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Query: UMLS:C0002453 (amenorrhea)
 6,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia nervosa (AN), a psychosomatic disorder, has serious negative effects on multiple organs and systems of the human body. A large number of endocrine and metabolic anomalies have been described, including amenorrhea/oligomenorrhea, delayed puberty, hypothyroidism, hypercortisolism, and alterations in the growth hormone (GH) axis and bone metabolism. The role of different peptides, including ghrelin, leptin, neuropeptide Y and serotonin, in the regulation of appetite is discussed. In addition, isolated hypogonadotropic hypogonadism that occurs in these patients is analyzed in detail, as well as the abnormalities in the growth hormone axis. Alterations in bone mineral density, bone markers and the degree of osteopenia in these patients, depending on the age at which amenorrhea began and its duration, are also discussed. Finally, our current understanding of the possible benefits of treatment with estrogens and progestogens is also analyzed.
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PMID:New concepts in anorexia nervosa. 1513 10

Anorexia Nervosa (AN) is a psychiatric disorder characterized by the classic triad: amenorrhea, weight loss, and behavioral changes. It is generally seen in young, white women under 25 and is particularly common in adolescence. The mortality of the disease varies between 5.1% and 13%. The endocrine changes associated with AN have been studied in depth and provide strong evidence for hypothalamic dysfunction. All are secondary and reverse with weight gain. In general, gonadotropin (FSH, LH) levels are decreased in patients with AN, as well as the response to Gonadotropin releasing hormone (GnRH). Fasting growth hormone levels are elevated, but the stimulated response of Growth hormone (GH) to Growth hormone releasing hormone (GHRH) is normal and inversely correlated to body weight. Serum Growth hormone binding protein (GHBP), insulin growth factor I (IGF-I) and IGF binding protein (IGFBP) - 3 levels are all significantly decreased in patients with AN and return to normal with refeeding. IGFBP-1 and 2 are increased and return also to normal with weight gain. Serum IGF-II is decreased but not significantly. The IGFBP-3 proteolytic activity is normal. Thyroxine (T4) and Triiodothyronine (T3) while reverse T3 (rT3) is elevated. Thyrotropin stimulating hormone (TSH). TSH levels are normal with a delayed response to thyrotropin releasing hormone (TRH). Cortisol levels are normal or elevated as well as urinary free cortisol. Corticotropin (ACTH) levels are normal with decreased response to Corticotropin releasing hormone (CRH). Dexamethasone suppression test is abnormal. Sex steroids are decreased. Finally leptin levels are decreased in patients with AN while ghrelin levels are elevated. Both leptin and ghrelin levels return to control values after renutrition.
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PMID:Endocrine abnormalities in Anorexia Nervosa. 1643 12

Patients with anorexia nervosa (AN) may develop multiple endocrine abnormalities, including amenorrhea, hyperactivity of the hypothalamus-pituitary-adrenal axis, hypothyroidism and particular changes in the activity of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis. Exaggerated GH secretion and reduced IGF-I levels are usually found in AN, as well as in conditions of malnutrition and malabsorption, insulin-dependent diabetes mellitus, liver cirrhosis and catabolic states. In AN, GH hypersecretion at least partially reflects malnutrition-induced peripheral GH resistance, which leads to reduced IGF-I synthesis and release; this implies an impairment of the negative IGF-I feedback action on GH secretion. On the other hand, primary alterations in the neural control of GH secretion cannot be ruled out. The neuroendocrine alterations include enhanced somatotroph responsiveness to growth hormone releasing hormone (GHRH) and impaired GH response to most central nervous system-mediated stimuli. Particular resistance to cholinergic manipulation has also been demonstrated, thus suggesting a somewhat specific alteration in the somatostatin (SS)-mediated cholinergic influence on GH secretion. Moreover, paradoxical GH responses to glucose load, thyrotropin releasing hormone (TRH) and luteinizing hormone releasing hormone (LHRH) have also been reported. The effect of reduced leptin levels on GH hypersecretion in AN is still unclear, but ghrelin (the gastric hormone that is a natural ligand of the GH secretagogue receptor and strongly stimulates somatotroph secretion) is thought to play a major role. Regardless of the supposed central and peripheral alterations, it has to be emphasised that the activity of the GH/IGF-I axis in AN is generally restored by nutritional and stable weight gain. It therefore reflects an impaired nutritional state and cannot be considered a primary hallmark of the disease.
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PMID:GH/IGF-I axis in anorexia nervosa. 1764 63

