This article is part of the Arthritis Archives.
Editor note: On 04/07/2005, Following scrutiny of the class of arthritis drugs known as NSAIDs and COX-2 inhibitors, the FDA announced planned regulatory actions. See: Questions & Answers: FDA Actions On COX-2 Inhibitors & NSAIDs
Dateline: June 3, 1999
COX-2 And Inflammation
A report in the June 1999 issue of Nature Medicine points to new information about the role of COX-2 in the inflammation process.
Paul Colville-Nash and colleagues at the William Harvey Research Institute in London report that a new study of lung inflammation in rats indicates that the COX-2 enzyme (cyclooxygenase 2) may have anti-inflammatory properties which occur later in the inflammation process. By blocking the COX-2 enzyme, inflammation may be ultimately prolonged, which is contrary to the intent of COX-2 selective inhibitors such as Celebrex and Vioxx.
COX-2 Selective Inhibitors
Celebrex (celecoxib) and Vioxx (rofecoxib) are two recently approved COX-2 selective inhibitors and many more are in development. They are collectively nicknamed "super-aspirins" and were developed after it was discovered that two types of COX exist, COX-1 and COX-2. It is COX-2 which is associated with pain and inflammation. COX-1 has a more extensive role including protection of the gastrointestinal lining.
When the selective COX-2 inhibitors were developed it was exciting news since it was thought that finally a drug was developed which would decrease inflammation yet have much less potential to damage the gastrointestinal tract.
The latest findings though from Colville-Nash and colleagues indicate that COX-2 is associated with an inflammatory reaction during the early phase of an inflammatory response (at about 2 hours). However later in the inflammatory process a swell of COX-2 exists which has been shown to have anti-inflammatory effects in the studied rats.
While the new COX-2 inhibitors and older NSAIDs (nonsteroidal anti-inflammatory drugs) serve to interrupt inflammation early on, it appears they may serve to aggravate inflammation later on. This may also help explain why older NSAIDs, although having anti-inflammatory properties, fall short of stopping disease progression.
The new findings may contribute important concepts towards better use of COX-2 inhibitors and NSAIDs. It may be found that continuous use of these drugs may not be the best application but rather reducing their use at times may enhance their efficacy. It need also be realized that conclusions may not directly apply to humans since the study involved lung inflammation in rats, not joint inflammation in humans. A correlation must be made implementing human clinical trials.
Sources:Study Questions Role Of "Super-Aspirins", Yahoo!News, 6/1/99; Remedy Brings More Pain, ABCNEWS, 6/2/99
First published: 6/03/1999