Apoptotic and anti-apoptotic seromarkers for assessment of disease severity of non-alcoholic steatohepatitis

This study aimed to find out non-invasive markers for the assessment of severity of non-alcoholic steatohepatitis [NASH] in an attempt to decrease the need for liver biopsy. It also aimed to evaluate the key role of apoptosis in the pathogenesis of the disease and the suggested role of anti-apoptotic factors in therapeutic modalities and disease prognosis. The serum levels of soluble Fas [s. Fas], s. Fas ligand, cytokeratin 18 [CK-18] fragment and Bcl-2 were measured in 80 patients and 15 non-hepatic subjects as control. The patients were divided based on histological examination of liver biopsy into three groups. Group I included 40 patients with NASH, group II had 40 patients with non-alcoholic fatty liver disease [NAFLD] non-NASH and group III had 15 non-hepatic subjects as control. Apoptosis of hepatocytes was assessed by morphological examination using a light microscope and expressed as number per square millimeter. There was a significant increase in the serum levels of s. Fas, s. Fas ligand and CK-18 fragments in the NASH group. The anti-apoptotic protein Bcl-2 showed significantly low levels in NASH patients. Apoptosis of hepatocytes was significantly higher in the NASH group. The degree of apoptosis was inversely correlated with the level of Bcl-2. A significant correlation between both s. Fas and CK-18 fragment with liver histology with regard to lobular inflammation and ballooning was found. Increased serum levels of s. Fas and CK-18 fragment in the NASH group and its correlation with the severity of disease suggested the key role of apoptosis in NASH pathogenesis which can be used for the assessment of the severity of NASH. A high level of anti-apoptotic Bcl-2 in NAFLD suggests its protective role in disease progress

Serum level of interleukin-10 with its gene polymorphism can be predictors of response to treatment in Egyptian patients with chronic hepatitis C virus

The aim of this study was to demonstrate the role of interleukin-10 [IL-10] gene polymorphism and its serum level in predicting response to treatment in patients with chronic hepatitis C virus. This study was carried out on 35 Egyptian patients with chronic HCV [Hepatitis C Virus] and 15 age- and sex-matched healthy subjects as control. They were divided as follows: Group I: 35 chronic HCV patients. They were subdivided according to their response to combination therapy of pegylated interferon alpha 2b and ribavirin into: Group I [a]: 21 responder patients. Group I [b]: 14 non responder patients. Group II: 15 healthy subjects as a control group. IL-10 serum level was assessed by ELISA [Enzyme Linked Immunosorbent Assay] before, during and after treatment. IL-10 gene polymorphism and genotype were analyzed using polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP]. A significant higher level of serum IL-10 was detected in HCV patients compared to the control group. A significant reduction was detected during treatment and a persistent decrease was found in patients with SVR. Low serum level of IL-10 pretreatment was associated with high treatment response. High pretreatment of the serum level of IL-10 was associated with the severity of chronic necroinflammation and non response to treatment. A positive correlation was found between IL-10 and serum ALT. The frequency of IL-10 592 genotype polymorphism was higher in HCV patients compared to control. A significant higher frequency of the IL-10 592 C/C polymorphism was found in the responder group compared to non responder. No correlation was observed between IL-10 polymorphism and liver histopathology. Serum IL-10 level pretreatment is useful for predicting treatment response in HCV patients. IL-10 may be a useful marker to assess necroinflammation and to monitor the evolution of liver damage. IL-10 gene polymorphism has no relation to liver histopathology. IL-10 592 C/C genotype was more frequent in responder patients