INTERNAL SECRETIONS AND TOXEMIA OF LATE PREGNANCY

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Abstract
The primary etiology of toxemia of late pregnancy has yet to be detd., no definitive treatment has been rewarded with spectacular cure, such as usually occurs following delivery of the products of conception, and prevention of the disease by the administration of hormones has not yet been proved. Certain aberrations from the normal in hormonal or hormonal-like findings and in placental morphology appear to be established in [female] [female] with pre-eclampsia and eclampsia: 1, excessive antidiuretic substance in urine and placenta; 2, a melanophore-expanding principle in the blood and placenta; 3, a hypersensitivity to the injn. of post. pituitary secretions; 4, high titers of chorionic gonadotrophin in a large percentage of cases; 5, decreased excretion of estrogens and pregnanediol, and 6, histological and histo-chemical changes in the placenta similar to but more marked than those of the normal placenta at term and primarily involving degeneration of the syncytial cells which probably secrete the steroid hormones. Of these established abnormalities, the last 3 are underway prior to clinical manifestations and occur normally at term. The predisposing factors such as essential hypertension, diabetes, primi-gravidity, hydatidiform mole, twins and hydramnios suggest that the primary etiology of toxemia may consist of a number of causes. Evidence establishes premature senility of the placental syncytium and premature withdrawal of the placental steroid hormones as the final intermediary pathology. This disturbance, which-occurs normally at term, must be brought about prematurely by the working of the primary etiology, which probably involves either an intrinsic metabolic abnormality affecting the placenta or a decrease in blood supply to the placenta or both. Since the syncytial-steroid aberration from the normal characterizes all cases, it may logically be assumed to be contributory factor to the development of toxemia in all cases. It cannot, however, be assigned the role of the sole precipitating cause of the toxemic syndrome. Recent incomplete work suggests that withdrawal of hormonal support from the pregnant as from the non-pregnant uterus may result in the formation of a menstrual-like toxin in the placenta (?) maternal portion, i.e., decidua); that the primary etiology may, in conjunction with the steroid deprivation it causes, do the same thing; and that release of this toxin may prove to be the final cause of toxemia of late pregnancy.

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