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A New Approach in Research on the Therapy of Peptic Ulcer

FRANKLIN HOLLANDER, Ph.D.; HENRY D. JANOWITZ, M.D.

AMA Arch Intern Med. 1956;97(2):194-200.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

According to our current ideas concerning the pathogenesis of peptic ulceration, this disease is essentially a matter of localized autodigestion of the wall of the digestive tract by active gastric juice. This process does not occur unless there is a breakdown of some kind in the normal defensive mechanism of the gastrointestinal mucosa, the two-component mucous barrier.¹ Since we do not yet know how to strengthen or repair this defensive structure directly, all the medications in general use today for the therapy of this disease are designed to reduce the intensity of the aggressive agent, acid-pepsin juice— directly, by way of the enzyme, and indirectly, by reducing the intragastric acidity, upon which peptic action is dependent. Many of the pharmacological agents which reduce gastric acidity also, in some measure, relieve muscle spasm which makes for prolonged retention of stomach contents. Hence, a review of all chemotherapeutic agents presently in . . . [Full Text PDF of this Article]

Author Affiliations
New York

Footnotes
Submitted for publication Aug. 12, 1955.

Gastroenterology Research Laboratory, The Mount Sinai Hospital.

Much of the experimental work discussed in this paper was carried out with the aid of grants from the Altman Foundation.

Read before the Section on Pathology and Physiology at the 104th Annual Meeting of the American Medical Association, Atlantic City, June 7, 1955.

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