Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002453 (amenorrhea)
 6,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with hypothalamic amenorrhoea and a poor response in terms of pituitary growth hormone (GH) to acute administration of growth hormone-releasing factor has been treated with pulsatile gonadotrophin-releasing hormone (GnRH) combined with GH to induce ovulation. GH was administered daily until signs of ovulation were detected. The luteal phase was supported by pulsatile GnRH only. Combined treatment gave an improved follicular recruitment, higher plasma levels of 17 beta-oestradiol and an earlier ovulation, compared to the previous cycle with pulsatile GnRH only. The result was a twin pregnancy which ended with the birth of two healthy male babies. The role of GH in potentiating the ovarian response to gonadotrophins, as well as the GH secretion abnormalities associated with dysfunctions of the hypothalamic - pituitary - gonadal axis, might provide a rationale for combined GH and pulsatile GnRH treatment in such patients.
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PMID:Pregnancy following combined growth hormone--pulsatile GnRH treatment in a patient with hypothalamic amenorrhoea. 211 57

The effects of cholinergic muscarinic receptor antagonist pirenzepine on the GHRH-induced GH release were studied in 10 adolescent females with anorexia nervosa at different stages of the disease, in 5 adolescent females with eating disorders and in 5 normal adolescents. The patients were characterized according to psychological (DSM III-R), endocrinological (GnRH test), nutritional (Somatomedin-C, T3), and clinical (% IBW, duration of the amenorrhoea) criteria. On two separate occasions, each subject received an i.v. bolus injection of GHRH 1-40 (1 microgram/kg) alone or preceded by pirenzepine (0.6 mg/kg i.v. 5 min before GHRH 1-40). GHRH 1-40 injection induced a significantly (P less than 0.05) higher GH increase in the patients with anorexia nervosa at the acute stage as compared with the controls. Pirenzepine did not abolish opportunely the exaggerated GH response to GHRH 1-40 in anorectic patients at the acute stage unlike the control, who showed the blockade of GHRH-induced GH release by the cholinergic muscarinic antagonist (P less than 0.05). The anorectic adolescents at the non acute stage and the adolescents with eating disorders showed varying reductions of GH response; however, pirenzepine produced a blunted suppression of GHRH-induced GH increase as compared to the controls, which was not statistically significant. Somatomedin-C values were significantly (P less than 0.05) lower in anorectic patients at the acute stage as compared with controls. The abnormal activity of cholinergic system in anorectic patients, as our data show, could induce the GH hypersecretion through an inhibitory influence on the somatostatinergic function. The reduced somatomedin-C levels, a specific malnutrition index in anorectic patients, produce a modified feed-back on the hypothalamic site (somatostatin) and/or directly on the pituitary, following the GH hypersecretion.
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PMID:Effects of cholinergic muscarinic antagonist pirenzepine on GH response to GHRH 1-40 in patients with anorexia nervosa. 211 57

We studied growth hormone (GH) levels in 14 adolescents with anorexia nervosa (AN), 12-20 years of age. All had amenorrhea and the duration of symptoms ranged from 2-24 months. There was no difference in unstimulated GH between the girls with AN and endocrinologically normal girls. However, the GH response to the alpha-adrenergic agent clonidine was blunted (less than 10 ng/ml) in 11 of 14 girls with AN. Our results of a normal basal GH level and blunted response to stimulation is in contrast to some reports of high basal GH levels and an exaggerated response to pituitary stimulation although it agrees with other studies. Our patient population was younger and at an earlier stage of the disease (12 with symptoms for less than 1 year) than the AN patients previously reported to have elevated GH secretion. In view of studies that report an elevated GH response to growth hormone releasing factor, our results suggest that the AN patient's abnormalities in GH secretion may result from an abnormal hypothalamic response to adrenergic stimuli. This hypothalamic abnormality might also contribute to the growth failure seen in adolescent girls with AN.
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PMID:Blunted growth hormone responses to clonidine in adolescent girls with early anorexia nervosa. Evidence for an early hypothalamic defect. 231 12

To further elucidate the neuroendocrine regulation of anterior pituitary function in women with functional hypothalamic amenorrhea (FHA), we measured serum LH, FSH, cortisol, GH, PRL, TSH concentrations simultaneously at frequent intervals for 24 h in 10 women with FHA and in 10 normal women in the early follicular phase (NC). Using the same data, we separately analyzed the cortisol-PRL responses to meals in these women. In addition, the pituitary responses to the simultaneous administration of GnRH, CRH, GHRH, and TRH were assessed in 6 FHA and 6 normal women. The 24-h secretory pattern of each hormone except TSH was altered in the women with FHA. Compared to normal women, the women with FHA had a 53% reduction in LH pulse frequency (P less than 0.0001) and an increase in the mean LH interpulse interval (P less than 0.01); LH pulse amplitude was similar. The 24-h integrated LH and FSH concentrations were reduced 30% (P = 0.01) and 19% (P less than 0.05), respectively. The mean cortisol pulse frequency, amplitude, interpulse interval, and duration were similar in the two groups, but integrated 24-h cortisol secretion was 17% higher in the women with FHA (P less than 0.05). This increase was greatest from 0800-1600 h, but also was present from 2400-0800 h. Cortisol levels were similar in the two groups from 1600-2400 h, resulting in an amplified circadian excursion. In contrast, the 24-h serum PRL levels were markedly lower at all times (P less than 0.0001), the sleep-associated nocturnal elevation of PRL was proportionately greater (P less than 0.05), and serum GH levels were increased at night in the women with FHA (P less than 0.05). Although 24-h serum TSH levels were similar at all times, T3 (P less than 0.05) and T4 (P less than 0.01) levels were lower in the FHA women. The responses of serum cortisol to lunch (P less than 0.01) and dinner (P less than 0.05) and those of serum PRL to lunch (P less than 0.05) and dinner (P = 0.08) were blunted in the women with FHA. Pituitary hormone increments in response to the simultaneous iv administration of GnRH, CRH, GHRH, and TRH were similar in the two groups, except for a blunted PRL response to TRH in the women with FHA (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine aberrations in women with functional hypothalamic amenorrhea. 249 24

