave the rats
indomethacin, an NSAID available generically, or NS-398, a
COX-2 inhibitor.
At the early stages the drugs reduced inflammation, as they
are supposed to. But at the later stages NS-398 prompted a huge
increase in inflammation. Indomethacin increased inflammation,
also, but not by nearly as much.
They said if the results bear out in humans, there could be
implications for how COX-2 inhibitors should be used.
"In the treatment of rheumatoid arthritis, NSAIDs are
administered for several months or even years and yet they show
little evidence of decreasing disease progression or joint
destruction," they wrote.
Karen Seibert and colleagues from GD Searle & Co said
results in rats are often different from what happens in
humans. "The final analysis, as always, will come from clinical
data," they wrote in a commentary.
Copyright 1999, Reuters News Service |
