Plasmapheresis in the treatment of hepatic coma]

Fourteen patients, including 6 with viral hepatitis B and 8 with liver cirrhosis were treated with plasmapheresis for hepatic coma. Altogether 29 plasmaphereses were carried out. Complete recovery was achieved in one patient with viral hepatitis B and in 3 patients with liver cirrhosis. Plasmapheresis should be performed in patients with severe lesions to the liver. Classification of patients to the treatment should include clinical examination, biochemical and enzymatic tests, and evaluation of liver reserve with isotope hepatography. In case of the acute poisoning with hepatotoxic agents indications to plasmapheresis should be evaluated from the toxicologic point of view.     

Plasmapheresis in the treatment of hepatic coma complicating viral hepatitis]

Therapeutic plasmaphereses using CS 3000 Fenwal Cell Separator were performed in 4 women and 2 men, aged between 17 and 44 years, with hepatic coma complicating acute viral hepatitis type B. One to four plasma exchanges per patient were performed, usually at the volume of 3000 ml per procedure. Two patients at II and IVa period of the coma, according to Aboun classification, survived. Four patients at II, III and two at III/IV period of the coma died. The authors suggest that in some cases exchange of large volumes of plasma in the treatment of hepatic coma complicating acute viral hepatitis may be a lifesaving procedure.     

Genetic determinants of hepatic steatosis in man

Hepatic steatosis is one of the most common liver disorders in the general population. The main cause of hepatic steatosis is nonalcoholic fatty liver disease (NAFLD), representing the hepatic component of the metabolic syndrome, which is characterized by type 2 diabetes, obesity, and dyslipidemia. Insulin resistance and excess adiposity are considered to play key roles in the pathogenesis of NAFLD. Although the risk factors for NAFLD are well established, the genetic basis of hepatic steatosis is largely unknown. Here we review recent progress on genomic variants and their association with hepatic steatosis and discuss the potential impact of these genetic studies on clinical practice. Identifying the genetic determinants of hepatic steatosis will lead to a better understanding of the pathogenesis and progression of NAFLD.