A 29 year old woman with an enlarged pituitary fossa and classical acromegaly, possibly present for ten years, had biochemical and partial somatic resolution of the disorder after removal of a bronchial carcinoid tumour. In addition, galactorrhea stopped, menstruation returned after two years, and amenorrhea and elevated prolactin levels fell towards normal. Immunocytochemistry showed numerous growth hormone releasing factor (GRF) staining cells in the tumour. The tumour cells, when cultured, produced a supernatant selectivity stimulating human pituitary somatotrophic cell cultures to produce growth hormone (GH). The bronchial carcinoid did not secrete detectable GH, but extracts of it, and preoperative serum contained GRF immunoreactivity which coeluted with synthetic human pancreatic GRF.
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PMID:Resolution of acromegaly after removal of a bronchial carcinoid shown to secrete growth hormone releasing factor. 311 10

The authors report the case of a 35-year-old acromegalic woman who developed amenorrhea and decreased left vision, and who was found to have suprasellar and pulmonary hemangiopericytomas. Total removal of the suprasellar hemangiopericytoma resulted in normalization of the plasma human growth hormone (GH) level and a marked decrease in size of the pulmonary hemangiopericytoma. Immunoperoxidase studies for GH and human hypothalamic growth hormone-releasing factor (GHRF) demonstrated immunoreactive intracellular GH only in the suprasellar hemangiopericytoma, with no immunoreactive intracellular GHRF evident in either the suprasellar or pulmonary hemangiopericytoma.
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PMID:Acromegaly associated with suprasellar and pulmonary hemangiopericytomas. Case report. 392 70

A 48-year-old female presented with acromegaly, amenorrhea and hyperthyroidism associated with high serum free T4 levels and measurable TSH concentrations. The administration of GHRH induced significant increases in GH, PRL and TSH. Conversely, intravenous infusion of dopamine or oral administration of bromocriptine effectively inhibited GH, PRL and TSH secretion. Serum alpha-subunit levels were neither affected by GHRH, dopamine nor bromocriptine. Transsphenoidal surgery was performed and immunostaining of the tissue showed that the adenoma cells were positive for GH, PRL or TSH. The patient was treated with bromocriptine at a daily oral dose of 10 mg after surgery. Serum TSH were initially suppressed but returned within reference intervals with persistent normalized free T4 levels. Serum PRL became undetectable and GH levels were stable around 6 ng/ml except the periods of poor drug compliance, when serum TSH, GH and PRL levels rose considerably. The patient was followed-up for 10 years without any change in the residual adenoma tissues as detected by magnetic resonance imaging. These findings suggest that long-term bromocriptine therapy is effective in treating the hypersecretory state of a plurihormonal adenoma secreting TSH, GH and PRL.
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PMID:Long-term treatment with bromocriptine of a plurihormonal pituitary adenoma secreting thyrotropin, growth hormone and prolactin. 1042 81

Amenorrheic athletes exhibit a spectrum of neuroendocrine disturbances, including alterations in the GH-insulin-like growth factor I (IGF-I) axis. Whether these changes are due to exercise or amenorrhea is incompletely characterized. The present study investigates spontaneous (overnight) and exercise-stimulated GH secretion and associated IGF-binding proteins (IGFBPs) in amenorrheic (AA; n = 5), and eumenorrheic athletes ( n = 5) matched for age, percent body fat (dual energy x-ray absorptiometry), training history, and maximal oxygen consumption. Each volunteer participated in two hospital admissions consisting of a 50-min submaximal exercise bout (70% maximal oxygen consumption) and an 8-h nocturnal sampling period. Deconvolution analysis of serum GH concentration time series revealed increases in the half-life of GH (60%) and the number of secretory bursts (85%) as well as a decrease in their half-duration (50%) and the mass of GH secreted per pulse (300%) in the AA cohort. Time occupancy at elevated trough GH concentrations was significantly increased, and GH pulsatility (approximate entropy) was more irregular in the AA group. During exercise, AA exhibited a reversal of the normal relationship between IGF-I and GH, and a 4- to 5-fold blunting of stimulated peak and integrated GH secretion. Fasting levels of plasma IGF-I, IGFBP-3, and IGFBP-1 appeared to be unaffected by menstrual status. In ensemble, this phenotype of GH release in amenorrheic athletes suggests disrupted neuroregulation of episodic GH secretion, possibly reflecting decreased somatostinergic inhibition basally, and reduced GHRH output in response to exercise compared with eumenorrheic athletes. Accordingly, we postulate that the amenorrheic state, beyond the exercise experience per se, alters the neuroendocrine control of GH output in amenorrheic athletes.
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PMID:Increased pulsatility, process irregularity, and nocturnal trough concentrations of growth hormone in amenorrheic compared to eumenorrheic athletes. 1123 79