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Peptic Ulcer Disease, Cytoprotection, and Prostaglandins
Steven C. Fiske, MD
Arch Intern Med. 1988;148(10):2112-2113.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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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.
. . . [Full Text PDF of this Article]
Author Affiliations
Division of Gastroenterology St Michael's Medical Center 268 Dr Martin Luther King Jr Blvd Newark, NJ 07102
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