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
MITCHELL A. SPELLBERG, RONALD H. CHAIKOFF. Saluretic and Toxic Effects of Amphenone in a Patient with Cirrhosis and Ascites. AMA Arch Intern Med. 1959;104(3):396–401. doi:10.1001/archinte.1959.00270090050008