An endocrine basis for endometrial carcinoma

In 165 endometrial cancer cases in which ovariectomy was performed i n the course of the surgical treatment hilar regions were not included in the tissue sections of 1 or both ovaries in 32 cases. For controls ovarian sections from 86 postmenopausal women were studied including 52 cases of postmenopausal endometrial hyperplasia. The hilar or Leydig cells were suspected of being of major significance in the etiology of endometrial carcinoma. Since Leydig cells are hormonally dependent upon the pituitary gonadotropin LH or ICSH a corollary study of the urinary excretion of LH was done in selected patients using the ventral prostate weight technique described by MacArthur. In this study urine was assayed in 31 patients with primary adenocarcinoma of the endometrium 37 patients with other conditions 19 patients who had previously been treated for endometrial carcinoma and 4 cases in which LH determinations were repeated after administration of Delalutin (17-hydroxyprogesterone caproate). 133 cases of primary endometrial carcinoma had ovarian hilar tissue available for study in at least 1 section of 1 ovary. Leydig cell hyperplasia was present in 109 cases (81.9%). In the 29 cases of primary adenocarcinoma of the uterus studied since 1957 hilar-cell hyperplasia has been present in 100%. In the controls 14 of 86 cases contained hilar cells. In the 34 controls without evidence of postmenopausal endometrial hyperplasia the incidence of hilar cell clumps was 2 (5.88%). The 52 control patients with such hyperplasia had hilar cell components in 12 cases (23%). The number of hilar or Leydig cells was much lower in cases not associated with endometrial cancer. The urine assays for LH showed that the patients with primary adenocarcinoma of the endometrium had elevated LH levels in all 31 cases. Following bilateral oophorectomy the level of LH fell to normal in all the cases. According to the authors concept at birth a female destined to develop adenocarcinoma of the endometrium is endowed with an abnormal complement of hilar Leydig or theca cells which are LH responsive. During reproductive years these cells are mini mally functioning because of other hormonal activity. However they may cause increased sterilit y. After menopause this restraining activity is less the pituitary is stimulated to excrete excessive LH endometrial hyperplasia results and finally carcinoma of the endometrium.