GASTRIC SECRETION IN FEVER AND INFECTIOUS DISEASES

Abstract

In febrile conditions derangement of gastric function constitutes one of the common symptoms. It may be either in the form of motor disturbance or manifested as secretory anomaly. For instance, nausea or vomiting frequently marks the onset of many acute infections. Anorexia as a rule persists throughout the course of such illness. These phenomena point to an impairment of the tone and motility of the stomach and have been attributed to the action of toxins on the gastric musculature (1) (2). They usually disappear after the disease process subsides. The secretory disturbance, on the other hand, may not be quite so apparent. Nevertheless it is not any less common. Achlorhydria has been found in various acute and chronic febrile diseases (3) (4). Faber (5) in discussing the etiology of achylia especially emphasized the importance of these febrile diseases as factors causing complete suppression of the gastric secretion. He believes that typhoid fever, more than any other infectious disease, is frequently complicated or followed by achlorhydria because in this disease there exists an intestinal infection and the stomach is there- fore more easily affected. Faber also interprets the secretory changes on the basis of an anatomical lesion, probably in the form of gastritis. It is his opinion that the postfebrile anacidity is very likely to remain for the rest of the patient's life. While infection and intoxication have been generally held as the explanation of the observations quoted above, Meyer, Cohen and Carlson (6) have approached the relationship from another point of view. In their animal experiments these authors were able to obtain the same change in the gastric juice from fever and from application of external heat. Under both of these conditions gastrin, injected subcutaneously, failed to induce a normal secretion. When the temperature became normal the restoration of gastric function was prompt. This definite but transitory depression of the gastric gland cells was therefore considered to be directly produced by the elevation of temperature.