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Biomedical subjects

B Corenblum

Publications and source records attributed to B Corenblum.

At least 37 records · Page 2Linked to original sources
PubMed1988

Induction of ovulation with luprolide acetate and human menopausal gonadotropin.

Four women with unexplained infertility and two anovulatory oligomenorrheic women who experienced repeated premature luteinization when treated with human menopausal gonadotropin (hMG) or gonadotropin-releasing hormone (GnRH) were given the gonadotropin-releasing hormone agonist (GnRHa), luprolide acetate, in order to effect medical hypophysectomy. This was followed by hMG for induction of ovulation. Four of the six patients had hMG-only cycles, which were compared with the luprolide acetate/hMG cycles. The luprolide acetate/hMG cycles resulted in normal folliculogenesis with presumptive ovulation. In luprolide/hMG cycles, significantly more hMG was needed for induction of ovulation than in hMG-only cycles. Premature luteinization was abolished with luprolide acetate treatment.

Adult↗
PubMed1987

Utilization of the biochemical response to clomiphene citrate for the selection of women with hypothalamic amenorrhea who require further investigation.

Clomiphene citrate (CC) 100 mg daily for 5 days was given to 41 women with hypothalamic amenorrhea. CC also was given to 6 similar women with known organic suprasellar disease and to 8 normal women in the early follicular phase. Serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol (E2) were measured both before the first tablet of CC and again on the fifth day. Biochemical evidence of ovulation occurred in 12 of the 41 women. The remaining 29 women included 14 with a significant rise in one or more of serum LH, FSH, and E2 similar to the normal group. The 15 women without rise in any hormonal parameter were investigated further because their response was similar to the organic suprasellar disease group. Serious organic sellar/suprasellar disease was initially found in 4 women, while 2 of the remaining 11 subsequently developed previously unrecognized organic disease over the ensuing year. The authors conclude that the biochemical response to CC is useful to indicate which women with hypothalamic amenorrhea--without any other obvious clinical stigmata--should be further investigated for underlying organic disease.

Amenorrhea↗
PubMed1987

Augmentation of gonadotropin-releasing hormone induced follicular growth with exogenous gonadotropins.

Three women with hypothalamic amenorrhea (HA) were treated with pulsatile gonadotropin-releasing hormone (GnRH). They responded with high luteinizing hormone (LH) values, minimal increments in follicle-stimulating hormone (FSH) values, and failure of follicular development. In subsequent GnRH-stimulated cycles, 1 ampule of human menopausal gonadotropin (hMG) was given intramuscularly for 3 consecutive days once the dominant follicle had attained a diameter of 7 to 8 mm. In all women, subsequent administration of human chorionic gonadotropin (hCG) produced presumptive evidence of ovulation. Five cycles were induced in three women using this regimen. A conception occurred in all three. One woman has conceived a second time. It was concluded that some women with HA respond to GnRH with an inappropriate LH and suppressed FSH response that may be overcome successfully using small doses of hMG.

Amenorrhea↗
PubMed1986

Pregnancy in the hyperprolactinaemic patient.

Once other causes of hyperprolactinaemia have been excluded it is reasonable to assume that the cause lies within the hypothalamus or the pituitary. The pituitary may be the site of lactotroph hypertrophy and hyperplasia, a micro-adenoma or a macro-adenoma. Sixty-nine pregnancies in 53 patients, who required treatment of hyperprolactinaemia prior to the onset of pregnancy, have been observed. It is the purpose of this review to describe these patients, discuss the effects of pregnancy upon any pituitary lesion, and to discuss the effects of hyperprolactinaemia or the treatment of hyperprolactinaemia upon pregnancy. Based upon experience and the discussion of these data, recommendations for treatment of the hyperprolactinaemic pregnant patient will be made.

Adenoma↗
PubMed1986

Subtle abnormalities in follicular development and hormonal profile in women with unexplained infertility.

A prospective study of six unselected couples diagnosed as having unexplained infertility was done. In three of six patients, subtle abnormalities in follicular development were detected. In the first case poor follicular growth was observed. There was a premature small rise of luteinizing hormone (LH) with subsequent low levels of estradiol (E2) in the late follicular phase and unusual wide LH peak. This was followed by low progesterone levels in the luteal phase. In the second case follicular growth was abrupted by premature LH surge. This surge was triggered by early rise of E2 level while the follicle was still small in size. In the third case luteinized unruptured follicle syndrome was diagnosed, on ultrasound examination. All of the abnormalities were repetitive.

Adult↗
PubMed1985

The medical treatment of the hypersecreting pituitary gland.

Pituitary adenomas may produce local endocrine and neurological effects, as well as systemic metabolic complications due to hormonal hypersecretion. Medical therapy with pharmacological agents has been developed and is based on the neurotransmitter regulation of normal pituitary hormonal secretion. 189 patients with secretory pituitary adenomas underwent medical therapy for the hypersecretory state. 156 of these were prolactin-secreting adenomas, 16 of which were in males. The response of bromocriptine was almost universal with lowering of serum prolactin and reversal of the clinical symptoms, as well as tumor shrinkage of most large adenomas with suprasellar extension. 23 patients with acromegaly were treated with bromocriptine, with 11 noting clinical improvement, and decreased tumor size in two. Five patients with Cushing's disease were treated with cyproheptadine, with only one showing a biochemical and clinical improvement. Two patients with Nelson's syndrome each had progressive tumor growth stabilized with cyproheptadine and bromocriptine in one, and sodium valproate in the other. There appears to be a role for medical therapy in the majority of prolactin-secreting pituitary tumors, some growth hormone secreting pituitary tumors, and selected adrenocorticotropin secreting-pituitary tumors.

