Abstract
Background: Approximately 3% of the world population is infected with hepatitis C virus (HCV). Protein of hepatitis C virus modulates apoptosis and steatosis, liver cell injury, activates liver stellate cells and liver fibrosis. Hepatitis C virus infection will cause injury to the hepatocytes. This injury to the hepatocyte will activate liver stellate cells. Stellate cells have a huge role in the development of liver fibrosis. The objective of this study is to evaluate the difference of active CD38+ liver stellate cells in various degree of fibrosis as well as its relation with aspartate transaminase (AST), alanine transaminase (ALT), and quantitative amount of hepatitis c virus ribonucleic acid (HCV RNA) in chronic hepatitis C.Method: This study was a cross-sectional study performed in 32 patients with chronic hepatitis C who had undergone liver USG, did not suffer from hepatoma, had undergone liver biopsy. Paraffin block of patients’ liver tissue was further stained using Haematoxylin and Eosin technique to identify the Metavir degree which is categorized into mild-moderate or severe degree. Special staining is performed to evaluate liver stellate cells that were then counted in averagely in five fields of view.Results: In this study, we found significant difference in the amount of CD38+ stellate liver cells between severe and mild-moderate fibrosis (p 0.001), there was no association between CD38+ stellate liver cells with AST (p = 0.2) or ALT (p = 0.7), and there was association between CD38+ stellate liver cells with quantitative HCV RNA (r = -0.372).Conclusion: Total amount of CD38+ stellate liver cells in severe fibrosis was higher compared to the total amount of CD38+ liver stellate cells in mild-moderate fibrosis. There was no association between the value of AST, ALT, and quantitative HCV RNA with the number of CD38+ stellate liver cells.
Highlights
3% of the world population is infected with hepatitis C virus
The results of this study revealed the increase of CD38+ liver stellate cells in accordance with the advancing degree of ¿EURVLVIURPPLOGWRVHYHUH7KLVZDVFRQVLVWHQWZLWK the hypothesis that CD38+ liver stellate cells would increase in concordance with the advancing degree of ¿EURVLVRIWKHOLYHUFHOOV$UHWURVSHFWLYHVWXG\ZKLFK was conducted by Tomanovic et al, studied 20 liver biopsy samples of chronic hepatitis C patients and 10 normal liver biopsy samples
Study conducted by Nadeem et al in 107 non-cirrhotic hepatitis C patients and had not received treatment for hepatitis C revealed that there was no association between aspartate transaminase (AST) YDOXH DQG GHJUHH RI OLYHU ¿EURVLV ZKLFK LPSOLFLWO\ showed that there was no correlation between AST value and number of CD38+ liver stellate cells.[11]
Summary
3% of the world population is infected with hepatitis C virus. Protein of the hepatitis C virus modulates apoptosis and steatosis, liver cell LQMXU\DFWLYDWHVOLYHUVWHOODWHFHOOVDQGOLYHU¿EURVLV Around 10-20% will develop into liver cirrhosis and hepatocellular carcinoma. While the body immune system tries to eliminate the virus, liver cells injury DQG¿EURVLVLQFKURQLFLQIHFWLRQKDSSHQWKURXJKGLUHFW FHOOXODUWR[LFLW\DQGUHOHDVHRIORQJWHUPLQÀDPPDWRU\ cytokines.[1,2] Hepatitis C virus infection will cause injury to the hepatocytes. This injury to the hepatocytes will activate liver stellate cells. By ceasing the injury to liver FHOOVOLYHUP\R¿EUREODVWZLOOGLVDSSHDU3 it has been known that other mesenchymal liver cells contribute in the accumulation of extracellular matrix, stellate cells activation pathway is still considered as the PDLQSDWKZD\LQWKHSURFHVVRIOLYHU¿EURVLVWKURXJKLWV response towards liver tissue injury.[4] These cells have
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