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)

Twenty-four women, 11 with endometriosis and 13 with fibrocystic mastopathy, were treated with a medium dose (300-400 mg daily) of Danazol for 6 months. The circulating level of progesterone, the 34K insulin-like growth factor-binding protein (IGF-bp) and endometrial protein PP14 (placental protein 14) were measured by specific radioimmunoassays before and during treatment. The serum progesterone concentration decreased significantly during Danazol treatment, as did the serum levels of 34K IGF-bp and PP14. By the third month of therapy amenorrhoea was observed in 22 out of 24 women and this was accompanied by a further decline in the IGF-bp and PP14 levels. In light of the previous observations on the IGF-bp and PP14 synthesis by secretory endometrium and the fact that Danazol causes endometrial atrophy, these results suggest that Danazol treatment has an effect on endometrial protein secretion.
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PMID:The effect of Danazol on the circulating levels of 34K insulin-like growth factor-binding protein (PP12) and endometrial secretory protein PP14. 368 Apr 85

Insulin has been shown to regulate insulin-like growth factor-binding protein-1 (IGFBP-1) in vivo and in vitro. Insulin resistance is a feature of the polycystic ovary syndrome (PCOS). We have studied the relationship between insulin sensitivity (S1) and the circulating concentration of IGFBP-1 in a group of young women and in some who had PCOS. A case-control study has been carried out comparing reproductively normal women with women with PCOS (defined as women with oligo- or amenorrhea associated with androgen excess). Fifteen women with clinical PCOS and ten age- and weight-matched controls were studied. S1 was measured by the frequently sampled intravenous glucose tolerance test (FSIGT) using the minimal model technique. IGFBP-1, insulin-like growth factor-I (IGF-I) and growth hormone levels were measured before and during the FSIGT. Circulating testosterone, dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) levels were measured while the subjects were fasting. S1 and IGFBP-1 levels were significantly lower in the PCOS group than in controls (S1/10(-5) min-1/pM] mean +/- SE 3.8 +/- 0.8 vs. 8.5 +/- 1.3, p < 0.03; IGFBP-1 [ng/ml] mean +/- SE 26.6 +/- 4.2 vs. 56.0 +/- 5.9, p < 0.005). In women with PCOS, IGFBP-1 concentrations related negatively to the body mass index (BMI) (r = -0.77, p < 0.003) and positively to S1 (r = 0.76, p < 0.003). S1 remained a significant predictor of IGFBP-1 concentrations when controlled for BMI (combined r2 = 0.35, p < 0.05). No relationship was found between androgen levels and IGFBP-1. Insulin sensitivity contributed to the difference in IGFBP-1 levels found in women with PCOS. Whether the reduced concentrations of IGFBP-1 play a role in the pathophysiology of PCOS is uncertain, but it may act to alter delivery of IGF to peripheral tissues in insulin-resistant individuals.
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PMID:The relationship between insulin sensitivity and insulin-like growth factor-binding protein-1. 903 68

We investigated the relationship between the growth hormone and prolactin response to stimulation of growth hormone-releasing hormone (GHRH) and changes in body weight in pre- and postmenopausal women before and after 4 and 20 weeks of oral hormone replacement therapy (HRT). Ten postmenopausal women (with levels of follicle-stimulating hormone (FSH) of > 30 mIU/ml) were compared to ten premenopausal women suffering from post-pill amenorrhea (FSH < 10 mIU/ml). Both patient groups reported anamnestic body weight increases in the course of the former use of sex hormones. Additionally, ten postmenopausal women without anamnestic weight changes were studied. A significant reduction in the growth hormone response to GHRH was observed during the first month of HRT in women gaining weight, which was restored to pre-therapeutic levels after 6 months of HRT. A small but statistically significant increase in insulin-like growth factor (IGF)-I levels occurred in the course of HRT in all patients studied. These changes in growth hormone stimulation testing and IGF-I levels were accompanied by distinct changes in body weight. No reduction in the GHRH response was observed in those patients who did not gain body weight. Although GHRH stimulation induces a significant rise of prolactin concentrations in all patients before therapy no influence on prolactin levels could be demonstrated during HRT.
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PMID:Effects of estradiol valerate on growth hormone and prolactin response to growth hormone-releasing hormone stimulation in pre- and postmenopausal women. 908 39

