Abstract
THE cessation of menstruation at the time of the menopause is not invariably accompanied by atrophic changes in the genital tract. Moreover the speed of the onset of atrophy and its completeness vary greatly in different individuals and even in different parts of the genital tract of the same woman. Novak and Richardson (1) found active hyperplasia and proliferation of the endometrium in patients many years past the menopause. In a series of patients studied by the author previously (2) it was shown that atrophic changes were present in over 95 per cent. In many instances the atrophy was accompanied by cystic changes in the glands, either diffusely throughout the endometrium or in a polyp of the senile type. In the remaining cases the endometrium exhibited hyperplasia or proliferation and in 1 case a secretory pattern was noted. Endometrial activity is generally assumed to be the result of ovarian hormone secretion, particularly of estrogen. In view of the varying endometrial patterns, some writers have tried to demonstrate possible continued action of estrogens in the normal postmenopausal woman. Mack (3), using the glycogen content of the vaginal cells as an index of estrogenic activity, estimated that in 30 per cent of elderly women there was evidence of continued estrogen secretion. Previously Robson et al. (4) by bioassay methods found estrogens in the urine of postmenopausal women. The picture was complicated by reports that estrogens could be demonstrated by biologic methods in the urine of surgically castrated women. The inference was that estrogens, if present, were not of ovarian origin.