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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine dysfunction and parameters of metabolic syndrome were assessed in 91 patients aged 4.3-32.5 years who underwent allogeneic or autologous BMT in childhood. Final short stature, found in five of the 35 patients who attained final height, was associated with the underlying disease (specifically, Fanconi anemia) (P=0.0013), previous cranial irradiation (P=0.0007), type of conditioning irradiation (P<0.05) and allogeneic BMT (P=0.05). Growth hormone deficiency (n=10) was associated with previous cranial irradiation (P<0.005) and conditioning total body irradiation (P<0.001). Twelve patients had primary hypothyroidism, one had hyperthyroidism and one papillary thyroid carcinoma. Hypothyroidism was associated with neck/mediastinal (P<0.005) and conditioning irradiation (P<0.05). Primary gonadal failure was found in 24 of the mature patients (62.5% females). Hypogonadism was associated with the underlying disease (especially hematological malignancies) (P<0.05), pretransplant treatment (P<0.05), irradiation conditioning (P<0.001), older age (P<0.005) and advanced pubertal stage at BMT (P<0.05). Obesity (body mass index >2 s.d.) was found in 4.4% and type II diabetes and impaired glucose tolerance in 3.3% each. Dyslipidemia was found in 27.9% of the 43 patients tested. These findings emphasize the need for long-term follow-up of endocrine and metabolic parameters in young patients after BMT in order to offer proper treatment and improve quality of life.
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PMID:Endocrine dysfunction and parameters of the metabolic syndrome after bone marrow transplantation during childhood and adolescence. 1669 34

In the last 15 years, it has been recognised that growth hormone deficiency (GHD) in the adult leads to increased morbidity (metabolic syndrome, osteoporosis, muscle wasting, impaired quality of life) and increased incidence of cardiovascular events, a main cause of the increased mortality observed in this population. Pituitary adenomas and their treatment (surgery, radiation) are the most common cause of GHD in adults. Patients with biochemical diagnosis of severe GHD must be offered growth hormone replacement therapy only in the presence of GHD associated morbidity. This treatment improves morbidity, but its effect on mortality remains to be proven. Continuation of treatment for GHD patients in late adolescence to early adulthood, who have reached final height with growth hormone replacement, requires careful clinical judgement.
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PMID:Adult growth hormone deficiency: to treat or not to treat. 1742 74

Along with the growing epidemic of obesity, the risk of atherosclerosis, cardiovascular disease morbidity, and mortality are increasing markedly. Several risk factors for cardiovascular disease, such as visceral obesity, glucose intolerance, arterial hypertension, and dyslipidemia commonly cluster together as a condition currently known as metabolic syndrome. Thus far, insulin resistance, and endothelial dysfunction are the primary events of the metabolic syndrome. Several groups have recommended clinical criteria for the diagnosis of metabolic syndrome in adults. Nonetheless, in what concerns children and adolescents, there are no unified definitions, and modified adult criteria have been suggested by many authors, despite major problems. Some pediatric disease states are at risk for premature cardiovascular disease, with clinical coronary events occurring very early in adult life. Survivors of specific pediatric cancer groups, particularly acute lymphocytic leukemia, central nervous system tumors, sarcomas, lymphomas, testicular cancer, and following bone marrow transplantation, may develop metabolic syndrome traits due to: hormonal deficiencies (growth hormone deficiency, thyroid dysfunction, and gonadal failure), drug or radiotherapy damage, endothelial impairment, physical inactivity, adipose tissue dysfunction, and/or drug-induced magnesium deficiency. In conclusion, some primary and secondary prevention remarks are proposed in order to reduce premature cardiovascular disease risk in this particular group of patients.
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PMID:Detection of metabolic syndrome features among childhood cancer survivors: a target to prevent disease. 1906 99

