COMPARISON OF THE PROTECTIVE EFFECTS OF R OXATIDINE AND MISOPROSTOL ON DICLOFENAC-INDUCED GASTRODUODENOPATHY - AN ENDOSCOPIC, CONTROLLED-STUDY IN HEALTHY-VOLUNTEERS
P. Muller et al., COMPARISON OF THE PROTECTIVE EFFECTS OF R OXATIDINE AND MISOPROSTOL ON DICLOFENAC-INDUCED GASTRODUODENOPATHY - AN ENDOSCOPIC, CONTROLLED-STUDY IN HEALTHY-VOLUNTEERS, Arzneimittel-Forschung, 44-2(10), 1994, pp. 1127-1129
For prophylaxis of gastroduodenal lesions induced by non-steroidal ant
irheumatic drugs (NSAID) acid-lowering as well as mucosa protective su
bstances are used Direct comparison of both therapeutic regimens are l
acking. In randomized parallel studies the gastroduodenal tolerability
of 100 mg diclofenac daily in slow-release form was evaluated in the
presence and absence of 150 mg roxatidine (CAS 78273-80-0) daily as we
ll as in the presence of 75 mg bid roxatidine or 200 mu g bid misopros
tol (CAS 59122-46-2). The drugs were taken over a period of 14 days. E
ndoscopic controls were performed at entry as well as after 14 days of
treatment. A quantitative damaging score was used. Study A: Both trea
tment groups (n = 20) had at entry comparable mucosal damages: placebo
/ diclofenac: 0.9 +/- 0.1 (+/- SEM), roxatidine/diclofenac: 0.9 +/- 0
.1; after 14 days of treatment the score increased in the diclofenac /
placebo group to 7.6 +/- 1.9 and, in the corresponding diclofenac / r
oxatidine group, only to 2.1 +/- 0.9. The difference between the two t
reatment groups after 14 days was significant (p < 0.05). Study B: Bot
h treatment groups (n = 24) had comparable mucosal damages at entry: d
iclofenac / roxatidin: 0.9 +/- 0.1, diclofenac / misoprostol: 0.8 +/-
0.1. Following 14 clays treatment with 100 mg diclofenac daily the dam
aging score in both group rose to comparable levels: roxatidine group
2.1 +/- 0.7 and misoprostol group 2.0 +/- 0.4 (n.s.). The data suggest
that for prophylaxis of NSAID-induced gastroduodenal lesions substanc
es with different mechanism of action can be used. The findings underl
ine the complex way by which NSAID can damage the mucosa of the upper
gastrointestinal tract.