CORTICAL STEROID EXCRETION IN EDEMA OF PREGNANCY, PRE-ECLAMPSIA, AND ESSENTIAL HYPERTENSION*

Abstract

THE syndrome seen in desoxycorticosterone intoxication is in many respects strikingly similar to toxemia of late pregnancy (pre-eclampsia and eclampsia). In both syndromes one may find hypertension (1, 2, 3, 4), edema (2, 3, 4, 5), and albuminuria (2, 4, 6). In both syndromes the hypertension is greatly alleviated by drastic dietary sodium restriction (7, 8, 9). In both syndromes the hypertension and albuminuria may be markedly increased by an excessive sodium intake in the diet (6, 7). Excessive DCA administration to animals usually causes atrophy of the adrenal cortex, presumably because of an inhibition of corticotropic hormone secretion by the anterior pituitary (10, 11, 12). Paralleling the DCA findings, Fauvet found abnormally small adrenals in women dying of eclampsia (13) and reported a decreased concentration of corticotropic hormone in the serum of eclamptic women (14). Women with essential hypertension have a greatly increased susceptibility to toxemia of pregnancy (15a). They are also more susceptible to the pressor effects of DCA (16). Renal disease which produces hypertension also increases susceptibility to toxemia. Unilateral nephrectomy (17) and Masugi nephritis (18) in animals increase the toxic effects of DCA.