Hepatic steatosis: A benign disease or a silent killer

Abstract

Steatosis is a common feature of many liver diseases, namely non-alcoholic steatohepatitis (NASH) and hepatitis C virus (HCV) infection, but the pathogenic mechanisms differ. Insulin resistance (IR), a key feature of metabolic syndrome, is crucial for NASH development, associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis. This may have potential implications for new drug therapy. In HCV-related disease, steatosis impacts both fibrosis progression and response to treatment. Steatosis in HCV-related disease relates to both viral factors (HCV genotype 3), and host factors (alcohol consumption, overweight, hyperlipidemia, diabetes). Among others, IR is a recognized factor. Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors. Thus, hepatic steatosis should not be considered a benign feature, but rather a silent killer.

Clinical characteristics associated with hepatic steatosis on ultrasonography in patients with elevated alanine aminotransferase

“…The conventional methods include abdominal ultrasonography, computed tomography (CT) and MRI . 4 Ultrasonography is the method of choice for the initial assessment of hepatic steatosis, since it presents a number of advantages over oth- Table 3. Distribution of biochemical variables among 94 blood donors with elevated ALT, according to the presence of hepatic steatosis on ultrasonography xLSn = times the upper limit of normality; AST = aspartate aminotransferase; ALT = alanine aminotransferase; DB = direct bilirubin; ALP = alkaline phosphatase; GGT = gamma glutamyltransferase; *Student's t test or Mann-Whitney test, as appropriate for group comparisons.…”

“…In viral hepatitis, liver fibrosis progression to cirrhosis is due to the presence of chronic active hepatitis. 4 Even if the evolution of NAFLD depends on the causative factor, the early stages may be reversible if early intervention is taken to remove the offending factor. Individuals with advanced fibrosis exhibit an increased risk of developing hepatocellular carcinoma, although this risk is less common in NAFLD than is seen in cirrhosis due to alcohol or the hepatitis C virus.…”

Management of Chronic Hepatitis C Virus Infection: Current Perspectives

“…Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops [66].Usually (80% of the time) this change affects less than a third of the liver [66].Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25 % hepatocellular carcinoma [35].About 10 t0 30% of those infected develop cirrhosis over 30 years [13,7]..Cirrhosis is more common in those also infected with hepatitis B, Schistosoma, orHIV,inalcoholics and those of male gender [7].In those with hepatitis C,excess alcohol increases the risk of developing cirrhosis 100 fold [67].Those who develop cirrhosis have a 20 fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1-3% per year [13,7].Being infected with hepatitis B in addition to hepatitis C increases this risk further [68].Liver cirrhosis may lead to portal hypertension, ascites(accumulation of fluid in the abdomen) easy bruising or bleeding, varicose (enlarged veins, especially in the stomach and esophagus),jaundice, and a syndrome of cognitive impairment known as encephalopathy [69].Ascites occurs at some stage in more than half of those who have chronic infection [70].…”

Liquid-Crystal in Embryogenesis and Pathogenesis of Human Diseases

“…Maltese-crosses, indicating liquid-crystals, have also been found in lipid depositions accumulating in smooth muscle and foam cells [Kruth H 2001]. These liquid crystal depositions in the vascular wall were found to be low density lipoproteincholesteryl esters mediated by cell surface receptors [Goldstein JL et al 1977, 1979, 2008Brown MS et al 1974, 1974]. …”