Pregnancy in a woman with active acromegaly is very rare, because amenorrhea, due to hyperprolactinemia and disturbed pituitary gonadotropin secretion may cause infertility. We report a 28-year-old pregnant woman with untreated acromegaly, who was followed up from early pregnancy to delivery. Her pregnancy was uneventful, and she went into spontaneous labor at 38 weeks and delivered a normal infant. Her serum GH levels were further increased in late pregnancy, followed by decreased in postpartum periods, which may be associated with enlargement of pituitary adenoma during pregnancy. In contrast with serum GH, her serum insulin-like growth factor-1 (IGF-1) levels were dissociated with her serum GH levels during late pregnant and postpartum period. Her serum GH and IGF-1 levels in late pregnancy were different from the levels in pregnant women with acromegaly reported previously.
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PMID:A case of active acromegalic woman with a marked increase in serum insulin-like growth factor-1 levels after delivery. 915 23

The development of functional hypothalamic amenorrhea (FHA) in weight-stable, nonathletic women has long been thought to be psychogenic in origin. This study was designed to gain insight into the possibility that nutritional deficits and compensatory endocrine-metabolic adaptations contribute to the development and maintenance of FHA of the psychogenic type. Nutritional intake, insulin sensitivity, and 24-h dynamics of insulin/glucose, cortisol, leptin, somatotropic, and LH axes were simultaneously assessed in eight women with FHA not associated with exercise or weight loss and in eight age- and body mass index-matched regular cycling controls (NC). The percent fat body mass was lower and lean body mass was higher in FHA than in NC (P < 0.05). The FHA subjects scored higher (P < 0.05) on two Eating Disorder Inventory subscales and had a higher (P < 0.05) Beck depression rating than NC, although all were in the subclinical range. Although daily caloric intake did not differ, FHA consumed 50% less (P < 0.001) fat, twice (P < 0.05) as much fiber, and more carbohydrate (P < 0.05) compared to NC. During the feeding phase of the day, FHA exhibited lower glucose (P < 0.05) and insulin (P < 0.01) levels than NC, and the degree of hypoinsulinemia was directly related to relative dietary fat (r = 0.73). Although 24-h mean GH levels did not differ, the pattern of GH release in FHA was distinctly altered from that in NC. GH pulse amplitude was blunted, pulse frequency was accelerated 40% (P < 0.01), and interpulse GH concentrations were elevated 2-fold (P < 0.01) throughout the day for FHA compared to NC. This distorted pattern of GH pulses was associated with a 40% decrease (P < 0.01) in GH-binding protein levels. Levels of the insulin-dependent insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) were elevated (P < 0.001) during the feeding portion of the day in FHA and were inversely related to insulin (r = -0.50) and directly related to cortisol (r = 0.64) levels for FHA and NC groups together. Although levels of IGF-I and IGFBP-3 did not differ, the elevation of IGFBP-1 levels in FHA resulted in a reduced (P < 0.01) ratio of IGF-I/IGFBP-1, which may decrease the bioactivity and hypoglycemic effect of IGF-I. Twenty-four-hour mean leptin levels and the diurnal excursion of leptin in FHA did not differ from those in NC. LH pulse frequency was slowed 50% (P < 0.001) in FHA, with unaltered pulse amplitude, resulting in 45% lower (P < 0.01) 24-h mean LH levels for FHA compared to NC. LH pulse frequency for the two groups was related positively to insulin (r = 0.80) levels and the ratio of IGF-I/IGFBP-1 (r = 0.70) and negatively with cortisol (r = -0.61) and IGFBP-1 (r = -0.72) concentrations. In summary, we found evidence of subclinical eating disorders in weight-stable, nonathletic women with FHA accompanied by a severe restriction of dietary fat intake. Unbalanced nutrient intake in psychogenic FHA was associated with multiple endocrine-metabolic alterations. Among these, reduced levels of plasma glucose and serum GHBP, a decrease in the ratio of IGF-I/IGFBP-1, accelerated GH pulse frequency, and elevated interpulse GH levels are indicative of a hypometabolic state. In addition, the magnitude of glucoregulatory responses (increased cortisol secretion and decreased insulin/IGF-I action) were directly related to the degree of suppression of GnRH/LH pulse frequency. These results are remarkably similar to those seen in highly trained athletes with FHA(1). Thus, nutritional deficits may represent a common contributing factor to the development and maintenance of multiple neuroendocrine-metabolic aberrations underlying both psychogenic and exercise-related FHA.
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PMID:Nutritional and endocrine-metabolic aberrations in women with functional hypothalamic amenorrhea. 943 12