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

Visceral adipose tissue-derived serine protease inhibitor (vaspin) is a recently discovered adipocytokine mainly secreted from visceral adipose tissue, which plays a main role in insulin sensitivity. In this study, we have investigated the regulation of vaspin gene expression in rat white adipose tissue (WAT) in different physiological (nutritional status, pregnancy, age and gender) and pathophysiological (gonadectomy, thyroid status and growth hormone deficiency) settings known to be associated with energy homeostasis and alterations in insulin sensitivity. We have determined vaspin gene expression by real-time PCR. Vaspin was decreased after fasting and its levels were partially recovered after leptin treatment. Chronic treatment with metformin increased vaspin gene expression. Vaspin mRNA expression reached the highest peak at 45 days in both sexes after birth and its expression was higher in females than males, but its levels did not change throughout pregnancy. Finally, decreased levels of growth hormone and thyroid hormones suppressed vaspin expression. These findings suggest that WAT vaspin mRNA expression is regulated by nutritional status, and leptin seems to be the nutrient signal responsible for those changes. Vaspin is influenced by age and gender, and its expression is increased after treatment with insulin sensitizers. Finally, alterations in pituitary functions modify vaspin levels. Understanding the molecular mechanisms regulating vaspin will provide new insights into the pathogenesis of the metabolic syndrome.
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PMID:Regulation of visceral adipose tissue-derived serine protease inhibitor by nutritional status, metformin, gender and pituitary factors in rat white adipose tissue. 1947 Jul 78

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

Short stature associated with GH deficiency has been estimated to occur in about 1 in 4000 to 1 in 10,000 in various studies. In the last decade new genetic defects have been described in all the levels of the growth hormone-releasing hormone (GH-RH)-GH-IGF (insulin-like growth factor) axis. Genetic defects in the GHRH and in various parts of the Insulin-like growth factor system have been demonstrated. Genetic defects causing isolated GH deficiency (GHD), as well as multiple pituitary hormonal deficiencies have been analysed in detail. Signalling molecules and transcription factors leading to the development of the pituitary gland have been discovered and their function recognized. In animal models and in humans the importance of the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, TBX19, SOX2 and SOX3 has been extensively studied. Genetic alterations of those transcription factors dictate the highly variable phenotype: from isolated hypopituitarism to multiple pituitary hormonal deficiencies with or without malformations (e.g. septo-optic dysplasia or holoprosencephaly). Small for gestational age (SGA) children are increasingly recognized to be a heterogeneous group in which new mechanisms of growth retardation and metabolic disturbances have been proposed. Since SGA is considered to be the main reason for the short stature in 10% of short adults this is a large group with a great potential for novel insights into mechanisms of growth and metabolic disturbances. A group of signalling proteins are involved in prenatal (SGA) growth retardation: IRS-1, PDK1, AKT1, and S6K1. In addition, an attractive modern theory supposes that a disturbed mother-placenta-foetus relation results in the activation of the so-called "thrifty phenotype" of which the IGF system is a vital part. The mechanisms assure short-term postnatal survival in conditions of deficient nutritional supply. However, as a consequence, the abundant postnatal nutritional supply and the "thrifty phenotype" result in increased adult risk of metabolic syndrome, diabetes mellitus type 2 (DM2) and cardiovascular disease. The manuscript reviews in brief genetic alterations in humans leading to growth hormone deficiency (GHD), multiple pituitary hormone deficiencies (MPHD) and SGA.
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PMID:Growth hormone deficiency (GHD) and small for gestational age (SGA): genetic alterations. 2008 48

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

Survivors of pediatric hematopoietic stem cell transplantation (HSCT) are known to be at risk of developing endocrine abnormalities, but occurrence of diabetes mellitus (DM) is a relatively recent observation. We present a 17.5-year-old girl with DM after high-dose radio- and chemotherapy followed by allogeneic HSCT for the treatment of acute lymphoblastic leukemia, diagnosed when she was 10 years old. In the posttransplantation period, multiple acute and chronic complications occurred. Among them, we observed graft versus host disease requiring corticosteroid therapy, pancreatitis and some endocrine complications like primary hypothyroidism, growth hormone deficiency and hypergonadotropic hypogonadism. DM with some components of metabolic syndrome-like insulin resistance, high arterial blood pressure and dyslipidemia developed during the first year after HSCT. Five years later, a trend towards increased requirement of insulin with deterioration in metabolic control of DM was observed, despite a normal level of C-peptide and negative diabetes autoantibodies. After the addition of metformin to continuous subcutaneous insulin infusion in the therapy of DM, an improvement in metabolic control was observed. Due to the possible mechanism of insulin resistance which is associated with impaired insulin receptors after HSCT procedure, metformin with insulin appears to be effective in the treatment of this type of diabetes.
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PMID:Diabetes mellitus after allogeneic hematopoietic stem cell transplantation. 2329 12


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