Fatty Liver ; Humans

Elasticity Imaging Techniques ; Fatty Liver ; diagnostic imaging ; Humans

Genetic Predisposition to Disease ; Humans ; Non-alcoholic Fatty Liver Disease ; diagnosis ; genetics ; therapy

Controlled attenuation parameter (CAP)is a noninvasive,quantitative,fast,and reliable novel tool for the assessment of fatty liver disease (FLD),and it has been a hotspot in the noninvasive diagnosis of FLD.This paper introduces factors associated with CAP asses-sing FLD,the cut -off value for the diagnosis of liver steatosis,and the causes of the failure of CAP measurement and unreliable CAP meas-urement.The paper believes that even though the noninvasive and quantitative diagnosis of FLD by CAP has been confirmed by many stud-ies,most of the results were obtained with a limited sample size.Therefore,the factors associated with the cut -off value for CAP diagnosing liver steatosis and factors influencing the measurement results still need validation with larger samples and multi -centered research reports.

Evidence-based guideline of the diagnosis and treatment in the nonalcoholic fatty liver disease was formulated by Chinese Medical Association of fatty liver disease and alcoholic liver disease in order to simplify medical decision making and to help physicians make good decisions about NAFLD,which was published in 2006.Compared with some international guidelines or recommendations,Chinese guideline is more wide and complete for diagnosis and therapy of NAFLD.Meanwhile,there is significant difference in evaluation and treatment between these guidelines.

Nonalcoholic fatty liver disease(NAFLD) is the most common liver disorder in the world.A significant,albeit relative small,proportion of NAFLD patients can advance from steatohepatitis to liver cirrhosis and hepatocellular carcinoma.Moreover,NAFLD is associated independently with an increased incidence of type 2 diabetes and cardiovascular disease.The mortality of patients with NAFLD is significantly higher than that among the general population and cardiovascular risk may compete with liver-related risk in dictating the final outcome.From a clinical point of view,it has become mandatory to evaluate the metabolic risk factors in NAFLD patients and to consider careful surveillance and aggressive treatment of both hepatic and cardiovascular outcomes.Nowadays,there are substantial advances in the ability to make the diagnosis of NAFLD as well as both grade and stage the disease,however,liver biopsy remains the gold standard.Lifestyle changes are the first line and mainstay of management of NAFLD,weight loss and treatment of insulin resistant remain central to the therapeutic process.Specific pharmacological treatment is currently not recommended for routine clinical practice.

Hepatolenticular Degeneration ; diagnosis ; therapy ; Humans

Humans ; Non-alcoholic Fatty Liver Disease ; diagnosis ; therapy

Objective To study the pathogenesis of nonalcoholic steatohepatitis(NASH) in rat model. Methods Male SD rats were fed with a high fat diet for 12 weeks. Non alcoholic ateatohepatitis serum lipid, aminotransferase values and free fatty acid (FFA) levels were tested, the malondialdehyde (MDA) and superoxide dismutase (SOD) activity of hepatic tissue were also detected. Hepatic cytochrome P450ⅡE 1 (CYPⅡE 1) were detected in liver section by immunohistochemistry using CYPⅡE 1 specific antibodies and also with an immunohistochemical procedure for detecting the number of Kupffer cells. Results FFA concentrations of the serum and hepatic tissue were markedly increased, which was accompanied by an increase of MDA in hepatic tissue, whereas SOD activity of hepatic tissue was decreased. CYPⅡE 1 immunostaining was markedly increased, especially in the perivenous region. The number of Kupffer cells in NASH was significantly increased compared with control livers. Correlation analysis revealed that the increases in the levels of FFA correlated positively with the hepatic CYPⅡE 1 expression, the lipid peroxidation, and the pathological scores in the liver of NASH rats. Conclusion The increased FFA, highly expressed CYPⅡE 1, activated kupffer cells and increased lipid oxidate were all contributed to NASH.

Amyloidosis ; Gastrointestinal Hemorrhage ; Humans ; Immunoglobulin Light-chain Amyloidosis