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MITCHELL A. SPELLBERG, M.D.; RONALD H. CHAIKOFF, M.D.

AMA Arch Intern Med. 1959;104(3):396-401.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The precise pathogenesis of ascites in cirrhosis of the liver remains obscure. Portal hypertension,¹,² decreased plasma osmotic pressure due to hypoalbuminemia,³,⁴ increased lymphatic exudation from the liver,⁵,⁶ increase of antidiuretic hormone,⁷ and increase of sodium-retaining adrenocortical hormone⁸ are among the factors considered in the pathogenesis of ascites. The marked decrease of sodium excretion and the presence of increased amounts of aldosterone in the urine of patients with cirrhosis and ascites⁹ point to this sodiumretaining hormone as the possible culprit in the pathogenesis of ascites. The complexity of the pathogenesis of ascites is demonstrated schematically in Figure 1.

Amphenone B (3,3-bis[p-dimethylaminophenyl]butanone-2-dihydrochloride) (Fig. 2) was synthesized by Allen and Curwin,¹¹ in 1950, and has been shown to have principally an inhibiting effect on thyroid and adreno-cortical function.^12,13 Among its other effects are a progesterone- or estrogen-like effect on the female genitalia, with uterine enlargement 12 and a depressing effect on the central . . . [Full Text PDF of this Article]

Author Affiliations
Chicago

Attending Physician in Medicine, Michael Reese Hospital, and Associate Professor of Clinical Medicine, University of Illinois College of Medicine, Chicago (Dr. Spellberg); Resident in Medicine, Michael Reese Hospital (Dr. Chaikoff).

Footnotes
Submitted for publication Nov. 11, 1958.

The Amphenone used in this investigation was obtained from Dr. C. H. Sullivan of Ciba Pharmaceutical Products, Inc., Summit, N. J.

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