1,721,153 research outputs found

    Non-alcoholic fatty liver disease and cardiovascular disease: Epidemiological, clinical and pathophysiological evidences

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    Non-alcoholic fatty liver disease is recognized as the most common and emerging chronic liver disease in western countries. The disease has been traditionally interpreted as a possibly progressing condition to liver fibrosis and cirrhosis. However, recently, a large number of publications have demonstrated that people with non-alcoholic fatty liver have an increased chance of developing cardiovascular diseases, which represent the major causes of death in this setting. This association is mainly explained by the atherogenic profile of the metabolic syndrome a condition frequently associated with fatty liver, which may represent its hepatic component. Some studies have also shown an association independent of traditional risk factors or of the clinical features of the metabolic syndrome. In this setting, cardiovascular disease seems to be the consequence of low-grade chronic inflammation and increased oxidative stress. Most studies did not differentiate cardiovascular risk between simple steatosis and non-alcoholic steatohepatitis, although the latter seems to be at higher cardiovascular risk. Few studies have investigated the direct correlation between hepatic inflammation and atherosclerosis. Genetic studies will probably improve the interpretation of the increased cardiovascular risk in patients with fatty liver and no metabolic syndrome. © 2012 SIMI

    PLASMA-LIPOPROTEINS IN DIET-RESISTANT POLYGENIC AND FAMILIAL HYPERCHOLESTEROLEMIA - THE EFFECTS OF 3-HYDROXY-3-METHYLGLUTARIC ACID (HMGA, MEVALON

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    The effects of 3-hydroxy-3-methylglutaric acid (HMGA; Mevalon), a serum cholesterol-lowering agent, were studied in five patients with heterozygous familial hypercholesterolaemia (FH) and in 17 patients with polygenic hypercholesterolaemia. After 8-9 weeks of treatment (1 g twice daily) the mean reduction in total and LDL-cholesterol was -11.4% and -18.0% respectively in heterozygous FH. However, the response was markedly heterogeneous. In patients with polygenic hypercholesterolaemia, HMGA produced a considerably greater mean reduction in total and LDL-cholesterol (-14.4% and -19.0% respectively) and a significant reduction in total serum triglyceride concentration (-11.6%). In all patients HDL-cholesterol levels tended to decrease during treatment. In Type IIa polygenic hypercholesterolaemia a transitory slight increase in VLDL-cholesterol levels was also observed. The drug was well tolerated. No clinically significant changes in liver funtion occurred. HMGA appears to be a useful drug for the treatment of most patients with diet-resistant polygenic hypercholesterolaemia and of some patients with heterozygous FH. Hence, the genetic classification of the form of hypercholesterolaemia is to some extent predictive of the lipid-lowering effects of HMGA

    Treatment with atorvastatin and albumin infusions in a patient with congenital analbuminemia

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    Congenital analbuminemia is a rare autosomic recessive inherited disorder characterized by low plasma albumin and hypercholesterolemia, which may increase cardiovascular risk. We report a case of congenital analbuminemia (1,0 g/dL) in a 38 yrs-old male with hypercholesterolemia (range 406-475 mg/dL) and severe arterial dysfunction (no brachial artery flow-mediated dilation). Long-term, cholesterol-lowering treatment with atorvastatin was associated with the appearance of peripheral edema. Two-months infusions of albumin improved flow-mediated dilation (7%) and reduced serum cholesterol (273 mg/dL), supporting the hypothesis of a compensatory role of hypercholesterolemia. Statin treatment, together with periodical albumin infusions, may safely contribute to decrease cardiovascular risk

    Intracranial hemorrage due to brain metastases in an Italian HCV patient with hepatocellular carcinoma

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    Brain metastases from hepatocarcinoma are exceptional and only a few cases have been reported in the literature, mainly from Far-Eastern countries. Clinical diagnosis in asymptomatic patients with preserved liver function is difficult and usually late. In some cases, cerebral metastasis is the initial manifestation of HCC and patients may develop intracerebral hemorrage and have a stroke-like presentation. We report on the first Italian case of cerebral metastases from multifocal hepatocellular carcinoma in an asymptomatic HbsAg negative patient with unknown HCV related chronic hepatitis and no evidence of liver cirrhosis. For many years he had a mild liver enzyme elevation and the presence of multiple misinterpreted hypoechogenic hepatic lesions. The hepatic tumor spread to the lungs and the brain and the patient developed two major episodes of intracranial hemorrage. He had two nodular lesions in the brain and alpha-fetoprotein levels were more than 10,000 ng/ml. He died from neurologic causes, without major signs of liver failure
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