MANAGEMENT OF NSAR-ASSOCIATED GASTROPATHY

Treatment with non-steroidal antirheumatics (NSAR) results in the deve lopment of stomach ulcers six times more often than in the development of suodenal ulcers. Bleeding NSAR lesions and erosions also occur mos tly in the stomach. The actual side effect potency of a NSAR drug cann ot be predicted with certainty in any particular patient, just as it i s not possible to forecast safely its antirheumatic efficacy in that i ndividual. If gastropathy persists, it may be advisable to try a diffe rent antirheumatic. If NSAR therapy is continued, lesions of the mucos a can be treated with ranitidine or omeprazol. The efficacy of other u lcer therapeutics may be correlated with their acid-inhibitory potency . Prostaglandin derivatives in high, antisecretorially effective dosag e, should not be used as first-choice drugs in the treatment of NSAR-a ssociated mucosal damage, because they possess a potentially diarrhoeo genic action. NSAR gastric lesions and ulcers may be prevented by miso prostol in low dosage (2-3 x 200-mu-g), but not by H-2 antagonists and omeprazol. The rarer duodenal mucosal damage can be reduced by both m isoprostol, H-2 antagonists and omeprazol. Other drugs have not been s uccessfully tested to date against this particular indication. In all patients undergoing antirheumatic treatment in whom there is a certain amount of risk associated with this treatment, mucosa-protective come dication should always be considered. Prophylactic relief of NSAR-indu ced epigastric pain and complaints has not been sufficiently investiga ted to date.