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)

Bone density of lumbar vertebrae (L2 to L4) and the whole body in 29 patients with anorexia nervosa were measured by dual photon absorptiometry, and the results were compared with those of 10 age-matched normal controls. The patients had significantly lower bone mineral density (BMD) in L3 and L2-4 than controls. However, there was no difference in whole-body BMD. L3 and L2-4 BMD was positively correlated with body weight and was negatively correlated with duration of illness and amenorrhea. Patients who had been more active 6 months before the time of the study had significantly higher L3 BMD than the less active patients. Most patients had an abnormally low serum estrogen level, whereas the mean serum levels of thyroid hormone (T3, T4), cortisol, calcitonin, parathyroid hormone and vitamin D were within the normal range. No correlation was found between L3 or L2-4 BMD and the levels of these hormones. These results suggest that severe weight loss, low physical activity, longer duration of amenorrhea and deficiency of estrogen contribute to bone loss in patients with anorexia nervosa, whereas calcium-regulating hormones such as parathyroid hormone, calcitonin and vitamin D are unlikely to be a primary contributor to bone loss.
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PMID:Reduced bone density and major hormones regulating calcium metabolism in anorexia nervosa. 148 25

The prevention of female osteoporosis is based on: a) promoting the achievement of optimal bone mass at the time of menopause; b) minimizing subsequent rarefaction especially in fast bone losers. Both these objectives can be partly attained by appropriate behaviour (balanced diet with adequate calcium intake, physical exercise) but often with additional preventive treatment that is undoubtedly easier to undertake since the introduction of new therapeutic approaches like the use of transdermal estradiol (TDE) and the salmon calcitonin (CT) nasal spray. Certain situations, chronic hypo-estrogenism (amenorrhea caused by primary ovarian deficit and primary or secondary hypothalamic hypogonadotropinemia) should be rectified by replacement estrogen-progestin treatment before the onset of menopause. Protracted treatment of this kind can also be used beneficially in patients identified as at risk of osteoporosis during the climacteric and where it is advisable to minimise the hepatocellular action of the estrogens TDE will be the treatment of choice. In both phases the CT spray can be used preventively wherever there are contraindications to the use of the estrogens and a real risk of osteoporosis.
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PMID:[Application of new therapeutic approaches in the prevention of osteoporosis in women]. 273 48

A case of carcinoid tumor of the pancreas with the watery diarrhea, hypokalemia, and hypochlorhydria syndrome in association with hyperparathyroidism and the amenorrhea-galactorrhea syndrome is presented. Resection of the three grossly enlarged, hyperplastic parathyroid glands restored eucalcemia in this patient. A subsequent excision of the 370 gm pancreatic carcinoid tumor resulted in a cure of the watery diarrhea and a return of the gastric acid secretion to normal. Immunocytochemical studies of the pancreatic tumor demonstrated a positive stain only for serotonin, and negative results for vasoactive intestinal polypeptide, pancreatic polypeptide, glucagon, insulin, cholecystokinin, gastrin, and calcitonin were obtained. These studies suggest that in this patient, serotonin was a causative agent of the watery diarrhea syndrome.
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PMID:Carcinoid tumor of the pancreas causing the diarrheogenic syndrome: report of a case combined with multiple endocrine neoplasia, type I. 286 11

The pathophysiology of primary osteoporosis and the various therapeutic regimens that have been used are reviewed. Osteoporosis is a major public health problem because the incidence of hip, wrist, and vertebral fractures associated with bone loss is high. Postmenopausal women are at increased risk for developing osteoporosis because bone mineral content is lower in women than in men, dietary calcium intake is frequently insufficient, intestinal absorption of calcium decreases with age, and the rate of bone loss accelerates at menopause. The efficacy of many single and combination therapies in preventing or treating osteoporosis has been studied. Differences in study design and diagnostic techniques and the heterogeneous nature of osteoporosis make evaluation of clinical trials difficult. Exercise helps to maintain skeletal mass, but amenorrhea caused by vigorous activity may be harmful. The efficacy of estrogen replacement therapy is documented best; many studies have shown that estrogens slow the rate of bone loss and reduce the incidence of fractures, but the association of estrogen use with endometrial cancer and breast cancer is of concern. Progesterones may protect against endometrial cancer, but undesirable effects of oral contraceptives have resulted in a hesitancy to use combination hormonal therapy. All adults should meet daily nutritional requirements for calcium, but this intake may be insufficient for elderly persons and is below recommended doses for treating osteoporosis. A daily intake of at least 1000-1500 mg of elemental calcium has been shown to slow the rate of bone loss. Nutritional requirements for vitamin D should be met, but benefits from pharmacologic doses have not been demonstrated. The role of fluoride, calcitonin, anabolic steroids, and vitamin D metabolites is unclear. Fluoride has the potential to increase bone mass, but effects on bone histology and fracture rates require further study. The major goals for the management of osteoporosis are maintenance of bone mass and prevention of fractures. An adequate intake of calcium and regular weight-bearing exercise are important preventive measures. Despite the documented effectiveness of estrogens, risks associated with long-term use are of concern.
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PMID:Pathogenesis and management of primary osteoporosis. 352 28

