title: Therapeutic aspects of prostaglandins in the treatment of peptic ulcer disease.
abstract: Studies of antisecretory compounds such as the H2-receptor antagonists have altered therapy and enhanced the understanding of peptic ulcer disease (PUD). While it is agreed that the dictum "no acid, no ulcer" is valid, acid hypersecretion does not appear to be the major determinant in a significant number of ulcer patients. More careful consideration of mucosal integrity in the pathogenesis of PUD is therefore necessary. A small but significant number of patients (5-15%) do not heal, despite the use of effective antiulcer drugs. Moreover, the posthealing recurrence rate may reach 75% after treatment is discontinued, and nearly one third of cigarette-smoking patients on maintenance therapy may suffer recurrences. Prostaglandins (PGs) are particularly important as potent antisecretory and effective antiulcer agents. In addition, recognition of their cytoprotective effects has stimulated research into the understanding and importance of mucosal protection and mucosal defense mechanisms. Animal studies show that PGs at nonantisecretory dosages prevent the development of gastric ulcers caused by virtually any insult. In humans, PGs prevent the mucosal damage caused by aspirin and ethanol. In some studies, the maintenance of normal mucosal integrity has been linked to normal mucosal production of PGs. Therefore, it is possible that exogenous PGs may be effective in patients whose ulcers do not heal with conventional therapy. They may reduce the recurrence of ulcers, particularly in those patients whose defect in mucosal integrity appears to be the major problem. Furthermore, in those patients subjected to the toxic effects of alcohol ingestion, nonsteroidal antiinflammatory drugs, antineoplastic drugs, and stress, exogenous PGs may prevent mucosal lesions. As such, PGs could be the ideal antiulcer drug.
mesh_terms: D001639:Bicarbonates / Q000378:metabolism; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism; D009093:Mucus / Q000378:metabolism; D010437:Peptic Ulcer / Q000188:drug therapy*; D011453:Prostaglandins / Q000494:pharmacology / Q000627:therapeutic use*; D012907:Smoking
chemical_list: D001639:Bicarbonates; D011453:Prostaglandins