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There were significantly fewer upper gastrointestinal clinical events with the COX-2
selective inhibitor etoricoxib than with the traditional NSAID diclofenac due to a
decrease in uncomplicated events, but not in the more serious complicated events.
The reduction in uncomplicated events with etoricoxib is maintained in patients
treated with PPIs and is also observed with regular low-dose aspirin use.
The overall incidence of GI symptoms experienced by patients taking celecoxib was
significantly lower than by those taking NSAIDs, as was the rate of withdrawal due to GI
intolerability (Table 4). Of the most commonly reported GI adverse effects, dyspepsia,
abdominal pain, nausea, and constipation were significantly less common with celecoxib
than with NSAIDs, although there was no difference in the incidence of diarrhea
The overall incidence of bleeding-related adverse events, and specifically, anemia and
hematochezia, experienced by patients taking celecoxib was significantly lower than that
among patients taking NSAIDs for all patients and for those not taking aspirin (Tab
This study determined that celecoxib, a COX-2specific inhibitor, when used for 6
months in a dosage 2 to 4 times the maximum therapeutic dosage, is associated with a
lower incidence of combined clinical upper GI events than comparator NSAIDs
(ibuprofen and diclofenac) used at standard therapeutic dosages. patients taking NSAIDs
had significantly higher rates of symptomatic ulcers or ulcer complications than did
patients taking celecoxib, but the rate for ulcer complications did not differ
However, stopping the NSAID therapy may exacerbate the underlying arthritis
In previous studies, the use of standard doses of H 2-receptor antagonists has been
disappointing with respect to preventing NSAID-associated ulcers. A 400-mg dose of
cimetidine each night for 10 months was ineffective. 25 Two large placebo-controlled trials
of ranitidine showed a substantial reduction in the incidence of duodenal ulcers during
NSAID treatment, but no effect on gastric ulcers. 9,10 This is a problem, since most ulcers
that develop during NSAID treatment are gastric, 27-29 as we also found. A large,
prospective evaluation showed that therapy with H 2-receptor antagonists does not
reduce the risk of ulcer complications in NSAID users. 30 Findings such as these led to
the conclusion that NSAID-associated gastric ulcers are not caused by acid. However,
our findings challenge this view. The rate of continued remission was significantly higher
with omeprazole than with ranitidine, presumably because of the greater inhibition of
acid induced by omeprazole.32 In keeping with the view that acid suppression is required
to prevent NSAID-associated gastric damage, Taha et al. recently showed that highdose famotidine (40 mg twice daily) gave better protection against NSAID-associated
gastric ulcer than the standard dose (20 mg twice daily) or placebo.
In fact, misoprostol is the only drug with established long-term efficacy in preventing
NSAID-induced gastroduodenal ulcers in rheumatic patients
gastric antisecretory drugs are not effective in preventing NSAID-induced gastric ulcers,
and (3) misoprostol is the only antiulcer drug proven to be effective for preventing
NSAID-induced gastric and duodenal ulcers in patients receiving chronic NSAID.
Misoprostol represents a major therapeutic advance for the management of NSAIDinduced mucosal injury.
The rates of healing of gastric ulcers, duodenal ulcers, and erosions were all better with
either 20 mg or 40 mg of omeprazole than with ranitidine. Use of the higher dose of
omeprazole provided no obvious advantage overall (rate of successful treatment, 79
percent).