| [ Summary ] |
Nonsteroidal anti-inflammatory drugs (NSAIDS) frequently ca-use gastric mucosal damage. The major mechanism may be muco-sal prostaglandin (PG) deficiency. Therefore, a PG-analogue may be a very reasonable tool for prevention and treatment of such damage, but is often poorly tolerated because of as-sociated diarrhea and abdominal pain. The mucosal damage ca-used by NSAIDS is also gastric acid-dependent and so, an H2-receptor antagnoist is to some extent effective, although the efficacy is far lower than that of a PG-analogue. Recently, a proton-pump inhibitor has been reported to exert the same effect as a PG-analogue, in healing of gastroduodenal mucosal damage caused by NSAIDs, and a superior effect in preventing recurrence of the damage along with better tolerance hasbeen observed. These results suggest that strong acid inhibition is highly effective for treating such damage. Whether such strong acid inhibition causes disturbance of absorptlon of NSAIDS is not clear. If so, it might result in poor antiinflammatory effects. |