ABSTRACT
Activation of hepatic stellate cells [HSC] and transforming growth factor-b [TGF-bl] signaling are one of the important events at the beginning of fibrosis. Steatosis is present in liver biopsy in approximately 50% of patients with hepatitis C and its association with stage of fibrosis has been reported. The aim of this work is to study the relation between TGF-beta 1, steatosis, and fibrosis and hepatitis C genotype 4. We studied 47 patients [33 males, 14 females, mean age 43.46 +/- 13.54 years] with chronic HCV infection. Serum TGF-beta 1 was determined in all participants. Hepatitis C virus RNA was detected in patients' sera by reverse transcriptase-polymerase chain reaction [RT-PCR]. Liver biopsies were taken to evaluate steatosis, fibrosis, and tissue level of TGF-pL. Serurn levels of TGF-B1 [p < 0.001] were significantly higher in chronic hepatitis C patients compared with controls. Aspartate aminotransferase [AST], alanine aminotransferase [ALT] [p < 0.001], were significantly higher in chronic hepatitis C patients compared with controls. There was a significant difference between chronic hepatitis subgroups [as regard degree of steatosis] grading and staging [p< 0.001]. There was a significant correlation between steatosis grading and tissue level of TGF-Bl but not with serum level of TGF-B1. There was a significant correlation between fibrosis staging and tissue level of TGF-B1. Also, serum level of TGF-B1 was significantly correlated with advance of fibrosis. HCV-genotype 4 infection is associated with a significant higher serum level of TGF-B1 than those of normal subjects. We have confirmed that steatosis is associated with increased fibrosis and necroinflammation in chronic HCV biopsies
Subject(s)
Humans , Male , Female , /blood , Fatty Liver , Liver Cirrhosis , Liver Function Tests/blood , GenotypeABSTRACT
Iron overload may cause or contribute to hepatic injuiy and fibrosis. Mutations in tbr HFE gene may influence development or progression of chronic liver disease by increasing iron stores or modulating immune responses. The aim of this work was to assess the influence of HFE mutations and serum and hepatic measures of iron status on fibrosis severity and steatosis in patients with chronic hepatitis C genotype 4. We studied 47 patients [33 males, 14 females, mean age 43.46 +/- 13.54 years] with chronic HCV infection. Serum iron indices were determined in all participants. Hepatitis C virus RMA was detected in patients' sera by reverse transcriptase-polymerase chain reaction [RT-PCR]. Liver biopsies were taken to evaluate steatosis, fibrosis, and hepatic iron depositions. We used the method of polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP] to analyze the HFE mutations. Twenty-three patients 23/47 [48.936%] had increased serum iron stores and only eleven patients 11/47 [23.40%] had positive hepatic iron stain. There was a significant difference between hepatic steatosis subgroups as regards inflammatory grading and fibrosis staging [p <0.001]. Ferritin level was significantly correlated with fibrosis severity and steatosis grading. Hepatic iron deposition was significantly correlated only with steatosis grading but not with fibrosis severity. Heterozyosity for H63D allele was noted to be five patients 5/47 [10.638%] in CHC patients. Our data demonstrated no significant difference in the prevalence of HFE mutations between the HCV patients with increased serum iron store and others without Also, the same results were noticed in patients with and without hepatic iron deposition. Ferritin level should be better considered as a surrogate marker of severe fibrosis in chronic hepatitis C. The prevalence of HFE mutations associated with hereditary hemochromatosis is not increased in the patients with CHC. The HFE mutations may not contribute to iron accumulation in the CHC patients even when serum iron overload is observed in these patients