Abstract

Abstract 1.1. Partial inhibition of adrenal steroid production by Amphenone in patients with cirrhosis and ascites, who were maintained on prednisone and sodium restriction, was associated with increased urine sodium excretion in 5 of 7 cases, although a clinically significant loss of ascites occurred in only one. A complete inverse correlation between sodium and aldosterone excretion was not observed, and it is suggested that other factors as well as aldosterone secretion are operative in causing the sodium retention of these patients. In addition, the data indicate that patients with cirrhosis may have an impaired ability to excrete conjugated aldosterone. 2.2. Prednisone was found consistently to cause a water diuresis when administered to patients with cirrhosis, and this was associated with an increased response to mercurial diuretics and frequently a rise in serum sodium. Increased sodium excretion followed prednisone administration in 5 of 10 cases but was clinically significant in only 3 and could not be correlated with decreased aldosterone excretion. 3.3. The adverse neurologic manifestations following Amphenone administration to patients with cirrhosis, even though ameliorated by concomitant prednisone administration, create a severe limitation to its clinical usefulness. Prolonged prednisone administration to these patients with cirrhosis was associated with overwhelming infection in 2 instances.

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