Ovulation Stigma Research Articles

Ovulation stigma and concentration of progesterone and estradiol in peritoneal fluid: relation with fertility and endometriosis

The relationship between the presence or absence of an ovulation stigma and (1) the fertility status, (2) the incidence of endometriosis, (3) the concentration of progesterone and estradiol in the peritoneal fluid, and (4) the blood levels of luteinizing hormone, follicle-stimulating hormone, progesterone, and estradiol in 21 fertile and 45 infertile patients who underwent a laparoscopy in the early (n = 48) or late luteal phase (n = 18) was investigated. An ovulation stigma was observed in about half of the patients, irrespective of their fertility status (past and subsequent), the presence of endometriosis, or the time of the luteal phase. Progesterone and estradiol concentrations in the peritoneal fluid were highest in the early luteal phase, but they were not correlated with the presence or absence of an ovulation stigma. No significant differences were observed in peripheral hormone levels between women with and those without an ovulation stigma nor between women with high or low concentrations of progesterone in the peritoneal fluid. From the data, it is concluded that hormone assays are of no aid in the diagnosis of the luteinized unruptured follicle syndrome and that the absence of an ovulation stigma on laparoscopic examination cannot be equated with the luteinized unruptured follicle syndrome.

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.

Luteal phase insufficiency in the ewe as a consequence of premature induction of ovulation by intrafollicular injection of gonadotropins.

The largest ovarian follicle of ewes was injected on d 15 of the estrous cycle (2 to 3 d before the anticipated preovulatory surge of gonadotropins) with saline or either luteinizing hormone (LH) or follicle-stimulating hormone (FSH) in saline (5 micrograms). Ovulation was assumed based on the presence of an ovulation stigma at d 5 post-treatment. Control animals expressed estrus 2 to 3 d after treatment with saline, and during the estrous period ovulated from the treated follicle. Gonadotropin-treated animals ovulated from injected follicles prematurely and did not exhibit estrus. The stated observations with respect to time of ovulation were established by visual and hormonal criteria: (1) control follicles appeared to have ruptured within a day or two prior to relaparotomy (corpora hemorrhagica), whereas gonadotropin-treated follicles were in a more advanced stage of luteal development (corpora lutea); and (2) concentrations of systemic sera progesterone rose (P less than .05) in LH- and FSH-treated ewes 2d before such an increase in control animals. Luteal function was assessed by comparing sera concentrations of progesterone throughout the induced and spontaneous (vehicle controls) luteal phases. Premature stimulation of ovulation with either gonadotropin was followed by suppressed luteal function (maximum sera levels of progesterone in gonadotropin-treated animals and controls were slightly greater than 1 ng/ml and nearly 2.5 ng/ml, respectively; P less than .01). No differences in the level of luteal function due to treatment with LH or FSH were observed. The duration of the luteal phases of gonadotropin-treated animals were similar to controls (approximately 17 d).(ABSTRACT TRUNCATED AT 250 WORDS)

Ovulation stigma in fertile women

Ovulation stigma in fertile women

DIAGNOSIS OF THE LUTEINIZED UNRUPTURED FOLLICLE SYNDROME BY STEROID HORMONE ASSAYS ON PERITONEAL FLUID

The luteinized unruptured follicle syndrome is a frequent phenomenon, occurring in half of our women with regular cycles and infertility. Progesterone concentrations and 17 beta-oestradiol concentrations were assayed in peritoneal fluid of women during the luteal phase. Up to day 20 of the cycle, the concentrations were significantly higher in women with an ovulation stigma than in women without an ovulation stigma on their corpus luteum. The range of concentrations was sufficiently different in the early luteal phase to be used diagnostically, the only limitation being the presence of a cystic corpus luteum. We suggest that the assay of progesterone and 17 beta-oestradiol in peritoneal fluid should be done in all women with infertility and biphasic basal body temperature charts in order to diagnose the luteinized unruptured follicle syndrome.

Origin of Peritoneal Fluid in Women: An Ovarian Exudation Product

Department of Obstetrics and Gynaecology, Academic Hospital, St. Rafaël Katholieke Universiteit Leuven, B-3000 Leuven, Belgium

Origin of peritoneal fluid in women: an ovarian exudation product.

The volume of peritoneal fluid was measured after laparoscopic aspiration in 303 women. Contamination with blood was estimated at 4.2 per cent by haemoglobin assay. In 120 women with regular menstrual cycles, the volume of peritoneal fluid increased progressively during the follicular phase, was highest during the early luteal phase (20.0 +/- 6.3 ml) and declined thereafter. In 89 women with moderate and mild endometriosis the amounts of peritoneal fluid were similar, but 9 women with severe endometriosis had lower (P less than 0.05) volumes during the luteal phase. Women with inactive ovaries had uniformly low amounts of peritoneal fluid: 4.2 +/- 2.3 ml in 31 women taking combined oral contraceptive pills; 4.7 +/- 5.8 ml in 17 women taking 5 mg of lynoestrenol daily and 1.2 +/- 1.9 ml in 20 postmenopausal women with an inactive endometrium. In contrast, two postmenopausal women with proliferative endometrium had 7 and 10 ml of peritoneal fluid. Women with active ovaries, 5 with absent or distally occluded Fallopian tubes and 7 without a uterus had normal amounts of peritoneal fluid. The volume of peritoneal fluid was not affected by pelvic varicose veins, a visible corpus luteum or an ovulation stigma. Peritoneal fluid appears to be predominantly an ovarian exudate, neither an exudate from the pelvic peritoneum nor a tubal secretion.