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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult survivors of childhood cancer, particularly brain tumours and acute lymphoblastic leukaemia demonstrate evidence of increased rates of metabolic complications and cardiovascular disease in later life. Evidence is accumulating that risk factors for these complications include obesity, physical inactivity, lipid abnormalities, insulin resistance and development of the metabolic syndrome. Cranial radiotherapy-induced growth hormone deficiency, other direct adverse effects of radiotherapy and anthracycline-induced left ventricular dysfunction are clearly identified risk factors for developing these complications. Growth hormone replacement, where appropriate, has been of some benefit in reducing the prevalence of metabolic complications in some long-term survivors. In others, it is clear that multidisciplinary interventions will need to be developed which focus on modifying aspects of lifestyle including increasing levels of habitual physical activity, improving diet and prevention of smoking along with the use of lipid-lowering medication.
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PMID:Metabolic disorders. 1929 4

This article reviews evidence that causally links hormonal disorders with hepatobiliary disease, and gives particular focus to nonalcoholic steatohepatitis (NASH). The downstream mechanisms by which endocrine disturbances cause liver disease might be similar to those involved in the development of primary liver disease. Hypothyroidism, for example, might lead to NASH, cirrhosis and potentially liver cancer via the development of hyperlipidemia and obesity. Patients with growth hormone deficiency have a metabolic-syndrome-like phenotype that is also associated with the development of NASH. Polycystic ovary syndrome is a common endocrine disorder that is often associated with insulin resistance, the metabolic syndrome, altered levels of liver enzymes and the development of NASH. Recent findings support a role of dehydroepiandrosterone sulfate deficiency in the development of advanced NASH. In addition, adrenal failure is increasingly reported in patients with end stage liver disease and in patients who have received a liver transplant, which suggests a bidirectional relationship between liver and endocrine functions. Clinicians should, therefore, be aware of the potential role of endocrine disorders in patients with cryptogenic liver disease and of the effects of liver function on the endocrine system.
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PMID:Endocrine and liver interaction: the role of endocrine pathways in NASH. 1934 15

Craniopharyngioma is a rare, benign, suprasellar brain tumor associated with a significant number of endocrine and metabolic impairments. Growth hormone deficiency, caused by the tumor itself or by its subsequent surgical treatment, is the most common hormone deficiency in these patients and replacement is frequently necessary. Hypothalamic obesity observed after surgery treatment, whether combined with radiotherapy or not, presents with increased abdominal fat and altered lipid profiles and is likely caused by both disruption of the mechanisms controlling satiety, hunger and energy balance and impairment of sensitivity to leptin, insulin and ghrelin axis. It is well known that hyperlipemia is associated with acute pancreatitis, both as a precipitant and as an epiphenomenon. Moreover, the increased incidence of acute pancreatitis during growth hormone therapy is possibly due to increased enzyme production (e.g., amylase, lipase and elastase). We report the case of a 13-year-old girl affected by craniopharyngioma on growth hormone replacement treatment who developed acute pancreatitis. We suggest including routine evaluation of lipid profile during follow-up of all children on growth hormone treatment, especially those affected by hypopituitarism secondary to craniopharyngioma, given pancreatic adverse effects of growth hormone replacement therapy and associated metabolic impairment due to hypothalamic obesity.
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PMID:Acute pancreatitis in a girl with panhypopituitarism due to craniopharyngioma on growth hormone treatment. A combination of risk factors. 1950 96

