American Journal of Clinical Nutrition, Vol 2, 252-264, Copyright © 1954 by The American Society for Clinical Nutrition, Inc.

The PROTEIN STATUS in PULMONARY TUBERCULOSIS

¹ From the Creedmoor Institute for Psychobiologic Studies, Creedmoor State Hospital, Queens Village 27, N. Y., Harry A. LaBurt, Director, and the New York City Department of Health
² The Chest Division of the Bellevue Hospital, New York, N. Y.

Nitrogen equilibrium studies in a limited number of patients suffering from advanced chronic pulmonary tuberculosis with weight loss and a poor prognosis showed that there is, as a rule, no increased azoturia, so that the weight loss is not due to a "catabolic response" or "toxic" destruction of proteins. The weight loss is probably caused by disturbance of the appetite and is reflected by the presence of one or more changes in the body fluid compartments associated with hypoproteinia.

The use of high protein therapy is followed by a highly positive nitrogen balance and rapid weight gains; there does not seem to be an antianabolic factor in the disease.

The adverse effect on erythropoiesis and blood protein formation in pulmonary tuberculosis does not appear to be due to hypoproteinia alone; but the disease itself seems to play a role.

The effect of rapid protein replacement on increased respiratory activity associated with the specific dynamic action of high protein ingestion is discussed.

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