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Severe Steatosis (severe + steatosi)
Selected AbstractsLiver steatosis in chronic hepatitis C: a morphological sign suggesting infection with HCV genotype 3HISTOPATHOLOGY, Issue 2 2001L Rubbia-Brandt Liver steatosis in chronic hepatitis C: a morphological sign suggesting infection with HCV genotype 3 Aims:,To identify factors associated with liver steatosis in chronic hepatitis C. Methods and results:,Occurrence and severity of liver steatosis in 254 chronic hepatitis C patients were compared with presence of alcohol abuse, body mass index (BMI) >26, history of intravenous drug addiction and hepatitis C virus (HCV) genotype. Steatosis was found in 109 (43%) patients. The occurrence of steatosis was significantly associated with ongoing alcohol abuse (P=0.03) or HCV genotype 3 (P= 0.003), but not with BMI >26. A moderate to severe steatosis was present in 60% of patients infected with HCV genotype 3, irrespective of the presence of alcohol abuse, BMI >26 or history of intravenous drug addiction. Using a multivariable stepwise logistic regression analysis, infection with genotype 3 had an odds ratio (OR) of 10 (95% confidence interval (CI)=4.56,22) for a liver steatosis, whereas the presence of a cirrhosis at histology had an OR=0.256 (95% CI=0.07,0.92). Conclusions:,A moderate to severe degree of steatosis of the liver is a morphological sign suggestive of infection with HCV genotype 3, independent of other risk factors of a fatty liver, but it may disappear at late stages of the disease. [source] Non-alcoholic fatty liver syndrome: A hepatic consequence of common metabolic diseasesJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2003FRANCESCO ANGELICO Abstract Background and Aims: The association of liver steatosis with a number of common metabolic conditions has been suggested. The aim of the present study was to evaluate the clinical features of subjects with different severities of steatosis. Methods: The present study was performed in 282 consecutive patients with ,bright liver' at ultrasonography and in 58 subjects without steatosis. They had no history of alcohol abuse and negative tests for the presence of hepatitis B and C virus. Patients underwent clinical examination, anthropometry, laboratory tests and routine liver ultrasonography. Steatosis was graded as absent, mild, moderate and severe. Results: A progressive increase in the prevalence of obesity (P < 0.001), type 2 diabetes (P < 0.001), alanine aminotransferase (ALT) elevation (P < 0.001) and hypertriglyceridemia (P < 0.001), and a decrease of hypercholesterolemia (P < 0.05) was observed from the control group to the groups with mild, moderate and severe steatosis. More than half the subjects with liver steatosis had insulin resistance metabolic syndrome. Obesity, diabetes and hypertriglyceridemia were more common by 5.3-fold, 4.0-fold, and 6.7-fold, respectively, in subjects with severe steatosis, as compared to controls. Prevalence of obesity, diabetes and hyperlipidemia was significantly higher in subjects with fatty liver and ALT elevation. Conclusion: Fatty liver can be considered as the hepatic consequence of common metabolic diseases. © 2003 Blackwell Publishing Asia Pty Ltd [source] Predictors of a sustained virological response in patients with genotype 4 chronic hepatitis CLIVER INTERNATIONAL, Issue 8 2008Rita Raafat Gad Abstract Objectives: To determine the clinical, biological, virological and histological predictive factors associated with a sustained virological response (SVR) to combined interferon therapy among Egyptian patients infected by genotype 4 hepatitis C virus (HCV). Patients and Methods: Individual data from 250 patients with genotype 4 chronic hepatitis C, treated with different regimens of combined interferon, were analysed. The primary end point was SVR defined as undetectable HCV RNA by polymerase chain reaction (PCR) 24 weeks after the end of treatment. Multivariate logistic regression analysis was performed to select the independent prognostic parameters associated with SVR. Results: A sustained virological response was achieved among 137/250 (54.8%) patients. Baseline factors independently and negatively associated with SVR were serum ,-fetoprotein (AFP) level (above 0.3 upper limit of normal) [odds ratio (OR)=0.5, 95% confidence interval (CI): 0.2,0.8], severe fibrosis (Metavir score >F2) (OR=0.4, 95% CI: 0.2,0.8), presence of steatosis (OR=0.5, 95% CI: 0.3,0.97) and standard interferon treatment (OR=0.4, 95% CI: 0.2,0.8). Conclusions: Among genotype 4 chronic hepatitis C patients, severe fibrosis, severe steatosis, treatment with standard interferon and a high serum AFP level were all negatively associated with SVR. Pretreatment serum AFP level should be considered in the routine assessment of factors predictive of a treatment response. [source] Recurrent familial hypobetalipoproteinemia,induced nonalcoholic fatty liver disease after living donor liver transplantationLIVER TRANSPLANTATION, Issue 7 2009Noboru Harada Familial hypobetalipoproteinemia (FHBL) is one of the causes of nonalcoholic steatohepatitis (NASH) and a codominant disorder. Patients heterozygous for FHBL may be asymptomatic, although they demonstrate low plasma levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein B. Here we report a nonobese 54-year-old man with decompensated liver cirrhosis who underwent living donor liver transplantation with his son as the donor. Low albuminemia and refractory ascites persisted after transplantation. A biopsy specimen obtained 11 months after liver transplantation revealed severe steatosis and fibrosis, and recurrent NASH was diagnosed on the basis of pathological findings. Both the patient's and donor's laboratory tests demonstrated low LDL cholesterol and apolipoprotein levels. Because mutations in messenger RNAs of microsomal triglyceride transfer protein and apolipoprotein B genes were excluded neither in the recipient nor in the donor, both were clinically diagnosed as being heterozygous for FHBL. We successfully treated the recipient with heterozygous FHBL,induced recurrent NASH after liver transplantation using our diet and exercise programs. Liver Transpl 15:806,809, 2009. © 2009 AASLD. [source] Impairment of Hepatic Microcirculation in Fatty LiverMICROCIRCULATION, Issue 6 2003SAMIA IJAZ ABSTRACT Fatty liver or hepatic steatosis, which is the result of the abnormal accumulation of triacylglycerol within the cytoplasm of hepatocytes, is a common histological finding in human liver biopsy specimens that is attributed to the effects of alcohol excess, obesity, diabetes, or drugs. There is a general consensus that fatty liver compromises hepatic microcirculation, the common exchange network upon which hepatic arterial and portal inflows converge, regardless of underlying etiology. A significant reduction in hepatic microcirculation has been observed in human fatty donor livers and in experimental models of hepatic steatosis. There is an inverse correlation between the degree of fat infiltration and both total hepatic blood flow and flow in microcirculation. Fatty accumulation in the cytoplasm of the hepatocytes is associated with an increase in the cell volume that reduces the size of the hepatic sinusoid space by 50% compared with a normal liver and may result in partial or complete obstruction of the hepatic sinusoid space. As a result of impaired hepatic microcirculation, the hepatocytes of the fatty liver have reduced tolerance against ischemia-reperfusion injury, which affects about 25% of the donors for liver transplantation because severe steatosis is associated with a high risk of primary nonfunction after liver transplantation. [source] | ||||||||||