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
HOLLANDER F, JANOWITZ HD. Suppression of Gastric Hydrochloric Acid Secretion by Enzyme Inhibitors: A New Approach in Research on the Therapy of Peptic Ulcer. AMA Arch Intern Med. 1956;97(2):194–200. doi:10.1001/archinte.1956.00250200070006
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