The undesirable side effects of non-steroidal anti-inflammatory drugs (antiphlogistics) (NSAIDs) are manifested most frequently in the gastrointestinal tract. Prostaglandin synthesis inhibition, which is the principal mechanism of action of NSAIDs, is closely associated with these undesirable side effects. The side effects in the gastrointestinal tracts are 1. the complex of signs and symptoms of dyspepsia (epigastric pain, nausea, vomiting), 2. peptic lesions (erosions of mucous membrane and gastric ulcers), 3. intestinal disturbances (constipation - in rare cases diarrhoea), and 4. rare toxic hepatoses.The NSAID-induced dyspeptic complaints occur without correlation with the endoscopic-morphological pattern of peptic lesions of the stomach and duodenum. In this respect NSAID-induced dypsepsia is comparable with dypsepsia known as non-ulcer dypsepsia. Hence, the therapeutic approach applied to date in NSAID-induced dypsepsia, namely, administration of antacids or acid inhibitors, has become rather questionable. Significant relief from the dyspeptic complaints induced by NSAIDs was seen only in double-blind studies with pirenzepine. Selective motility effects are possibly of decisive importance in this connection. Erosions which are localised mainly in the distal antrum occur very frequently during NSAID therapy. Case control studies also show a highly disproportionate share of patients taking ASA or NSAIDs in groups of gastric ulcer patients. Extrapolated incidence rates indicate a 6 to 30fold increase of incidence of gastric ulcer under NSAIDs. The point prevalence for NSAID-induced gastric ulcer is between 11 and 29 per cent, the general prevalence being about 5 per cent. NSAID-conditioned ulcers are significantly larger than normal ulcers, often occur in multiple form, bleed significantly more often and have an increased tendency to perforation of the ulcer in women over 65 years of age.A certain amount of prophylaxis of peptic lesions is achieved by using special application forms of NSAIDs (preparations that are soluble in the small intestine, prodrug principle, suppositories) as well as by the use of antacids. It is well documented that inhibition of acid secretion via H2 antagonists results in a decrease of occult gastric blood losses and also of the frequency and/or extent of NSAID-induced peptic lesions. It is questionalbe as to what extent the mucoprotective approach with oral prostaglandin analogues explores new avenues, since optimal prevention and treatment of NSAID-induced microhaemorrhage and possibly also of the peptic gastroduodenal lesions appears possible only by means of antisecretory effective doses of the prostaglandin analogues. NSAID-induced ulcers show after discontinuation of NSAID a rate of healing under H2 antagonists - as well as in case of necessity of continuing NSA treatment - that is comparable with the rate of healing of non-NSAID-induced ulcers. However, as is the case with "normal" peptic ulcers, the size does have an influence on the rate of healing. If NSAID therapy is continued, it will be necessary to closely control healing of the ulcer by endoscopy even if there are no complaints (freedom from complaints having been achieved via H2 antagonists), since even asymptomatic NSAID-induced ulcers have an increased tendency to haemorrhage and to perforation.