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ORIGINAL ARTICLE
Year : 2013  |  Volume : 41  |  Issue : 4  |  Page : 327-335

Serum leptin and ghrelin concentrations in chronic hepatitis C genotype-4 patients with steatosis: their effect on the response to antiviral therapy


1 Department of Internal Medicine, Faculty of Medicine, Mansoura University, Mansoura, Egypt
2 Department of Diagnostic Radiology, Faculty of Medicine, Mansoura University, Mansoura, Egypt
3 Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt

Correspondence Address:
Mohamed S Abd El Gawad
Department of Internal Medicine, Mansoura University Faculty of Medicine, Elgamaa street, Mansoura City
Egypt
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DOI: 10.4103/1110-1415.126198

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Background The precise pathogenic mechanisms of steatosis among patients with chronic hepatitis C (CHC) still remain largely unknown. Recent evidences identified various adipokines and gut hormones as relevant modulators of the pathophysiology of liver fibrosis and steatosis progression. We assessed whether pretreatment serum leptin and ghrelin concentrations differ in steatotic patients infected with hepatitis C virus (HCV) genotype-4 and whether these concentrations are associated with response to antiviral treatment. Participants and methods This study was conducted on 50 patients with CHC genotype-4 and steatosis and 25 age-matched healthy participants as a control group. Patients were treated with Peg-interferon and ribavirin for 48 weeks, independent of virologic response. Serum HCV-RNA concentrations were measured before the initiation of treatment and at weeks 12, 24, and 48 during the treatment. The genotype was determined using INNO-LIPA HCV assays, and serum leptin and ghrelin concentrations were measured using enzyme-linked immunosorbent assay. Biopsy specimens were scored according to the Ishak system, and steatosis was graded as mild, moderate, or severe. Results We found high insulin resistance and serum leptin concentrations and low plasma ghrelin concentrations at baseline in patients with CHC compared with the healthy controls (P = 0.000). Serum leptin levels tend to increase (P = 0.023), whereas plasma ghrelin levels tend to decrease (P = 0.004) as the grade of steatosis worsens. Plasma ghrelin at baseline showed significant negative correlations with insulin resistance and leptin. However, we did not find any correlations between leptin, ghrelin, insulin resistance, hepatic fibrosis, and hepatic steatosis with viral load. Sustained virological response (SVR) was achieved in 28 patients (56%) and was associated with a lower grade of liver steatosis (P = 0.013), milder fibrosis (P = 0.002), low value of insulin resistance (P = 0.001), lower leptin levels (P = 0.005), and higher ghrelin levels (P = 0.001), whereas patients who did not achieve SVR (nonresponder) had significantly higher leptin and lower ghrelin concentrations at baseline, with significant difference as the severity of steatosis worsened. Conclusion Increased serum leptin before treatment may predict non-SVR, whereas increased ghrelin may predict SVR. Ghrelin exerts antifibrotic effects on the liver and may represent a novel antifibrotic therapy.


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