Reproduction is a physiologically costly process that consumes significant amounts of energy. The physiological mechanisms controlling energy balance are closely linked to fertility. This close relationship ensures that pregnancy and lactation occur only in favourable conditions with respect to energy. The primary metabolic cue that modulates reproduction is the availability of oxidizable fuel. An organism's metabolic status is transmitted to the brain through metabolic fuel detectors. There are many of these detectors at both the peripheral (e.g., leptin, insulin, ghrelin) and central (e.g., neuropeptide Y, melanocortin, orexins) levels. When oxidizable fuel is scarce, the detectors function to inhibit the release of gonadotropin-releasing hormone and luteinizing hormone, thereby altering steroidogenesis, reproductive cyclicity, and sexual behaviour. Infertility can also result when resources are abundant but food intake fails to compensate for increased energy demands. Examples of these conditions in women include anorexia nervosa and exercise-induced amenorrhea. Infertility associated with obesity appears to be less related to an effect of oxidizable fuel on the hypothalamic-pituitary-ovarian axis. Impaired insulin sensitivity may play a role in the etiology of these conditions, but their specific etiology remains unresolved. Research into the metabolic regulation of reproductive function has implications for elucidating mechanisms of impaired pubertal development, nutritional amenorrhea, and obesity-related infertility. A better understanding of these etiologies has far-reaching implications for the prevention and management of reproductive dysfunction and its associated comorbidities.
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PMID:Metabolic fuel and clinical implications for female reproduction. 1797 92

Functional hypothalamic amenorrhea (FHA) is defined as a non-organic and reversible disorder in which the impairment of gonadotropin-releasing hormone (GnRH) pulsatile secretion plays a key role. There are main three types of FHA: stress-related amenorrhea, weight loss-related amenorrhea and exercise-related amenorrhea. The spectrum of GnRH-luteinizing hormone (LH) disturbances in FHA is very broad and includes lower mean frequency of LH pulses, complete absence of LH pulsatility, normal-appearing secretion pattern and higher mean frequency of LH pulses. Precise mechanisms underlying the pathophysiology of FHA are very complex and unclear. Numerous neuropeptides, neurotransmitters and neurosteroids play important roles in the physiological regulation of GnRH pulsatile secretion and there is evidence that different neuropeptides may be involved in the pathophysiology of FHA. Particular attention is paid to such substances as allopregnanolone, neuropeptide Y, corticotropin-releasing hormone, leptin, ghrelin and beta-endorphin. Some studies reveal significant changes in these mentioned substances in patients with FHA. There are also speculations about use some of these substances or their antagonists in the treatment of FHA.
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PMID:Functional hypothalamic amenorrhea: current view on neuroendocrine aberrations. 1822 38

Adolescence is a critical time for bone mass accrual, and increases in bone mass through puberty are dependent on rising levels of gonadal steroids, growth hormone and insulin like growth factor-1. Many high school girls are involved in athletic activities, and as many as 23.5% of adolescent athletes have been reported to develop amenorrhea. This review focuses on (1) factors that determine which athletes are likely to develop amenorrhea, such as a negative energy balance state, low levels of leptin and high levels of ghrelin, and (2) the impact of hypogonadism in athletes on bone metabolism. Beneficial effects of increased mechanical loading from athletic activity do not appear to protect against the deleterious effects of hypogonadism in adolescent athletes.
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PMID:Bone density in the adolescent athlete. 1840 4

Caloric restriction caused by undernutrition or over-exercise is increasingly common and has significant health consequences such as hypothalamic amenorrhea, infertility, attainment of low peak bone mass, and bone loss leading to fracture. In these patients, the pathophysiology of amenorrhea and bone loss is multifactorial, involving hormones that integrate the nutritional state with the hypothalamic-pituitary-ovarian axis, including leptin and possibly ghrelin. The pathophysiology of bone loss includes nutritional deficiencies, possibly estrogen deficiency, and direct and indirect effects of leptin on bone. Identifying patients at risk for low bone mineral density and fracture is important, as is screening with dual energy radiograph absorptiometry. Treatment has focused on oral contraceptive use, yet improved bone mineral density is marked by nutritional recovery and anovulation reversal. Therefore, resolving the nutrition deficiency should be the cornerstone of treatment. Cognitive-behavioral therapy aims for weight recovery, which can lead to reversal of amenorrhea and improvement in other associated metabolic abnormalities. During treatment, estradiol levels can be followed to assess hypothalamic-pituitary-ovarian recovery because estradiol secretion may increase well before ovulation occurs. In patients failing the above interventions, hormone replacement should be considered, but bone mineral density should be followed because patients may continue to lose bone despite treatment with oral contraceptives if nutrition is not improved.
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PMID:Anorexia, bulimia, and the athletic triad: evaluation and management. 1843 Mar 90