Osteoporosis is a serious metabolic bone disorder that results in fractures of the wrist, hip and vertebrae. These fractures frequently occur with little or no trauma. Osteoporosis is seen more frequently in women than men. While the pathogenesis of osteoporosis is incompletely understood at this time, certain risk factors are emerging as important. Among the more important of these are family history, low calcium intake, early menopause and sedentary lifestyle. Other suggested risk factors include high intakes of protein, alcohol and caffeine; low body weight; exercise-induced amenorrhea; and cigarette smoking. No single therapy or combination of therapies for osteoporosis has proven to be uniformly successful. Indeed, once fractures occur, full restoration of the skeleton may not be possible. Currently, calcium, exercise and estrogen form the treatment for osteoporosis. When these conservative measures are ineffective or inadequate, treatment with fluoride, calcitonin, vitamin D or anabolic steroids may be attempted. Research to clearly identify and quantify risk factors and find an effective treatment for osteoporosis continues.
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PMID:Osteoporosis: significance, risk factors and treatment. 376 61

Hip fractures are common in the elderly, affecting 1 in 4 women by the age of 90 years and 1 in 8 men. These fractures have caused an "epidemic" during the last 20 years because the age specific rate for such fractures has doubled, and there has been a significant increase in the size of the elderly population in Europe. Hip fracture patients occupy a quarter of all orthopedic beds, the treatment is costly and the rehabilitation slow. Fifteen percent die in hospital; 33% are dead by one year. Of survivors only 2/3 return to their own home. There is now a move to prevent such fractures. Hip fractures arise in the elderly for two reasons: deteriorating bone stock and increasing falls. Hip fracture prevention needs to address both issues, but most work has looked at bone stock. Predictions of hip fracture risk even if based on bone density are poor, so preventive measures need to target the whole population. Bone density rises to a peak at 35 to 40 years in both sexes; men have a higher bone density at all times than women. Thereafter there is a steady loss of 1-2% per year. Women have 10 years of accelerated loss after the menopause. Hip fracture prevention starts by ensuring that peak bone mass is reached. This is under genetic influence but may be maximized by adequate dietary calcium and physical activity in adolescence. Smoking, alcohol and steroid use reduce bone density and their use should be moderated. In women amenorrhea reduces bone density. For women, estrogen may stop menopausal loss and maintain bone density for at least 15 years and in retrospective studies can reduce the fracture risk by 50%. Calcitonin may be an alternative. Five years beyond the menopause primary or secondary prevention may be started. Estrogen is still the best therapy but may be less popular because of the return of menstrual periods. Calcitonin or oral calcium supplements may also be of benefit. Drugs in combination may be more effective than alone. Over age 70, when calcium absorption diminishes, vitamin D, calcium and calcitonin may be effective. For men, treatment options are calcium, calcitonin or, later on, vitamin D. The role of exercise in bone density protection is unclear but should be encouraged for general health reasons. Bisphosphonates are new drugs that may be useful. Falls become increasingly common in the elderly such that up to 80% of all 80-year-olds may sustain at least one fall per year.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The epidemiology of hip fractures and methods of prevention. 805 45

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.
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PMID:Corticosteroid-induced bone loss. Prevention and management. 894 96

Typical modifications of cardiovascular activity and water and salt homeostasis throughout female reproductive life are well known. Differences in plasma levels of calcitonin gene-related peptide (CGRP) and atrial natriuretic peptide (ANP) have been observed in conditions characterized by different estrogenic levels, suggesting a correlation between female reproductive function and these cardiovascular hormones. The aim of our study was to investigate in hypothalamic amenorrhea the relationship between estrogen deficiency and plasma ANP and CGRP response to adaptive tests (saline infusion test and upright posture test, respectively). Women with hypothalamic amenorrhea (aged 18-28 years) (n = 6) and age-matched healthy controls (n = 6) underwent both functional tests. Plasma CGRP and ANP levels were measured by specific radioimmunoassays before and in course of the tests. Basal plasma CGRP levels of amenorrheic patients did not significantly differ from those of normal women, while basal plasma ANP levels were significantly higher compared to controls (p < 0.01). In amenorrheic women, plasma CGRP levels showed a significant increase in response to upright posture test, though lower than the increase observed in normal women. In contrast, saline infusion test determined a significant increase in plasma ANP levels only in control subjects. In women with hypothalamic amenorrhea, the altered response of CGRP and ANP to adaptive stimuli indicates a partial derangement in the control of the secretion of these cardiovascular hormones. Nevertheless, the differences between such modifications and those observed in other conditions of altered estrogenic levels, suggest that in amenorrheic women hypogonadism is not the major factor influencing CGRP and ANP response to adaptive stimuli.
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PMID:Hypothalamic amenorrhea and cardiovascular hormones: changes of plasma calcitonin gene-related peptide and atrial natriuretic peptide levels. 962

