Relationship of Serum Hepcidin, Ferritin and Iron in Chronic Hepatitis C Patients of District Hyderabad.

Evaluating Iron Metabolism Biomarkers among Patients of Chronic Hepatitis C

Abstract

Introduction: Hepatitis C Virus (HCV) is the 2nd largest infection in Pakistan. Roughly 20% of individuals with hepetitis C virus eventually develop liver scarring and cancer. The primary cause of the advancement of the disease is iron overload, with subsequent decreased levels of hepcidin. Objectives: The study aimed to determine the correlation of hepcidin, and ferritin levels with disease progression in chronic hepatitis C (CHC) patients. Methodology: A cross-sectional study was carried out in the Physiology department of L UM H S, in collaboration with clinical wards (Medicine ward, medicine outpatient department, gastroenterology ward, gastroenterology outpatient department) and D-R Lab, LUMHS. The study was conducted from 22^nd February 2022 to 22^nd September 2022. Diagnosed male and female patients aged between 20-45 years visiting the medicine and gastro outpatient department or admitted to the medicine and gastro ward at LUMHS Jamshoro were included in this study. A Self-structured questionnaire was used to collect data and blood samples were drawn from participants for serum hepcidin, and ferritin. SPSS 23.0. Results: The study involved 116 volunteer participants. Of these, 48 (41.3%) were male, and 68 (58.6%) were female, the mean age of the participants was 47.7 years. The serum hepcidin was negatively and non-significantly related to ferritin levels, at an R-value of 0.069 and a P-value of 0.459, and substantially negatively correlated at iron (R-value= 0.497) and (P value= < 0.0001). Conclusion: This study concludes that for the participants with hepatitis, low hepcidin levels are often observed as a result of excessive iron in the body. Our research suggested hepcidin as a predictive marker for monitoring iron load in patients of CHC, iron overload in CHC is the core reason for disease progression to cirrhosis. Hepcidin transcription is down-regulated by HCV-induced reactive oxygen species, increasing duodenum iron intake and macrophage release.