We compared bone mineral density (BMD) and content (BMC), menstrual and metabolic status between physically active women with 1) high cognitive dietary restraint (High-CDR) (score > or = 9, n=38) and Normal-CDR (score<9, n=46) and 2) across quartiles of CDR scores. Eighty-four physically active (500+/-35 min wk(-1)) premenopausal women participated and were categorized according to their CDR score. Primary outcomes included, BMD, BMC, menstrual status, estrone-3-glucuronide (E1G) and pregnanediol-3-glucuronide (PdG) area under the curve (AUC). Secondary outcomes included resting energy expenditure (REE), total triiodothyronine, and ghrelin. Measures of body mass (59.2+/-1.1 vs. 58.5+/-1.0 kg) and percent body fat (24.7+/-1.2 vs. 23.7+/-0.7%) were similar between women with Normal-CDR and High-CDR, however the High-CDR group had lower total body (1.140+/-0.011 vs. 1.179+/-0.010 g cm(-2); p=0.015) and lumbar spine (1.114+/-0.019 vs. 1.223+/-0.022 g cm(-2); p=0.001) BMD. The prevalence of oligo-amenorrhea was higher in the High-CDR group and became increasingly greater across the CDR quartiles. There were no differences in metabolic characteristics between the High-CDR and Normal-CDR groups, however REE and the ratio of measured to predicted REE were lower in the fourth quartile (CDR scores > or = 13) compared to the second and third quartiles. Our results provide evidence that high CDR scores are associated with reduced lumbar spine and total body BMD in physically active premenopausal women. A greater frequency of menstrual disturbances in women with higher CDR scores likely played a role in the reduced total body and lumbar spine BMD.
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PMID:Cognitive dietary restraint: impact on bone, menstrual and metabolic status in young women. 1850 99

The purpose of this study was twofold: (1) to determine if gastrointestinal hormones, associated with energy intake and energy balance, are altered in exercising women with hypothalamic amenorrhea and (2) to assess the association between gastrointestinal hormones and behavioural indicators of subclinical disordered eating in exercising women with hypothalamic amenorrhea. This cross-sectional study analyzed serum ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1), menstrual status (by E1G and PdG), resting energy expenditure (REE), and subclinical eating behaviours in sedentary ovulatory (SedOv), exercising ovulatory (ExOv), and exercising amenorrheic (ExAmen) women. Groups were similar with respect to age (23.8+/-0.6 years) and BMI (21.4+/-0.3 kg/m(2)). The ratio of REE to predicted REE (REE:predicted REE) was 0.94+/-0.02, 0.94+/-0.02, and 0.88+/-0.02 in the SedOv, ExOv, and ExAmen groups, respectively. The REE:predicted REE in the ExAmen group was consistent with an energy deficiency. LogPYY, ghrelin, dietary cognitive restraint, and drive for thinness were elevated in the ExAmen group compared to other groups. GLP-1 concentrations were similar among groups. LogPYY correlated with drive for thinness and REE/FFM. In conclusion, fasting PYY and ghrelin concentrations are elevated in exercising women with FHA and both gastrointestinal peptides may serve as a proxy indicator of energy deficiency in this population.
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PMID:Elevated PYY is associated with energy deficiency and indices of subclinical disordered eating in exercising women with hypothalamic amenorrhea. 1892 7

To date, the predominant mechanism underlying menstrual disturbances in exercising women supports an underlying energy deficiency-related aetiology, in which a failure to compensate dietary intake for the energy cost of exercise suppresses reproductive function. Increasing evidence demonstrates that energy deficiency plays a causal role in the induction of amenorrhoea in exercising women, and consistent with this mechanism are findings of glucoregulatory perturbations such as low triiodothyronine, reduced insulin secretion and elevated cortisol, growth hormone and ghrelin levels. The menstrual disturbance that may differ in its energetic characteristics and, perhaps in its androgenic and ovarian steroid environment, is oligomenorrhoea. We conducted a systematic review of the literature to begin to understand whether oligomenorrhoea in exercising women is a mild subclinical phenotype of polycystic ovarian syndrome (PCOS) in which exercise is conferring beneficial effects in protecting women from the classic PCOS phenotype, or whether oligomenorrhoea is part of the spectrum of menstrual disturbances caused by an energy deficiency that is often reported in exercising women with menstrual disturbances. We included observational, randomized controlled trials and cross-sectional studies that reported clinical, hormonal and metabolic profiles in exercising women with amenorrhoea or oligomenorrhoea and in women with PCOS. Previous studies examining the underlying mechanisms and consequences of exercise-associated menstrual disturbances have grouped exercising amenorrhoeic and oligomenorrhoeic women into a single group, and have relied primarily on self-reported menstrual history. Although scarce, the data available to date suggest that hyperandrogenism, such as that observed in PCOS, may likely be associated with oligomenorrhoea in exercising women, and may not always represent hypothalamic inhibition secondary to an energy deficiency. It is critical to closely examine the metabolic and endocrine status of women with menstrual disturbances because the treatment strategies for energy deficiency-related menstrual disturbances differ from that of disturbances traceable to hyperandrogenaemia. Further investigation is necessary to explore whether different endocrine aetiologies underly menstrual disturbances, particularly oligomenorrhoea, in physically active women.
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PMID:Oligomenorrhoea in exercising women: a polycystic ovarian syndrome phenotype or distinct entity? 1990 85


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