To the Editor: The results of the Celecoxib
Long-term Arthritis Safety Study (CLASS)1
support the hypothesis that celecoxib alone does not induce anatomical lesions
in the gastrointestinal (GI) tract.
However, in the subgroup of patients who were receiving aspirin for
cardiovascular disease there was no difference in nonsteroidal anti-inflammatory
drug (NSAID)–induced GI complications between celecoxib and aspirin
vs conventional ibuprofen or diclofenac and aspirin. Because cyclooxygenase
(COX)-1 is responsible for GI integrity under physiological conditions and
because COX-2–specific inhibitors alone do not cause anatomical lesions,
we would have expected a lower rate of ulcer complications in the group receiving
celecoxib and aspirin. As outlined in the accompanying Editorial by Drs Lichtenstein
and Wolfe,2 a possible explanation for this
surprising finding might be a type II error due to the small sample size.
However, the small numerical difference observed between the 2 groups suggests
that even a statistically significant result in a study with a much larger
sample size would translate into questionable clinical benefit. Alternatively,
healing of aspirin-induced anatomical lesions, which normally involves COX-2
induction, might be delayed by celecoxib.3
In the CLASS trial, there was no washout period, and many patients were receiving
NSAIDs at baseline. Therefore, many of these patients were at risk for asymptomatic
NSAID-induced gastropathy at the time they entered the study. Thus, although
COX-2–specific inhibitors are not specifically ulcerogenic, they may
interfere with repair of NSAID-induced gastropathy.