Controversial effects of weight reduction on gonadotropin secretion in obesity have been reported. As a result of pulsatility, single serum samples or frequent sampling studies are somewhat limited with regard to monitoring LH and FSH concentrations. We studied follicular phase nocturnal urinary (nu) LH and FSH secretion and glucose metabolism (150-min euglycemic hyperinsulinemic clamp) during 1 menstrual cycle/30-day period before and after weight reduction in 10 severely overweight infertility patients (age, 29 +/- 3.1 yr; body mass index, 37.1 +/- 3.3 kg/m2; +/-SEM). A 6-week very low calorie diet was followed by a 4-week normocaloric period. The urinary LH and FSH results reported represent samples taken 12 to 2 days before the LH surge, or 10 consecutive samples in the case of amenorrhea. We observed a decrease of 8% (P < 0.001) in percent body fat mass and a 5% (P < 0.005) reduction in waist to hip ratio. Mean nu-LH decreased by 45% [6.06 +/- 1.05 (+/-SEM) to 3.22 +/- 0.71 IU/L], whereas mean nu-FSH remained unchanged. Insulin-stimulated glucose uptake increased by 41% (P < 0.01), which was accounted for by a significant increase in nonoxidative glucose disposal (P = 0.003). Serum sex hormone-binding globulin concentrations increased by 39% (P < 0.01), and insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) levels increased by 46% (P < 0.05). Fasting serum insulin concentrations decreased by 38%, those of leptin by 37%, those of androstenedione by 32%, those of testosterone by 20% (all P < 0.01), and those of dehydroepiandrosterone sulfate by 13% (P < 0.05). The percent change in nu-LH correlated negatively with glucose uptake (r = -0.76; P < 0.01) and the increase in serum sex hormone-binding globulin (r = -0.85; P < 0.005) and positively with the percent change in waist to hip ratio (r = 0.79; P < 0.01). The absolute nu-LH levels after weight reduction correlated significantly with fasting insulin concentrations (r = 0.88; P < 0.001) and negatively with glucose uptake (r = -0.67; P < 0.05). No significant relationships were found between absolute levels or changes in nu-LH concentrations and leptin, IGF-I, IGFBP-3, or IGFBP-1 concentrations. Our findings suggest that weight reduction with a very low calorie diet results in a decrease in nu-LH concentrations, a reduction in the LH/FSH ratio, and FSH predominance favoring folliculogenesis. The decrease in LH concentrations is inversely related to the severity of insulin resistance. It is possible that the decrease in LH secretion with weight reduction is more dependent on the absolute levels of insulin sensitivity than on the degree of general adiposity.
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PMID:The decrease in luteinizing hormone secretion in response to weight reduction is inversely related to the severity of insulin resistance in overweight women. 1099 21

Adolescence is a period of rapid skeletal growth during which nearly half of the adult skeletal mass is accrued. This life stage is a window of opportunity for influencing peak bone mass and reducing the risk of osteoporosis later in life. Endocrine factors that may influence peak bone mass include insulin-like growth factor-1, which regulates skeletal growth, and gonadotropic hormones, which stimulate epiphyseal maturation. Estrogen deficiency and amenorrhea can reduce skeletal mass. Weight-bearing exercise can increase bone mass. Appropriate mineralization of the skeleton requires adequate dietary intakes of minerals involved in the formation of hydroxyapatite; the most likely to be deficient is calcium.
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PMID:Adolescence: the period of dramatic bone growth. 1201 3

