CD38+ Liver Stellate Cells in Chronic Hepatitis C Patients with Fibrosis

Authors

  • Titos Ahimsa Department of Internal Medicine, Cengkareng Hospital, Jakarta
  • Rino Alvani Gani Division of Hepatobiliary, Department of Internal Medicine, Faculty of Medicine, University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital, Jakarta
  • Ari Fahrial Syam Division Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital, Jakarta
  • Suhendro - - Research and Development, Department of Internal Medicine, Faculty of Medicine, University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital, Jakarta

DOI:

https://doi.org/10.24871/162201586-91

Keywords:

CD38 stellate cells, chronic hepatitis C, aspartate aminotransferase (AST), alanine aminotransferase (ALT), viral load hepatitis c virus ribonucleic acid (HCV RNA)

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.

Downloads

Published

2015-08-01

How to Cite

Ahimsa, T., Gani, R. A., Syam, A. F., & -, S. .-. (2015). CD38+ Liver Stellate Cells in Chronic Hepatitis C Patients with Fibrosis. The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy, 16(2), 86–91. https://doi.org/10.24871/162201586-91

Issue

Vol. 16 No. 2 (2015): VOLUME 16, NUMBER 2, August 2015

Section

Original Articles

License

Authors who publish with this journal agree to the following terms:

a. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.

b. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.

c. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).