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Biomedical subjects

B Corenblum

Publications and source records attributed to B Corenblum.

At least 19 recordsLinked to original sources
PubMed1991

Recurrent hypoglycemia secondary to drug-dispensing error.

We present three patients who developed hypoglycemia due to inadvertent dispensing of sulfonylurea drugs. Each patient had a similar clinical course characterized by hypoglycemia that remitted during hospitalization and recurred after discharge. The cause of the hypoglycemia was determined only after close inspection of the patients' medications, not the label on the container. Our experience suggests that hypoglycemia due to drug-dispensing error may be more common than is generally recognized.

Aged↗
PubMed1990

Asymptomatic hyperprolactinemia resulting from macroprolactinemia.

Five patients are presented who had moderate hyperprolactinemia as measured by RIA. The patients did not have any symptoms or signs that result from hyperprolactinemia, nor evidence of any underlying cause of hyperprolactinemia. Because of the lack of clinical features, laboratory search for macroprolactinemia was undertaken. In these patients no further investigation or therapy is indicated.

Adolescent↗
PubMed1990

Medical therapy for the syndrome of familial virilization, insulin resistance, and acanthosis nigricans.

UNLABELLED: In the syndrome of familial virilization, insulin resistance, and acanthosis nigricans, the interrelationships are not understood. Twin sisters were studied, along with a lesser affected sister and mother. They manifested amenorrhea, hirsutism, masculinization, hypertension, hyperinsulinemia, hypertriglyceridemia, and hyperprolactinemia. Medical therapy with a gonadotropin-releasing hormone agonist plus an antiandrogen resulted in reversal of the hirsutism, yet with preservation of potential fertility. In response to luteinizing hormone (LH) and follicle-stimulating hormone suppression, there was normalization of the serum androgens, but not of the hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, hypertension, or acanthosis nigricans. CONCLUSIONS: (1) This syndrome may be familial. (2) Medical therapy for the virilization is successful. (3) The hyperandrogenemia is primarily LH dependent and not primarily insulin dependent, although insulin may have an amplification effect. (4) Hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, and the hypertension are not androgen dependent.

Acanthosis Nigricans↗
PubMed1989

Hyperprolactinemia in hepatic encephalopathy may result from impaired central dopaminergic neurotransmission.

Ten patients with liver disease and hepatic encephalopathy (HE) and eight normal controls were studied. Five of the 10 HE patients had hyperprolactinemia. The administration of L-dopa produced a decrease of serum prolactin in all. Prior administration of Carbidopa, a peripheral decarboxylase inhibitor, did not change the prolactin suppression by L-dopa in the normal controls or in the patients with normal baseline prolactin levels. In the hyperprolactinemic group, Carbidopa significantly inhibited the response to L-dopa. Impaired central neurotransmission, at least involving the hypothalamic-pituitary dopaminergic system, may underlie the hyperprolactinemia in HE.

Adult↗
PubMed1988

Septuplet gestation following the use of human menopausal gonadotropin despite intensive monitoring.

Despite this good correlation supporting only four follicles, seven gestational sacs developed. The cause is unknown, but oocyte division cannot be ruled out. This case demonstrates that there are no absolute criteria for preventing high multiple pregnancies. While sophisticated cycle tracking using ultrasound and E2 values may alert the clinician to the development of multiple follicles, thus permitting discontinuation of the treatment, this report emphasizes that multiple gestations exceeding the anticipated number of follicles remains a possibility.

Adult↗
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↗