Athletes have enjoyed almost a thirty year amnesty of rhGH abuse, which they consider has contributed to the winning of medals and the breaking of world records. Such a reprieve is almost at an end, since WADA have identified a method to detect rhGH abuse. Or have they? The anecdotal word "on the street" is that rhGH is still undetectable and athletes believe that the benefits, at the dosages they administer, far outweigh the risks! Scientists are aware that in a hormone deficiency condition, replacement can halt and in certain situations reverse some of the adverse effects. Growth hormone deficiency can lead to a loss of skeletal muscle mass and an increase in abdomino-visceral obesity, which is reversed on replacement with rhGH. Since the availability of GH, athletes have been trying to extrapolate these effects from the deficiency state to the healthy corpus and increase their sporting prowess. Past confessions from athletes, such as Ben Johnson, Kelly White, Tim Montgomery, Marion Jones and currently Dwain Chambers have demonstrated that they are prepared to tread the very fine lines that separate the "men from the boys". Rewards are so great, that anonymous surveys have identified that athletes will risk ill health, if they believe they can cheat, win and not get caught. The question that still needs to be answered is, "does growth hormone enhance performance"? Recent research suggests that it could. There is also a suspicion that in "cycled" low supraphysiological doses, it is no where near as harmful as WADA claim it to be.
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PMID:Potential benefits of recombinant human growth hormone (rhGH) to athletes. 1953 5

Quality of life (QoL) has emerged as an important construct that has found numerous applications across healthcare-related fields, ranging from research and clinical evaluation of treatment effects to pharmacoeconomic evaluations and global healthcare policy. Impairment of QoL is one of the key clinical characteristics in adult GHD and has been extensively studied in the Pfizer International Metabolic Database (KIMS). We provide summarized evidence on GH treatment effects for both clinical and health economic applications based on the KIMS data. The primary focus is on those aspects of QoL research that cannot be investigated in the traditional clinical trial setting, such as specific patient subgroups, cross-country comparisons and long-term follow-up. First, the impact of age, gender, disease onset, primary aetiology, extent of hypopituitarism, previous radiotherapy and obesity on QoL before and during long-term GH replacement is discussed. Secondly, the studies on QoL in relation to country-specific normative values are reviewed. Finally, health economic data derived from KIMS including both burden of disease and utility assessment are evaluated. We conclude that the wide spectrum of analyses performed on the KIMS data allows for practical application of the results not only to research and clinical practice but also to health policy and global medical decision making.
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PMID:Assessment of quality of life in adult patients with GH deficiency: KIMS contribution to clinical practice and pharmacoeconomic evaluations. 1968 56

Growth hormone (GH) is the most important hormonal regulator of postnatal longitudinal growth in man. In adults GH is no longer needed for longitudinal growth. Adults with growth hormone deficiency (GHD) are characterised by perturbations in body composition, lipid metabolism, cardiovascular risk profile and bone mineral density. It is well established that adult GHD usually is accompanied by an increase in fat accumulation and GH replacement in adult patients with GHD results in reduction of fat mass and abdominal fat mass in particular. It is also recognized that obesity and abdominal obesity in particular results in a secondary reduction in GH secretion and subnormal insulin-like growth factor-I (IGF-I) levels. The recovery of the GH IGF-I axis after weight loss suggest an acquired defect, however, the pathophysiologic role of GH in obesity is yet to be fully understood. In clinical studies examining the efficacy of GH in obese subjects very little or no effect are observed with respect to weight loss, whereas GH seems to reduce total and abdominal fat mass in obese subjects. The observed reductions in abdominal fat mass are modest and similar to what can be achieved by diet or exercise interventions.
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PMID:Obesity, growth hormone and weight loss. 1972 58