Disruption of the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis has been reported and studied in menopause, hypothalamic amenorrhea, and anorexia nervosa, but not in weight-stable amenorrheic athletes. We investigated the effects of short-term transdermal estradiol on basal and exercise-stimulated serum GH, IGF-1, and associated binding proteins (IGFBP-1 and IGFBP-3) in seven weight-stable female amenorrheic athletes with percentage body fats greater that 12%. Each subject received a 72 h placebo patch followed by 144 h of transdermal estradiol. Serum samples for GH, IGF-1, IGFBP-1, and IGFBP-3 were obtained at baseline (t1), 72 hr (t2), 144 hr (t3), and during three 90-minute trials of aerobic exercise. Basal, and exercise GH, IGF-1, and IGFBP-1 were not different between trials. Baseline IGFBP-3 decreased from t1 to t2 (p = 0.04) and serum free fatty acids increased from t1 to t2, and t1 to t3 (p = 0.04, and 0.02 respectively). These findings differ from postmenopausal women, and women having weightloss-associated amenorrhea, suggesting that estrogen, exercise, and nutritional deficiencies may have independent effects on the GH/IGF-1 axis.
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PMID:Estradiol effects on the growth hormone/insulin-like growth factor-1 axis in amenorrheic athletes. 1267 Nov 96

A 40-year-old female presented with growth hormone (GH)-secreting pituitary adenoma associated with primary moyamoya disease manifesting as amenorrhea, acromegaly, and transient ischemic attack. Magnetic resonance (MR) imaging revealed a tumor mass extending from the sella turcica to the suprasellar cistern, and MR angiography demonstrated stenoses in the bilateral internal carotid arteries with basal moyamoya vessels. Her blood GH and insulin-like growth factor (IGF-1) levels were elevated to 78.94 and 923.0 ng/ml, respectively. The patient underwent removal of the pituitary adenoma because her ischemic symptoms disappeared after oral aspirin medication. Subtotal resection resulted in persistence of the high blood GH and IGF-1 levels. Postoperative MR angiography showed progression of the stenoses in the bilateral internal carotid arteries. Excess systemic GH and IGF-1 may participate in the progression of vascular disease and so could have caused the deterioration of the moyamoya disease.
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PMID:Growth hormone-secreting pituitary adenoma associated with primary moyamoya disease--case report. 1292 97

The kinetics of cervical and circulating phosphoisoforms of insulin-like growth factor-binding protein-1 (IGFBP-1) in normal and pathological early pregnancy are not well known. We investigated the profiles of IGFBP-1 in serum and in cervical secretion during medical termination of early pregnancy. Sixteen women requesting termination of pregnancy, with <63 days of amenorrhoea, received 200 mg of mifepristone on day 0, followed by either oral or vaginal administration of 0.8 mg of misoprostol on day 2. Serum and cervical swab samples, collected up to 6 weeks following the beginning of the treatment, were analysed for IGFBP-1 using two immunoenzymometric assays recognizing different patterns of IGFBP-1 phosphoisoforms. Serum mifepristone was also assayed. In the cervical samples, IGFBP-1 concentration, measured with both assays, increased substantially 2 days following administration of mifepristone. At 3 h after administration of misoprostol, IGFBP-1 had further increased several-fold in the cervix, but the increase was more pronounced as measured by the assay with preference for the amniotic fluid isoforms of IGFBP-1. A strong negative correlation was found between the time to abortion and the increase in cervical IGFBP-1 after administration of misoprostol, as measured by the assay preferring the phosphorylated isoforms of IGFBP-1. At 6 weeks, IGFBP-1 in the cervix had decreased to lower than pre-treatment levels, as measured by both assays. In serum, both assays showed a significant increase in IGFBP-1 concentrations after administration of mifepristone, and the highest values were measured on day 2, already before misoprostol administration. Thus, the kinetics of circulating and cervical IGFBP-1 differed from each other, indicating different sources and regulation of serum and cervical IGFBP-1.
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PMID:Differential kinetics of serum and cervical insulin-like growth factor-binding protein-1 during mifepristone-misoprostol-induced medical termination of early pregnancy. 1466 8


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