Canales Es

Ovarian refractoriness during lactation in women: Effect of gonadotropin stimulation

This study was to obtain information about the response of the ovari es when stimulated by im gonadotropins in women during lactation and to correlate the hormone changes in an attempt to define the activity of the ovaries during the postpartum period. Patients were 6 normal women aged 17-24 years who were studied for 6 weeks. Lactation was started in all patients immediately after delivery and continued during the study. Human menopausal gonadotropins (HMG) (Pergonal 500) were administered by im injection 3 ampules daily for 5 days starting Day 6 after delivery. Total HMG for each woman was 2250 IU. Levels of total estrogens were determined by the Beling technique. Pregnanediol and pregnanetriol were analyzed in 24-hour urine before gonadotropin stimulation then every 3 days for 2 weeks and then weekly for 4 more weeks. Total gonadotropin activity in urine by bioassay was estimated before stimulation. Daily blood samples were also obtained before stimulation. Plasma FSH was assayed by double-antibody radioimmunoassay. Endometrial biopsies were taken 10 and 30 days after the HMG course. The administration of gonado tropins elicited no significant increase in the output of urinary estrogens pregnanediol or pregnanetriol within 20 days after partuition. Significant changes were not observed in steroid output in the following 4 weeks. In all patients the endometrium remained inactive. Basal body temperature was monophasic type. Menstrual flow did not appear. The FSH values were half of those found during the follicular phase of a normal cycle. Results suggest that the ovaries are refractory during a part of the postpartum and lactation intervals. A relative delayed recovery of the pituitary gondotropin activity is also present.

Effect of Acute Administration of L-Dopa on Serum Concentrations of Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) in Patients with the Amenorrhea-Galactorrhea Syndrome

The effect of acute L-dopa therapy on serum FSH and LH concentrations was studied in 10 patients with the amenorrhea-galactorrhea syndrome. L-dopa ingestion was not followed by a significant alteratio

Endocrine aspects of lactation and postpartum infertility

The hormonal basis for human lactation and postpartum anovulation primarily based on studies of prolactin physiology is reviewed. Lactation is possible from midtrimester of pregnancy buy normally is initiated by abrupt decline in estrogen and progesterone that occurs at childbirth. These steroids take a week to fall to nonpregnant levels. Prolactin levels rise during pregnancy then fall at delivery to basal levels determined by the amount of suckling. Prolactin binds to receptors in the Golgi apparatus of the alveolar cells in the breast where casein lactose and alpha-lactalbumin are synthesized. Oxytocin acts on the myoepithelial cells to facilitate milk ejection. Suckling is so important a stimulus that it can overcome the effect of prolactin-blocking drugs. Suckling causes a surge of prolactin secretion most important in the 1st few moments of nursing. Another hormone involved in lactation is human placental lactogen only active in late pregnancy acting to prepare the alveoli for lactation. Thyroid releasing hormone can also cause prolactin release. Prolactin functions as a suppressor of ovulation rendering women infertile for 6-8 weeks after delivery. It suppresses follicle stimulating hormone more than luteinizing hormone postponing ovulation. Prolactin flattens the pulsating LHRH release pattern reduces ovarian responsiveness to gonadotropins and estrogens and reduces ovarian steroidogenesis. In women with defective lactation thyroid stimulating hormone or the drug metoclopramide will raise prolactin levels and bring on full lactation. This treatment will make lactation possible in nulliparous women who also have nipple stimulation.

Pituitary Response to Synthetic Luteinizing Hormone-Releasing Hormone in Prader-Willi Syndrome, Prepubertal and Pubertal Children

Pituitary responsiveness to the intravenous injection of synthetic luteinizing hormone-releasing hormone (LH-RH) was studied in a female patient with Prader-Willi syndrome and the response was compare

Feasibility of suppressing and reinitiating lactation in women with premature infants

4 puerperal women (19-33 years of age) who had vaginal deliveries after pregnancies of 34-39 weeks and delivered infants weighing between 1300-2500 gm were treated with 2.5 mg bromocriptine orally 3 times a day from the 1st through the 8th postdelivery days. The infants were under intensive care during this period. None of the patients nursed their infants. Blood samples were obtained during the nonnursing period and assayed for serum prolactin (hPRL) by radioimmunoassay. From Day 8 to 12 postpartum a dose of 20 mg of thyrotropin-releasing hormone (TRH) was administered 4 times a day. Breast-feeding was initiated at the 14th postdelivery day. Serum hPRL levels were suppressed by bromocriptine. Patients were without breast engorgement or milk flow. A bolus dose of 250 mcg TRH exhibited milk flow after TRH injection. Milk production was reinitiated in all the mothers are persisted for the following 4 weeks. These results suggest that the administration of TRH could have some therapeutic value in women for whom it is necessary to suppress and reinitiate lactation.

