Production of Experimental Endometrial Hyperplasia. ∗

Abstract

Endometrial hyperplasia has been known in this country since 1900, when it was described by Cullen 1 . Schroeder's 2 conclusion that endometrial hyperplasia was due to changes in the ovary resulting from a deficiency of the corpus luteum has been amply confirmed. Fluhmann 3 , and Burch, Williams, and Cunningham 4 have studied the condition from the hormonal standpoint, and consider that the endometrial pathology is due mainly to the action of oestrin. While in their experiments 4 the cellular changes of endometrial hyperplasia were faithfully reproduced, the characteristic gland pattern was lacking. This gland pattern, the most striking feature of the condition, was considered less important than the cellular changes. The characteristic gland pattern was experimentally produced and recognized as such by Hofbauer 5 . He repeatedly implanted anterior lobe substance in guinea pigs with intact ovaries. It is impossible to evaluate the relative effects of hypophyseal and ovarian hormones, as the formation of the ovarian hormones would be stimulated. The inference is clear that oestrin must be the major factor, as the hormone of the corpus luteum exercises little or no effect on an endometrium unless sensitized by oestrin.

To test further this conception of the etiology of endometrial hyperplasia, a series of 24 spayed guinea pigs and 20 spayed rats were given varying amounts of oestrin over relatively long periods of time. Sections of the uteri of these animals were removed at stated intervals during the injection period.

A large percentage of the guinea pigs which received the oestrin injections exhibited uteri in which the cellular and glandular picture was identical with that found in human hyperplasia. The glands, many of which were cystic, were very prominent throughout the greatly thickened mucosa.