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Hepatic Regulation of Sodium and Water in Ascites

John B. LaLonde, MD; Sankaran M. V. Valiathan, MB; Walter F. Ballinger II, MD
JAMA. 1964;187(2):117-118. doi:10.1001/jama.1964.03060150041009.
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FACTORS INVOLVED in the production and maintenance of ascites secondary to cirrhosis of the liver are not clearly understood. Outflow obstruction of the hepatic veins, hypoproteinemia,1 and hyperaldosteronism2 have been implicated in its etiology. More recently, additional factors have been suggested to play a role in the formation of ascites. Baronofsky3 succeeded in ameliorating experimental ascites in dogs by thyroidectomy. He postulated a thyroid-adrenal interrelationship in the causation of cirrhotic ascites. Mittlemann4 reported two patients with ascites secondary to cirrhosis who had a naturesis in the face of rising urinary aldosterone following portacaval shunts. This seeming paradox has not been adequately explained. Watson5 has called attention to the possibility of a humoral agent released by the cirrhotic liver that could cause ascites. More recently, Wolfman and associates6,7 have presented experimental evidence that dogs with portacaval shunts retain more sodium and water in response to


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