Induction of Ovulation with Clomiphene and Estradiol Benzoate in Anovulatory Women Refractory to Clomiphene Alone

Twenty-two infertile and clomiphene-nonresponding patients received a course of clomiphene, 100 mg/day for 5 days, followed 7 days later by an intramuscular injection of 1 mg of estradiol benzoate. The diagnosis of idiopathic chronic anovulation had been established. None of these patients had galactorrhea, hirsutism, or ovarian enlargement. Thirteen of the twenty-two women had surges of both luteinizing hormone and follicle-stimulating hormone after the estradiol injection; the peak gonadotropin levels occurred within 72 hours of the injection. These 13 patients ovulated and pregnancy ensued in 10 of them. The estradiol benzoate injection also elicited a significant increase in serum prolactin levels- This enhanced prolactin release had no apparent effect on the gonadotropin surge. These results suggest that the association of clomiphene and estradiol benzoate potentiates the action of clomiphene and may prove useful in clomiphene nonresponders.

Clinical use of metoclopramide test in the diagnosis of women with hyperprolactinemia.

UNLABELLED 14 women with elevated prolactin (PRL) serum levels (greater than 25 ng/ml) were given 2.5 mg of metoclopramide, by bolus intravenous injection, to evaluate its diagnosic potential as a stimulus for PRL release. Following metoclopramide injection there was a prompt increase in serum PRL in normal subjects and in patients with moderate PRL elevations associated with galactorrhea-oligomenorrhea. The women with amenorrhea-galactorrhea regardless of the presence of absence of a pituitary tumor, showed a blunted response. Metoclopramide failed to induce TSH secretion in all cases. IN CONCLUSION the use of the metoclopramide test provides no additional clinical information to that furnished by the basal serum PRL concentration for the hyperprolactinemic patient.

Effect of suckling on serum follicle-stimulating hormone and luteinizing hormone in nursing women.

The effect of breast feeding on serum FSH and LH concentrations was studied in 13 puerperal women. Despite the collateral increase in serum prolactin levels, nursing was not followed by significant changes in serum FSH or LH levels during a 30-min observation period. Our data indicate that nursing has no significant effect on pituitary FSH and LH release.

LH and FSH releasing mechanism in the testicular feminization syndrome

The effect of various stimuli on follicle stimulating hormone (FSH) and luteinizing hormone (LH) secretion was investigated in 7 patients with the complete form of the testicular feminization syndrome (TFS). Blood samples were obtained prior to and after an iv dose of 50 mcg of synthetic LH-releasing hormone (RH). This LH-RH test was carried out in some cases before and after gonadectomy. Basal LH and FSH were found to be elevated in comparison to normal males and females. The FSH serum levels increased two- to sevenfold following gonadectomy and ten- to fifteenfold 2 months after gonadectomy. LH-RH increased serum LH within 8 minutes and a maximal FSH increase occurred at 32-64 minutes. LH-RH released more FSH in the TFS than in adult normal subjects however LH release did not differ markedly. 2 weeks after castration 50 mg of progesterone was administered im and blood samples were drawn at intervals for 48 hours. 1 week later the 4 patients were treated orally with 80 mcg ethinyl estradiol/day for 4 weeks. Then 50 mg of progesterone was administered im to all subjects. The progesterone alone did not markedly alter the FSH or LH levels. However during the administration of ethinyl estradiol the levels of both FSH and LH decreased. The positive feedback effect of estrogen in patients with TFS was studied by the im administration of 50 mcg estradiol benzoate/kg body weight. FSH and LH were measured at intervals up to 72 hours postinjection. No positive gonadotropin response was obtained. These results demonstrate the presence of a partial feedback control of both FSH and LH secretion suggesting that this gonadotropic feedback control is exerted through gonadal factors.

Nomifensine Test Does Not Differentiate Hyperprolactinemia Associated with and without Radiologic Abnormalities in the Sella turcica

A group of 17 hyperprolactinemic women was given 200 mg of nomifensine orally to evaluate its diagnostic potential to discriminate between tumors and nontumorous hyperprolactinemia. The nomifensine suppressive effect on prolactin serum levels was not significantly different between patients with or without enlargement of the sella turcica. A control group of 5 women with normal prolactin levels exhibited a nomifensine suppressive effect below 65% of the baseline prolactin level, which was significantly different from that in the hyperprolactinemic group. In conclusion it is confirmed that the nomifensine test provides no value in the early diagnosis of the prolactinoma.