Etiology of infertility in monkeys with endometriosis: luteinized unruptured follicles, luteal phase defects, pelvic adhesions, and spontaneous abortions.
To elucidate the etiology of infertility due to endometriosis, we autografted endometrial or adipose tissue to the pelvic peritoneum of 21 cynomolgus monkeys. These primates were divided into five groups: control animals with adipose tissue autografts (n = 5), animals with microscopic endometriosis (n = 5), animals with mild endometriosis (n = 5), animals with moderate endometriosis (n = 4), and animals with severe endometriosis (n = 2). During three subsequent menstrual cycles, each animal underwent (1) serial assay of peripheral serum gonadotropins and steroids; (2) mating timed according to daily serum 17 beta-estradiol; and (3) laparotomy to document an ovulatory stigma. The chemical and term pregnancy rates were lower among monkeys with moderate or severe endometriosis, as compared with control animals. The impaired fertility in monkeys with endometriosis appeared to be mediated primarily by failure of follicular rupture and/or pelvic adhesions.
D000022:Abortion, Spontaneous / Q000209:etiology*; D000818:Animals; D004715:Endometriosis / Q000150:complications*; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D007247:Infertility, Female / Q000209:etiology*; D008183:Luteal Phase; D007986:Luteinizing Hormone / Q000097:blood; D008252:Macaca fascicularis; D008598:Menstruation; D006080:Ovarian Follicle / Q000473:pathology*; D000292:Pelvic Inflammatory Disease / Q000150:complications*; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D000267:Tissue Adhesions / Q000150:complications
D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone