Citations from the Literature herniorrhaphy of the right broad ligament through mini-laparotomy. The potential for bowel herniation exists whenever a closed loop is present in the abdominal cavity.
ENDOCRINOLOGY Dieting causes menstrual irregularities in normal weight young women through impairment of episodic luteiniziag hormone SC!CMiOtl
Pirke KM; Schweiger U; Strowitzki T; Tuschl RJ; Laessle RG; Broocks A; Huber B; Middendorf R Divtiion of Psychoneuroendocrinology, Max-Planck-Institut fur Psychiatric, D-8aw) Munchen 40; German Federal Republic Fertility and Sterility/51/2 (263-268)/1989/ Thirteen healthy, normal weight young women were studied throughout a control cycle and a diet cycle, during which they lost 1 kg per week on a vegetarian 800 kcal diet. Blood was sampled daily in the morning, and at weekly intervals, collected at lo-minute intervals for 6 hours. Follicle growth was monitored by ultrasonic measurement. All subjects showed normal cyclic gonadal function during the control cycle. Cyclic gonadal function remained unaltered in two subjects during the diet cycle. No dominant follicle developed in seven others, while another four showed apparently normal follicular development but impaired progesterone secretion by the corpus luteum. Comparison of both cycles revealed that episodic luteinizing hormone (LH) secretion during the follicular phase was altered by dieting. Average LH concentrations and the frequency of episodic secretions were significantly reduced during the follicular phase but not during the luteal phase. Follicle-stimulating hormone was unaltered. Gonadotropin-releasing hormone pacemaker sensitivity to negative feedback inhibition by estradiol in women with hypothalamic amenorrhea
Judd S; Stranks S; Michailov L Department of Medicine, Flinders Medical Centre, Bedford Park, SA 5042; Saudi Arabia Fertility and Sterility/51/2 (257-262)/1989/ To better understand the pathophysiology of hypothalamic amenorrhea (HA), the frequency of luteinizing hormone (LH) pulsatility and the LH response to gonadotropin-releasing hormone (GnRH) was assessed before and after clomiphene citrate (CC) in 18 women with HA and 10 normal women in the early follicular phase (EFF’). The HA women showed a greater acceleration of LH pulsatility after CC than EFP women but there was a decrease in their LH response to GnRH. Naloxone caused an increase in LH pulsatility in HA but not EFP women, although this effect was less than that seen with CC. We conclude that, in HA women, the GnRH pacemaker, but not the pituitary, is inhibited by increased sensitivity to the negative feedback effect of estradiol and increased opiate tone. Effectiveness of vaginal bromocriptine in treating women with byperprolactinemia
Kletzky OA; Vermesh M
389
Department of Obstetrics and Gynecology, University of Southern Calvornia School of Medicine, Los Angeles, CA 90509; USA Fertility and Sterility/5112 (269-272)/1989/ Treatment of hyperprolactinemia with oral bromocriptine has been associated with a high incidence of side effects. The authors recently demonstrated that, in normal women, the vaginal route of administration was an effective and safe alternative to oral bromocriptine. To evaluate the effectiveness of vaginal bromocriptine in treating women with hyperprolactinemia. the authors treated 15 hyperprolactinemia women with daily vaginal administration of 2.5 mg tablets of bromocriptine. Serum prolactin (PRL) levels and vital signs were measured daily for 6 days, then weekly for 4 weeks. Gastrointestinal side effects were limited to a single episode of mild nausea, and two cases of transient constipation. In all patients there was a dramatic initial reduction in PRL in response to a single 2.5 mg dose of bromocriptine. In 13 patients PRL level were maintained within the normal range with daily administration of 2.5 mg, whereas in two patients, PRL levels remained higher than normal despite an increase in bromocriptine dose to 5 mg. These results suggest that short term use of vaginal bromocriptine is a safe and effective method of therapy of hyperprolactinemia. Long-term follow-up of patients with uterine fibroids after treatment with the LHRH agonist buserelin
Matta WHM; Shaw RW: Nye M The Royal Free Hospital School of Medicine, London NW3 2QG; United Kingdom British Journal of Obstetrics and Gynecology19612 (200206)/1989/ Ten patients with uterine fibroids palpable abdominally were treated with the luteinizing hormone-releasing hormone (LHRH) agonist buserelin, administered intransally, 300 mu g three times daily, for 6 months, and were then followed for a further 12 months. Oestrogen levels were markedly reduced in all patients during treatment. At the end of treatment the mean volume reductions were 44.4% (SEM 3.5) for total uterine volume and 57.3qo (SEM (7.4) for volume of discrete fibroids as assessed ultrasonically. There was also marked improvement in associated symptoms. After buserelin therapy was stopped, the total uterine and discrete fibroid volumes returned to, or slightly exceeded pretreatment volumes within 6 months in five patients, and by 12 months in two patients. Three other patients who underwent surgery for their fibroids during the first 4 months after treatment showed regrowth of fibroids to pretreatment size. Four comparable asymptomatic untreated patients showed no significant change in the total uterine or fibroid volume during six monthly ultrasonic assessments. Buserelin therapy may facilitate rather than replace surgery in the management of uterine fibroids. Administration of pure follicle-stimulating hormone during gonadotropin-releasing hormone agonist therapy in patients with clomipheae-resistant polycystic ovarian disease: Hormonal evaluations and clinical perspectives
Remorgida V; Venturini PL; Anserini P; Lanera P; De Cecco L Int J Gynecol Obstet 29
390
Citations from the Literature
Department of Obstetrics and Gynecology, University of Genoa, 16100 Genova; Italy American Journal of Obstetrics and Gynecology/l60/1 (108113)/1989/ Nine women with chronic anovulation caused by polycystic ovarian disease, which was unresponsive to clomiphene citrate therapy, were given a gonadotropin-releasing hormone agonist (buserelin) to induce pituitary densensitization. After 4 weeks induction of ovulation was attempted with a step-up administration of urinary follicle-stimulating hormone. Buserelin treatment was discontinued only in the presence of a positive pregnancy test result. Different responses were observed between the first and subsequent cycles. Whereas estradiol production and follicular growth were closely correlated in the first attempt, we recorded a dissociation between these two parameters of ovarian response during subsequent stimulations. Four clinical pregnancies occurred in these nine patients, and there was one abortion. This therapeutic approach can be successfully used to induce ovulation; however, prolonging pituitary suppression between treatment cycles changes the type of ovarian response and is not followed by better results.
Binding sites for gonadotropins ovaries
Ferenczy A; Gelfand M Department of Pathology, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Que. H3T IE2; Canada American Journal of Obstetrics and Gynecology/l60/1 (126131)/1989/ Eighty-five menopausal women (mean age 56 years) with endometrial hyperplasia without (65 patients, group 1) and with cytologic atypia (20 patients, group 2) were followed up prospectively from 2 to 12 years (mean 7 years) to shed insight into their respective response to oral medroxyprogesterone acetate therapy. In group 1, 9 of 65 patients (14%) had persistence, 4 (SW) had recurrence, and none developed carcinoma. In group 2 10 of 20 patients (50%) had persistence and 5 had recurrence with cytologically atypical disease. Five of 20 patients (25%) developed adenocarcinoma at 2 to 7 years (mean 5.5 years) after starting medroxyprogesterone acetate therapy. The data suggest that most women with hyperplasia respond to progestogenic therapy and are not at increased risk of developing cancer. The patients with an unfavorable response to medroxyprogesterone acetate and a significant elevation in cancer risk can be identified on the basis of cytologic atypia.
Int J Gynecol Obstet 29
postmenopausal
Nakano R; Shima K; Yamoto M; Kobayashi M; Nishimori K; Hiraoka J-I Department of Obstetrics and Gynecology, Wakayama Medical College, Wakayama; Japan Obstetrics and Gynecology/73/2 (l%-200)/1989/ The binding of human LH and human FSH to postmenopausal ovarian tissue from 21 patients with cervical carcinoma was analyzed. The binding sites for FSH and LH were demonstrated in postmenopausal ovarian tissue. The surface-binding autoradiographic study revealed that the binding sites for gonadotropins were localised in the cells of cortical stroma of the postmenopausal ovary. In addition, diffuse cytoplasmic staining of endogenous estrogen and 3 beta-hydroxysteroid dehydrogenase activity were detected immunohistochemically and histochemically in the cells of the cortical stroma. Electron microscopic study also suggested steroidogenic function in the cells of the cortical stroma. The results of the present study suggest that postmenopausal ovaries contain specific binding sites for pituitary gonadotropins and play a role in ovarian steroidogenesis. Long-term oral contraceptive bone density
The biologic significance of cytologic atypia in progestogentreated endometrhd hyperplnsia
in human
use does not affect trabecular
Lloyd T; Buchanan JR; Ursino GR; Myers C; Woodward G; Halbert DR Department of Obstetrics and Gynecology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, PA 17033; USA American Journal of Obstetrics and Gynecology/l60/2 (402404)/1989/ To determine whether long-term exposure to exogenous estrogen in oral contraceptives influences trabecular bone mass in premenopausal women, we studied 25 closely matched, healthy, premonopausal women, who were recruited from an active obstetrics and gynecology practice. Eleven women had never used oral contraceptives, and 14 women had used oral contraceptives for a minimum of 67 months. All oral contraceptive users had used preparations that provided a minimum of 50 mu g mestranol per day. Trabecular bone density was determined by quantitative single-energy computerized tomography of the Ll-3 lumbar vertebral bodies. Trabecular bone density was similar for both the control group and the oral contraceptive users, 160.6 + 6.9 versus 161.2 f 7.4 mg/ml, respectively. The power to detect a 15% difference in bone density between these two samples was 0.87. We concluded that long-term, premonopausal oral contraceptive use has no effect on vertebral bone density.