October 1988

Peptic Ulcer Disease, Cytoprotection, and Prostaglandins

Author Affiliations

Division of Gastroenterology St Michael's Medical Center 268 Dr Martin Luther King Jr Blvd Newark, NJ 07102

Arch Intern Med. 1988;148(10):2112-2113. doi:10.1001/archinte.1988.00380100010002

In this issue of the Archives an illustrative report of the therapeutic benefit of an oral prostaglandin analogue for the treatment of an intractable benign gastric ulcer is presented.1

In the past decade the treatment of peptic ulcer disease has progressed dramatically from diet (did it really matter?) to antacids (did they really work?) to the class of drugs known as H2-receptor antagonists (cimetidine, ranitidine, and famotidine). Then the drug sucralfate was approved by the Food and Drug Administration because it was as efficacious as H2 antagonists and high-dose antacid therapy in the treatment of duodenal ulcers. There is no doubt that hydrochloric acid (HCl) and pepsin are requirements for the development of a peptic ulcer. However, only approximately 30% of patients with duodenal ulcer and only approximately 10% of patients with gastric ulcer are hypersecretors of acid and pepsin.2 Therapy

See also p 2275.

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