Osteoporosis is a condition associated with decreased bone strength and an increased fracture risk. It may be defined based on bone mineral density (BMD) with a T-score at the hip or spine of less than -2.5 standard deviations in young healthy individuals or from an osteoporotic fracture (i.e. a fracture occurring after low-energy trauma or no apparent trauma). Risk factors predisposing to fractures include: increasing age; female gender; low BMD; a prior fragility fracture; a family history of fragility fractures; low bodyweight; lack of estrogen in women (i.e. post menopause); corticosteroid use; smoking; a number of diseases; deficiency in calcium and vitamin D; an increased risk of falls (i.e. impaired vision); immobilization; and Caucasian race. The more risk factors that are present the higher the risk of fractures over the following 10 years. The need to initiate preventive therapy with anti-osteoporotic treatment increases steeply with the absolute fracture risk. Indications for referral for dual energy x-ray absorptiometry measurement of BMD include: age >65 years; age <65 years in postmenopausal women with any of the risk factors already mentioned; premature menopause (<45 years); prolonged amenorrhea (>1 year) in younger women; fragility fractures; and diseases or conditions known to lead to osteoporosis.Anti-resorptive therapies include calcium plus vitamin D, bisphosphonates (alendronate, etidronate, risedronate, ibandronate), selective estrogen receptor modulators (raloxifene), hormone replacement therapy, and calcitonin. Guidelines from several countries on when to initiate anti-resorptive therapy state that therapy may be started in patients with a prior fragility fracture (some guidelines state that in this situation no BMD measurements are necessary) or in patients with a T-score of less than -2.5 (some guidelines state that additional risk factors need to be present in this situation). Some guidelines state that anti-resorptive therapy may be initiated in patients with a T-score in the osteopenic range (from -1 to -2.5, i.e. not frank osteoporosis) in the presence of other risk factors. The cost effectiveness of anti-resorptive therapy increases with the absolute fracture risk. In some scenarios, treatment with bisphosphonates may be cost effective in a 50-year-old woman with an absolute hip fracture risk of >or=1.1% over the next 10 years.
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PMID:Anti-resorptive therapy for the prevention of postmenopausal osteoporosis : when should treatment begin? 1618 96

We describe a hitherto undocumented variant of dimorphic pituitary neoplasm composed of an admixture of neurosecretory cells and profuse leiomyomatous stroma around intratumoral vessels. Radiologically perceived as a macroadenoma of 3.8 cm in diameter, this pituitary mass developed in an otherwise healthy 43-year-old female. At the term of a yearlong history of amenorrhea and progressive bitemporal visual loss, subtotal resection was performed via transsphenoidal microsurgery. Discounting mild hyperprolactinemia, there was no evidence of excess hormone production. Histologically, solid sheets, nests and cords of epithelial-looking, yet cytokeratin-negative cells were seen growing in a richly vascularized stroma of spindle cells. While strong immunoreactivity for NCAM, Synaptophysin and Chromogranin-A was detected in the former, the latter showed both morphological and immunophenotypic hallmarks of smooth muscle, being positive for vimentin, muscle actin and smooth muscle actin. Architectural patterns varied from monomorphous stroma-dominant zones through biphasic neuroendocrine-leiomyomatous areas, to pseudopapillary fronds along vascular cores. Only endothelia were labeled with CD34. Staining for S100 protein and GFAP, characteristics of sustentacular cells, as well as bcl-2 and c-kit was absent. Except for alpha-subunit, anterior pituitary hormones tested negative in tumor cells, as did a panel of peripheral endocrine markers, including serotonin, somatostatin, calcitonin, parathormone and vasoactive intestinal polypeptide. Mitotic activity was absent and the MIB-1 labeling index low (1-2%). While assignment of this lesion to any established neoplastic entity is not forthcoming, we propose it is being considered as a low-grade neuroendocrine tumor possibly related to null cell adenoma.
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PMID:Leiomyomatoid angiomatous neuroendocrine tumor (LANT) of the pituitary: a distinctive biphasic neoplasm with primitive secretory phenotype and smooth muscle-rich stroma. 1652 Sep 66


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