Single fetal demise in a twin gestation: umbilical vein thrombosis.

BACKGROUND: Single fetal demise in a twin pregnancy is a rare event, the common causes being twin-twin transfusion syndrome, chromosomal or congenital anomalies and abnormalities of the umbilical cord and placenta. Umbilical vein thrombosis is a very rare cause of single fetal demise in twins. CASE: Three days after a reassuring biophysical profile, a 40-year-old primigravida with twin pregnancy presented at 38 weeks' gestation in early labor when demise of 1 of the twins was recognized. She underwent a cesarean section for arrest of labor, delivering twin A, a stillborn female weighing 2, 360 g and twin B, a liveborn male weighing 2,200 g. Umbilical vein thrombus was noted in twin A. CONCLUSION: Umbilical vein thrombosis is a rare and sudden cause of fetal demise.

Cytogenetics of müllerian agenesis. A case report.

A 38-year-old woman presented with primary infertility and primary amenorrhea. The evaluation revealed müllerian agenesis and mosaicism, 45,X/46,XX/47,XXX.

The treatment of luteal phase defects with pulsatile infusion of gonadotropin-releasing hormone.

Because pulsatile administration of gonadotropin-releasing hormone (GnRH) can initiate normal follicular maturation and corpus luteum function in women with hypothalamic amenorrhea, the authors attempted to treat five women with inadequate and one with short luteal phase with GnRH therapy. Pulsatile administration of GnRH (5 micrograms intravenously every 90 minutes) was begun on days 1 to 4 and continued throughout the cycle. Blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrogen, and progesterone were monitored daily throughout the control and treatment cycles. There were 12 GnRH treatment cycles, all of them ovulatory. The length of the induced luteal phases varied from 11 to 17 days in all patients. Mean progesterone levels during GnRH treatment were significantly increased over those of the matched control cycles (control cycle 3.5 +/- 0.5 ng/ml; treatment cycle 8.2 +/- 1.45 ng/ml [mean +/- standard error]). Endometrial biopsies obtained during the luteal phase (days 25 to 27) in five women were in phase during the GnRH treatment cycle, in contrast to the control cycle in which they were two or more days out of phase. One patient achieved pregnancy during the treatment cycle, but aborted spontaneously at 8 1/2 weeks. The data demonstrate that pulsatile GnRH infusion, when initiated in the early follicular phase, can restore normal corpus luteum function in women with luteal phase defects.

Treatment of hyperprolactinemic amenorrhea with pulsatile gonadotropin-releasing hormone therapy.

Pulsatile GnRH therapy has been shown effective in the treatment of infertility associated with hyperprolactinemia by direct action on the pituitary. Gonadotropin secretion was restored in the setting of moderate hyperprolactinemia. GnRH should be considered as a potential alternative to BCPT therapy in this setting.

Pulsatile administration of gonadotropin-releasing hormone for induction of ovulation.

Chronic pulsatile administration of gonadotropin-releasing hormone (GnRH) was used to induce ovulation in 12 women with various ovulatory disorders. In the first group of eight patients with normal to low baseline levels of gonadotropin, seven responded favorably to the treatment. Follicular maturation was observed in 57% of the treated cycles, and normal ovulatory cycles were induced in 24% of the patients. Two patients became pregnant. The intravenous route of administration was more effective than the subcutaneous one, possibly in response to the GnRH profile after each pulse. (The amplitude of GnRH peaks after an intravenous pulse was four times that seen after a subcutaneous one.) In contrast, follicular maturation and ovulation could not be induced in four women of a second group of patients with normal baseline levels of follicle-stimulating hormone but with high and frequent pulses of luteinizing hormone. The conclusion reached was that pulsatile administration of GnRH can be a new therapeutic tool in the treatment of ovulatory disorders in women who have an insufficient endogenous release of GnRH.

Gonadotropin-releasing hormone and its clinical applications.

PIP: Evidence has accumulated that the hypothalamus contains neurohumoral substances which, upon secretion into the hypothalamo-hypophyseal portal circulation, control the release of anterior pituitary hormones. Gonadotropin-releasing hormone (GnRH) is a decapeptide that has been synthesized and used in studies on the way the hypothalamus controls anterior pituitary secretion. Several therapeutic applications for GnRH have also been investigated. The greatest amount of GnRH in the brain is within the hypothalamus where GnRH immunoreactive perikarya are in a continuum from the septal-preoptic region anteriorly to the premammillary nucleus posteriorly. Two major GnRH pathways control gonadotropin release in the primate: 1 originates in the arcuate nucleus, while the other derives from cell bodies in the anterior hypothalamic region. Hypothalamic GnRH is essential not only for the release but also for the synthesis of both gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone (FSH). Intermittent gonadotropin release is the result of pulsatile activity by the hypothalamus, not of the pituitary gland. Various experiments have been done to modify pulsatile gonadotropin release through endocrine modulation by ovarian steroids. GnRH has been used successfully to stimulate ovulation and spermatogenesis. Advantages of GnRH treatment for hypogonadism include 1) a more physiologic approach, because stimulation of the anterior pituitary gland is intermittent; 2) LH/FSH responses are controlled by endogenous gonadal feedback mechanisms, reducing chance of target organ hyperstimulation; and 3) cost per treatment cycle is lower than that for other therapeutic modalities because GnRH is a simple molecule. Agonists and antagonists resemble each other in their end biologic action, and both classes of GnRH analogs have been used to decrease gonadotropin and gonadal activities.^ieng

Management of multifetal pregnancies: sixteen years' experience at the Sloan Hospital for Women.

An analysis is made of the management and outcome of 35 pregnancies involving triplets, quadruplets, and quintuplets. Bed rest does not seem to increase the gestational age at the time of delivery but definitely improves the fetal outcome. Administration of betamethasone as early as 24 to 26 weeks' gestation to enhance pulmonary maturity is recommended. Cesarean section is the best mode of delivery if the obstetrician is not confident enough with vaginal maneuvers. The rate in this series was 42%. An experienced medical and nursing staff is mandatory for the successful management of multifetal gestations.

Multiple gestations: management of pregnancy and delivery.

The antenatal management and outcome of 31 higher-order multiple gestations, 24 triplets, six quadruplets, and one set of quintuplets were analyzed. Bedrest was advised as soon as the diagnosis was made; hospitalization along with the administration of betamethasone and phenobarbital was begun during the second trimester. Caesarian section was performed on 13 women (42%). The overall mortality rate was 14.8%; excluding neonates less than 28 weeks of age, however, it became 7.5%. The primary cause of death was respiratory distress syndrome.

Apparent immunologic nonidentity of human placental and endometrial 17beta-estradiol dehydrogenase.

Immunohistochemical techniques were used to search for the presence of 17beta-estradiol dehydrogenase activity in human endometrial and placental tissues, with the use of antibodies raised against highly purified human placental 17beta-estradiol dehydrogenase. Sensitivity and specificity of the antibodies were documented by radioimmunoassay and immunodiffusion on cellulose acetate. Although staining was consistently demonstrated in the syncytiotrophoblast layer of term placentas, in both cytoplasm and nuclei, no immunohistochemical reaction was observed in endometrial samples. These results support the contention that placental 17beta-estradiol dehydrogenase is immunologically dissimilar from the endometrial enzyme.