Adenoma↗
PubMed1985

Ovarian hyperstimulation with exogenous pulsatile gonadotropin releasing hormone therapy.

Two cases are reported of women with hypothalamic amenorrhea who had sonographic and biochemical evidence of ovarian hyperstimulation during the first cycle of exogenous pulsatile gonadotropin releasing hormone (GnRH) therapy. In one case, it was demonstrated that, with early detection, decrease in the dosage of GnRH may stabilize the condition and prevent further progression of the hyperstimulation. Therefore, the authors suggest that sonographic monitoring should be performed at least in the initial ovulatory cycle so that adjustment of the dosage of GnRH can be made with early detection of hyperstimulation.

Adult↗
PubMed1985

Ovulation induction and pregnancy in women with hypothalamic amenorrhea treated with intermittent gonadotropin-releasing hormone.

We induced ovulation in 34 cycles in 16 women following the administration of gonadotropin-releasing hormone (GnRH). In two patients two control cycles were induced. The patients self-administered GnRH through an indwelling intravenous catheter every 2 hours for 18 hours per day. In subsequent cycles the dose interval, dosage and infusion site, intravenous or subcutaneous, were varied. In all patients the estradiol, follicle-stimulating hormone and luteinizing hormone were measured, and follicular development was assessed ultrasonographically. Based on this preliminary study, a total of 34 cycles were studied in 16 women treated with 10 mg of self-administered GnRH intravenously every two hours during the day. Apparent ovulation was documented in all 34 cycles, and 11 pregnancies occurred. It appears that self-administered GnRH is economical and safe and achieves satisfactory results with respect to both ovulation and pregnancy.

Adult↗
PubMed1985

Potentiation of GnRH response by clomiphene citrate.

The method whereby clomiphene citrate (CC) induces ovulation in anovulatory women is not known. It probably binds to cytoplasmic estrogen receptors throughout the reproductive axis, with a central hypothalamic site postulated as a major center of action. Three patients who had severe hypothalamic amenorrhea and were clinically and biochemically unresponsive to CC alone had ovulation induced with the intermittent intravenous administration of gonadotropin-releasing hormone (GnRH). When CC was added to the GnRH, an enhanced secretory response of estradiol was demonstrated in all the patients. One patient demonstrated hyperstimulation, with large increments of estradiol and the development of multiple follicles, similar to what occurred with a larger dosage of GnRH alone. This finding suggests that CC may potentiate the response to GnRH, indicating that the action of CC is, at least in part, extrahypothalamic.

Adult↗
PubMed1984

The effect of a progestin on gallbladder function in young women.

Female sex hormones have been considered to be a risk factor for the development of cholesterol gallstone disease, because of increased cholesterol saturation of bile. Impaired gallbladder function is an additional factor which is suspect but unproved. We investigated gallbladder function in 10 young women on two occasions: first during the follicular phase of the menstrual cycle, when endogenous progesterone is low, and again after the ingestion of medroxyprogesterone acetate, 10 mg/day for 10 days, just prior to the next menstrual period. Another group, 15 young women, was studied during their luteal phase, when endogenous progesterone is high. Gallbladder filling and emptying in response to cholecystokinin (0.02 U/kg-min) was quantitated by 99mTc-HIDA cholescintigraphy. Gallbladder filling and emptying were no different in women in the follicular phase than in women in the luteal phase of the menstrual cycle. In both menstrual phases, the administration of the exogenous progestin significantly (p less than 0.05) reduced the fraction of hepatic bile entering the gallbladder. Gallbladder emptying was also depressed: the total amount ejected was less, the time to empty half the contents was prolonged, and the rate was slower (p less than 0.05). Thus, different phases of the normal menstrual cycle do not appear to have any effect on gallbladder function. Administration of an exogenous progestin, however, significantly impairs both gallbladder filling and emptying, factors which could predispose to the formation of cholesterol gallstones.

Adolescent↗
PubMed1983

Long-term follow-up of hyperprolactinemic women treated with bromocriptine.

Seventy-five women with hyperprolactinemia and demonstrable or suspected prolactinomas were treated with bromocriptine only and followed for 5 to 9 years. Biochemical, radiologic, and clinical responses were generally maintained in the long term, once established in the short term. Underlying mass effects on neurologic and pituitary function tended to improve, and no tumor progression was noted. Hypogonadal symptoms normalized in 68 of 75 women. Bromocriptine responses in long-term follow-up do not demonstrate any cumulative problems not seen in short-term therapy.

Adenoma↗
PubMed1982

The hyperprolactinemic polycystic ovary syndrome may not be an distinct entity.

Thirteen women with hyperprolactinemia and clinical stigmata of the polycystic ovary syndrome (PCO) had their serum prolactin (PRL) response to thyrotropin-releasing hormon (TRH) compared with two other groups of PCO. One PCO group had an elevated ratio of basal luteinizing hormone (LH) to follicle-stimulating hormone (FSH), and another had a normal ratio of basal LH to FSH. The PRL response to TRH was similar in hyperprolactinemic PCO and elevated LH PCO, and both were significantly greater than normal LH PCO and normal women. This suggests the hyperprolactinemic polycystic ovary (HPCO) is probably produced by similar central and/or peripheral mechanisms that result in the production of an elevated serum LH. These two features are probably associated in a common pathophysiologic mechanism. The HPCO syndrome does not appear to be a distinct entity but clinically must be differentiated from other causes of mild hyperprolactinemia.

Adolescent↗