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

Although transjugular liver biopsy requires the availability of trained personnel, takes more time than percutaneous biopsy and is moderately expensive, it is a safe alternative technique for obtaining adequate liver tissue for diagnosis in special clinical situations. The usual indications for transjugular rather than percutaneous liver biopsy are (a) coagulation disorder (prothrombin time greater than 3 sec over control value and/or platelet count less than 60,000/cm3), (b) massive ascites and (c) desire to perform ancillary procedures, such as measurement of pressures or opacification of the hepatic veins and inferior vena cava. Less common indications for transjugular liver biopsy include failed percutaneous biopsy, massive obesity, small cirrhotic liver (increased risk and lower success rate) and suspected vascular tumor or peliosis hepatis. Results from several centers indicate that adequate or diagnostic liver tissue is obtained in 81% to 97% of cases. The typical length of the biopsy core ranges from 0.3 cm to 2.0 cm. Modification of the classic technique, particularly the adaptation of a Tru-Cut needle, shows promise in yielding longer cores of tissue with less fragmentation. Transjugular liver biopsy is performed with an acceptable complication rate that ranges 0% to 20%. The reported mortality of transjugular liver biopsy was 0 in three major centers and ranged from 0.1% to 0.5% in three other centers. Transjugular liver biopsy may be useful in obtaining diagnostic liver tissue not only in advanced chronic liver disease with coagulopathy, ascites or both, but also in patients with fulminant hepatic failure to better determine prognosis and the need for liver transplantation.
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PMID:Transjugular liver biopsy. 155 49

The incidence of deep-vein thrombosis was studied in 146 consecutive Korean patients who had a cementless total hip replacement with a porous-coated anatomic prosthesis. All of the patients had discontinued taking aspirin, aspirin-containing compounds, or other antiplatelet medications fourteen days before admission to the hospital for the operation. Deep-vein thrombosis was diagnosed by roentgenographic venography, and pulmonary embolism, by perfusion lung-scanning. There was an unusually low incidence (10 per cent) of deep-vein thrombosis in this series. In contrast to other reports, we did not identify a relationship between deep-vein thrombosis and so-called risk factors such as advanced age, number of venous valves (more than five) in the lower extremity, abnormal coagulation-assay data, certain diseases, or preoperative limitation of mobility. In addition, hypertension, blood group, surgical approach, and choice of cemented or cementless total hip replacement did not seem to affect the incidence of deep-vein thrombosis. There was a low incidence of deep-vein thrombosis in patients in whom obesity, prolonged immobilization postoperatively, varicose veins, and hyperlipemia were not factors.
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PMID:Low incidence of deep-vein thrombosis after cementless total hip replacement. 339 86

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.
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PMID:[Liver transplantation in halothane-induced liver necrosis]. 802 96

Most cases of postpartum haemorrhage are caused by uterine atony, maternal soft-tissue trauma, retained placenta or its parts, and obstetric coagulopathy. The factors most significantly associated with haemorrhage include advanced maternal age, prolonged labour, pre-eclampsia, obesity of mother, multiple pregnancy, a birth weight of more than 4000g, and previous postpartum haemorrhage. It seems that multiparity itself is only a weakly associated factor. The prophylactic use of oxytocic drugs (oxytocin or its combination with ergometrine at the third stage of labour is always recommended for decreasing the bleeding. Prostaglandins should be used as a second line treatment if uterine atony cannot be abolished by uterine massage and oxytocin infusion. In the surgical management, the role of hypogastric artery ligation is decreasing. The stepwise uterine devascularization may be a reasonable method in the most severe uncontrollable postpartum bleeding. The uterine tamponade with gauze or specific tubes may also be a useful alternative in some cases. Selective arterial embolization is a promising new method that seems to have success in controlling the heavy postpartum bleeding unresponsive to more usual measures. However, the value of this method should be evaluated in bigger series.
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PMID:Postpartum haemorrhage. 862 78

Twelve Caesarean section-associated maternal deaths were encountered over a 15-year period. The major operative risk factors were pregnancy-induced hypertension, obesity and general anaesthesia. Severe preeclampsia was the forerunner to postoperative cardiac failure, consumptive coagulopathy and difficult airway manipulation. We conclude that pregnancy-induced hypertension and its ramifications pose the greatest threat to maternal survival from a Caesarean section.
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PMID:Maternal deaths associated with caesarean section. 903 30

It is now recognized that growth hormone (GH) deficiency in adults represents a distinct clinical syndrome that encompasses reduced psychological well-being as well as specific metabolic abnormalities. The latter features, which include hypertension, central obesity, insulin resistance, dyslipidaemia and coagulopathy, closely resemble those of metabolic insulin resistance syndrome. The increased cardiovascular morbidity and mortality demonstrated in these GH-deficient (GHD) adults reinforce the close association between the two syndromes. Replacement of GH in GHD adults has resulted in a marked reduction of central obesity and significant reduction in total cholesterol but little change in other risk factors, in particular insulin resistance and dyslipidaemia. The persistent insulin resistance and dyslipidaemia, together with the elevation of plasma insulin levels and lipoprotein (a) with GH replacement in these subjects are of concern. Long-term follow-up data are required to assess the impact of GH replacement on the cardiovascular morbidity and mortality of GHD adults. Further exploration of the appropriateness of the GH dosage regimens currently being employed is also indicated.
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PMID:Growth hormone deficiency and cardiovascular risk. 1008 92

