SODIUM AND WATER DIURESIS IN CIRRHOTIC PATIENTS WITH INTRACTABLE ASCITES FOLLOWING CHEMICAL INHIBITION OF ALDOSTERONE SYNTHESIS

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Abstract
Su 4885, an inhibitor of the enzyme responsible for 11[beta]-hydroxylation within the adrenal cortex, was administered to 8 patients with hepatic cirrhosis, intractable ascites and "secondary" hyperaldosteronism. Aldosterone synthesis was effectively diminished by this compound; however, the adrenal cortex produced large quantities of 11-desoxycorticosterone (DOC) under the influence of Su 4885. The net effect of aldosterone inhibition and DOC production was continued retention of sodium and water in 7 of 8 patients. However, when suppression of ACTH release was achieved by the administration of prednisone, Su 4885 treatment resulted in inhibition of aldosterone synthesis without concurrent stimulation of DOC synthesis. Significant diuresis of sodium and water was produced by combined treatment with Su 4885 and prednisone in 3 of 5 patients. Urinary sodium excretion rose from less than 5 meq/day to values of over 100 meq/day in the patients who responded to this regimen. It is concluded that the hypersecretion of aldosterone plays a significant role in the pathogenesis of sodium and water retention in many patients with hepatic cirrhosis and ascites.