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Paracetamol is an effective agent for pain relief due to OA.

Although safer, it is less effective than


NSAIDs. For safety reasons paracetamol should be the first line treatment, with NSAIDs
reserved for those who do not respond

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

The MELISSA trial confirms earlier studies suggesting that meloxicam


has a significantly improved GI tolerability profile in comparison with
other NSAIDs, including diclofenac. These results may in part reflect
the preferential COX-2 selectivity of meloxicam, although the dose and
other aspects of tolerability may be important. These results may
provide support for the hypothesis that selective inhibition of COX-2
relative to COX-1 might be an effective approach towards improved
NSAID therapy.

In conclusion, in patients taking NSAIDs daily, we found that treatment with 20 mg


of omeprazole daily is superior to ranitidine with respect to healing and

preventing gastroduodenal ulcers and erosions, as well as controlling dyspeptic


symptoms.

Endoscopic examination before/after this treatment confirmed the cytoprotective


property of sucralfate, with normalization of the gastric mucosa and subsidence of
subjective symptomatology

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.

Significantly fewer adverse events were reported by patients receiving


meloxicam. This was attributable to fewer GI adverse events (13%)
compared to diclofenac (19%; P < 0.001).
In patients receiving chronic NSAID therapy for osteoarthritis, treatment with misoprostol
for 3 months was associated with a significantly lower frequency of gastric ulcer
formation, compared with treatment with sucralfate (P less than 0.001).
Sucralfate gel reduces both the incidence of acute gastroduodenal mucosal lesions and
symptoms in patients with arthritis receiving short-term nonsteroidal anti-inflammatory
drugs.

Misoprostol menimbulkan efek samping yang relatif ringan. Diare cukup


banyak ditemukan dan biasanya gejala ini hilang spontan setelah pemberian
dihentikan. Bila diberikan per oral, mual dan muntah dapat timbul 2 6 jam
setelah pemberian.17 Efek samping lain yang timbul adalah menggigil ( 19

62 % ) dan demam ( suhu > 38C ) sebanyak 2 34% dan erat


hubungannya dengan kenaikkan dosis.
Misoprostol, 200 micrograms twice or three times daily, offers substantial protection
against gastric and duodenal ulcers in patients receiving long-term NSAID therapy.
These dosages were better tolerated than the currently approved regimen of 200
micrograms four times daily.

In fact, misoprostol is the only drug with established long-term efficacy in preventing
NSAID-induced gastroduodenal ulcers in rheumatic patients

The histamine H2-receptor antagonist ranitidine has been shown to be effective in


preventing NSAID-induced duodenal ulcers, but has no efficacy in preventing NSAIDinduced gastric ulcers. In a direct comparative trial with ranitidine, misoprostol (200
micrograms qid) was significantly more effective than ranitidine (150 mg bid) in
preventing gastric ulcers in chronic NSAID users. The inactivity of ranitidine in
preventing gastric ulcers indicates that the pathogenesis of NSAID-induced gastric
ulcers is not related to gastric acid. Limited but conflicting data exist with omeprazole.
The mucosal-coating drug sucralfate has not been found effective in preventing NSAID
ulcers. In fact, in a direct comparative trial, misoprostol (200 micrograms qid) was
significantly more effective than sucralfate (1 g qid) in preventing gastric ulcers in
patients receiving chronic NSAID therapy

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).

Histamine (H2) antagonists, omeprazole, sucralfate and E-prostaglandin (PGE) analogs


are effective for the treatment of NSAID-induced gastric and duodenal ulcers, if NSAIDs
are discontinued. However, if NSAIDs are continued while GI damage is present, the
PGE analogs misoprostol, arbaprostil and enprostil have shown efficacy in healing
NSAID-induced ulcers. Furthermore, one limited clinical study demonstrated that

omeprazole has efficacy in healing NSAID-associated ulcers. Neither H2 antagonists,


sucralfate and sulglycotide (a cytoprotective drug) have shown efficacy in preventing
NSAID-induced gastric ulcers. However H2 antagonists have shown efficacy in
preventing NSAID-induced duodenal ulcers. In contrast, only misoprostol prevents the
development of NSAID-induced gastric and duodenal ulcers.

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