Insulin resistance is associated not only with the classic cardiovascular risk factors of hypertension and dyslipidemia, but also with several disorders of coagulation and fibrinolysis. Elevated concentrations of the fibrinolytic inhibitor plasminogen activator inhibitor-1 are associated with insulin resistance. In experimental systems, increased expression and secretion of plasminogen activator inhibitor-1 by hepatocyte and endothelial cell lines can be induced by insulin, proinsulin-like molecules, triglyceride-rich lipoproteins and oxidized LDL, as well as by inducing insulin resistance in isolated hepatocytes. Concentrations of the endothelial cell protein von Willebrand factor are elevated in insulin-resistant states, suggesting that abnormalities of capillary endothelium, as well as those reported for endothelium-dependent vasodilatation, may play a role in the etiology of insulin resistance. Levels of a third coagulation factor, fibrinogen, are elevated in insulin-resistant subjects, an association that suggests a possible role for acute-phase cytokines in the abnormalities of coagulation and endothelial function. It is proposed that the recent observations of secretion of interleukin-6 by adipose tissue, combined with the actions of adipose tissue-expressed tumor necrosis factor-alpha in obesity-induced insulin resistance, could underlie the associations of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease.
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PMID:Abnormalities of coagulation and fibrinolysis in insulin resistance. Evidence for a common antecedent? 1018 59

There is considerable evidence that insulin and insulin-like growth factors regulate a number of important physiological functions in a variety of tissues, some not considered to be classically insulin sensitive. Impaired biological responses to insulin and related insulin-like growth factors are referred to as insulin resistance. Persons with insulin resistance often display clinical abnormalities other than impaired glucose tolerance, including central obesity, hypertension, dyslipidemia, microalbuminuria, and abnormal coagulation and fibrinolytic systems. The mechanisms leading to development of insulin resistance are not fully understood. However, in addition to abnormalities of phosphorylation processes, it appears that alterations in cellular cation metabolism contribute to diminished cellular actions of insulin (i.e., glucose transport and hemodynamic actions). This review focuses on known cellular cation abnormalities and associated insulin resistance and cardiovascular disease.
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PMID:Insulin, cation metabolism and insulin resistance. 1021 36

Growth hormone (GH) deficiency in adults is characterized by central obesity, dyslipidemia, coagulopathy and glucose intolerance, all features of the "metabolic syndrome", explaining the increased cardiovascular morbidity and mortality associated with GH deficiency in adults. Employing the 2-step euglycemic-hyperinsulinemic clamp, we have demonstrated severe insulin resistance in GH-deficient adults, with a reduction in insulin-mediated glucose utilization of -50%. Basal glucose turnover and partitioning of whole body glucose utilization into glycolytic flux (GF) and glycogen synthesis/glucose storage (GS) pathways are normal, but insulin activation of these 2 pathways is reduced, predominantly in the GS pathway. Activation of muscle glycogen synthase by insulin is markedly decreased, as is glycogen content of muscle. Insulin-induced muscle hexokinase activity appears also to be attenuated in GH-deficient adults with raised intramuscular cellular glucose and normal-reduced concentrations of glucose-6-phosphate. Beta-cell function is not excessive in GH-deficient adults and is inappropriately low for the insulin resistance. Following treatment of GH-deficient adults with recombinant GH (rhGH), the insulin resistance is either unchanged or more pronounced by 3, 6 or 24 months of treatment, despite the significant reduction in general and central obesity. The GF and GS pathways and muscle glycogen synthase and hexokinase activities remain severely impaired. Abnormalities in free fatty acid (FFA) metabolism are present in rhGH-treated GH-deficient adults and correlate significantly with the degree of insulin resistance as do the concentrations of rhGH-induced insulin-like growth factor (IGF)-I, the post-basal insulinemia and the duration of the GHD, but is independent of obesity. In conclusion, long-term rhGH treatment in GH-deficient adults results in persistent insulin resistance and abnormalities in the GF and GS pathways due to reduced glycogen synthase and hexokinase activities, in the presence of an ongoing reduction of central obesity. We postulate that the insulin resistance is due to chronic rhGH-induced alterations in FFA metabolism, non-physiological levels of IGF-I and chronic basal hyperinsulinemia.
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PMID:Insulin sensitivity in growth hormone (GH)-deficient adults and effect of GH replacement therapy. 1044 67

Although adipose tissue has long been considered to be metabolically passive and primarily responsible for energy storage, recent scientific advances have dramatically altered our understanding of the function of this ubiquitous tissue. The fat cell is a transducer of energy supply for the changing metabolic needs of the body, modulating glucose homeostasis, hypothalamic function, sympathetic output, vascular tone, immune response, and reproduction. Through endocrine/autocrine and paracrine actions, adipocyte-derived molecules defend the body during periods of energy deficit and stress. With the development of obesity, maladaptive responses to adipose excess result in pathologic states of inflammation, coagulopathy, and altered insulin sensitivity.
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PMID:Leptin and the adipocyte endocrine system. 1238 4


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