The most frequent liver disorder in metabolic syndrome is the nonalcoholic fatty liver disease. Its pathogenesis is a complex, multifactorial process, characterized by insulin resistance and involvement of the endocrine system. Hypothyroidism may lead to nonalcoholic steatohepatitis via hyperlipidemia and obesity. Adult patients with growth hormone deficiency have a metabolic syndrome-like phenotype with obesity and many characteristic metabolic alterations. The chronic activation of the hypothalamic-pituitary-adrenal axis results in metabolic syndrome as well. Cushing's syndrome has also features of metabolic syndrome. Mild elevation of transaminase activities is commonly seen in patients with adrenal failure. Non-alcoholic steatosis is twice as common in postmenopusal as in premenopausal women and hormonal replacement therapy decreases the risk of steatosis. Insulin resistance, diabetes mellitus type 2, sleeping apnoe syndrome, cardiovascular disorders and non-alcoholic fatty liver disease are more frequent in polycystic ovary syndrome. Hypoandrogenism in males and hyperandrogenism in females may lead to fatty liver via obesity and insulin resistance. Adipokines (leptin, acylation stimulating protein, adiponectin) have a potential role in the pathogenesis of nonalcoholic fatty liver. The alterations of endocrine system must be considered in the background of cryptogenic liver diseases. The endocrine perspective may help the therapeutic approaches in the future.
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PMID:[Role of the endocrine system in the pathogenesis of non-alcoholic fatty liver disease]. 1992 96

Endocrine diseases (hypothyroidism, growth hormone deficiency, hypercortisolism) are exceptional in obese children and are searched only in case of short stature. It is not necessary to test systematically glucose tolerance (fasting glucose; oral glucose tolerance test) and lipids in order to look for obesity related comorbidities. Decreased caloric intake is the main goal for the treatment. Ways to succeed need to be adapted to each child with pragmatism and without dogmatism. Goals for treatment are reasonable (stabilization of weight excess). Weight loss surgery in obese children may be discussed in some cases with multidisciplinary expert team (doctors, surgeons, psychologist...) and close collaboration between adults teams and paediatricians.
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PMID:[Management of childhood obesity]. 2061 56

More than 80% of children with acute lymphoblastic leukemia can now be cured. Relapses are rare after five years of remission. The most frequent sites of relapse are bone marrow, the central nervous system, and the testicles. Long-term follow-up is needed to detect late adverse effects of treatment. This includes regular cardiac examination, owing to the cumulative-dose-dependent cardiotoxicity of anthracyclines. Endocrine disorders (early puberty, growth hormone deficiency, gonad and thyroid dysfunction) are mainly due to irradiation of the brain or testicles, which is now less widely used. Growth must be monitored closely to detect early obesity. Bone mineral density can also be altered. Cognitive function, school performance and socialization are usually normal in non irradiated patients. Secondary neoplasms are rare, but some are related to previous treatments. Currently, post-cure quality of life is a major concern when choosing the treatment strategy.
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PMID:[Outcome of children cured of acute lymphoblastic leukemia]. 2066 33

Patients with hypopituitarism have the feature of metabolic syndrome, including central obesity, insulin resistance, and dyslipidemia. Because metabolic syndrome, including insulin resistance, is the main pathogenesis of the development of nonalcoholic fatty liver disease (NAFLD), we considered that patients diagnosed with hypopituitarism have an increased risk of developing NAFLD. We compared control subjects and hypopituitary men in metabolic parameters and the frequency of fatty liver on abdominal ultrasonography, and analyzed associating factors with the severity of the fatty liver in patients with hypopituitarism. 34 male patients with hypopituitarism and 40 age and sex-matched control subjects were included. The frequency of fatty liver on abdominal ultrasonography was significantly higher in hypopituitary men compared to control subjects (32.5% vs. 70.6%, p=0.001). Ln CRP and free fatty acids were significantly elevated in hypopituitary patients with fatty liver compared to patients without fatty liver. Ln GH was significantly lower in hypopituitary patients with fatty liver. The severity of fatty liver on abdominal ultrasonography correlated with negatively Ln GH, after adjusting for the BMI effect (p=0.020). There is a difference only between the severe fatty liver group and normal liver group in the analysis of the mean Ln GH level between 4 groups according to the severity of fatty liver (p=0.036). In conclusion, NAFLD is more common in hypopituitary patients than control subject. Severe growth hormone deficiency in hypopituitarism was associated with the severe degree of hepatic steatosis in NAFLD.
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PMID:Metabolic parameters and nonalcoholic fatty liver disease in hypopituitary men. 2086 48


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