Abstract
The therapeutic effect claimed for histidine in the treatment of peptic ulcer seems to be based on the allegation that it prevents experimental ulcer in dogs. The exact mode of action has not been well explained. Those originally advocating the treatment claim that it probably supplies the missing product of protein digestion. However, there is no tangible evidence to show that peptic ulcer is a result of amino-acid deficiency. Martin 1 postulates the interesting theory that histidine may stimulate secretion of mucus which exerts a buffer action on the gastric juice and protects the ulcer. Volini and McLaughlin 2 actually observed in a series of 21 ulcer patients treated with this drug a uniform decrease in the amount and acid of the fasting and stimulated gastric juice. Sandweiss 3 failed to obtain similar results and could not correlate the clinical response to any change in gastric acidity. This report deals with a study of the fasting, basal, and histamine-stimulated gastric secretions following a single injection of 0.2 gm. of histidine monohydrochloride (Laros-tidin) in 2 normal subjects, one case of nutritional edema, 2 cases each of gastric neurosis, chronic appendicitis and chronic dysentery, and 5 cases of peptic ulcer, with various degrees of gastric acidity represented. The control and histidine observations were made on separate days but under exactly identical conditions. Histidine was injected intragluteally 30 minutes before the collection of basal secretion was begun. After 4 ten-minute samples of basal juice were obtained, histamine (Ergamine acid phosphate 0.5 mg.) was given subcutaneously and the specimen collected during the second 10-minute period was chosen as representing the stimulated secretion because the maximum acidity is usually attained in this sample.
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