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The Mechanism of Hyponatremia in Pulmonary Tuberculosis

ROBERT J. SHALHOUB, M.D., F.A.C.P.; and LUCY D. ANTONIOU, M.D.
Ann Intern Med. 1969;70(5):943-962. doi:10.7326/0003-4819-70-5-943
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SUMMARY:

The diuretic response to acute water loading was studied in six patients with pulmonary tuberculosis and hyponatremia. In one of these a pulmonary alveolar-cell carcinoma was also present. Five out of six patients responded abnormally (fractional excretion less than 65% ) when compared with a control group, but the response was consistently improved or corrected by ethanol. In two out of three patients, pretreatment with cortisone also resulted in improvement.

For comparison, similar studies were performed on two patients with bronchogenic carcinoma and inappropriate secretion of antidiuretic hormone (ADH). Unlike the tuberculous group, these patients could not excrete dilute urine in response to water, ethanol, or cortisone. These patients also suffered from severe chronic alcoholism and malnutrition. They gained weight during the course of antituberculous therapy, and the hyponatremia gradually disappeared in four patients in whom it could be followed.

We conclude that in this group an acquired disturbance of neurohypophyseal function exists resulting in unregulated ADH release. Whether this is related specifically to tuberculosis or to the associated alcoholism or malnutrition is not clear from our studies.

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