Brief Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jul 28, 2012; 18(28): 3738-3744
Published online Jul 28, 2012. doi: 10.3748/wjg.v18.i28.3738
Vitamin D deficiency: Correlation to interleukin-17, interleukin-23 and PIIINP in hepatitis C virus genotype 4
Mona F Schaalan, Waleed A Mohamed, Hesham H Amin
Mona F Schaalan, Department of Biochemistry, Faculty of Pharmacy, Misr International University, Cairo 1, Egypt
Waleed A Mohamed, Department of Chemistry, Cairo University, Cairo 11562, Egypt
Hesham H Amin, Department of Clinical Pathology, Faculty of Medicine, AL Azhar University, Cairo 147, Egypt
Author contributions: Mohamed WA and Amin HH contributed to the acquisition and analysis of data; Schaalan MF and Mohamed WA contributed to the interpretation of data and drafting the article; Schaalan MF revised the manuscript critically for important intellectual content and approved the final version to be published; all authors contributed equally to the conception and design of the study.
Correspondence to: Dr. Mona F Schaalan, PhD, Department of Biochemistry, Faculty of Pharmacy, Misr International University, Km 28, Cairo-Ismailia Road, Cairo PO Box 1, Heliopolis, Cairo 11562, Egypt. mona.schaalan@miuegypt.edu.eg
Telephone: +20-22-2400800 Fax: +20-10-2011100
Received: December 13, 2011
Revised: April 19, 2012
Accepted: April 27, 2012
Published online: July 28, 2012
Abstract

AIM: To assess vitamin D (Vit D) abnormalities in hepatitis C infected patients and their relationship with interleukin (IL)-17, IL-23 and N-terminal propeptide of type III pro-collagen (PIIINP) as immune response mediators.

METHODS: The study was conducted on 50 Egyptian patients (36 male, 14 female) with hepatitis C virus (HCV) infection, who visited the Hepatology Outpatient Clinic in the Endemic Disease Hospital at Cairo University. Patients were compared with 25 age- and sex-matched healthy individuals. Inclusion criteria were based on a history of liver disease with HCV genotype 4 (HCV-4) infection (as new patients or under follow-up). Based on ultrasonography, patients were classified into four subgroups; 14 with bright hepatomegaly; 11 with perihepatic fibrosis; 11 with hepatic cirrhosis; and 14 with cirrhosis and hepatocellular carcinoma (HCC). Total Vit D (i.e., 25-OH-Vit D) and active Vit D [i.e., 1,25-(OH)2-Vit D] assays were carried out using commercial kits. IL-17, IL-23 and PIIINP levels were assayed using enzyme linked immunosorbent assay kits, while HCV virus was measured by quantitative and qualitative polymerase chain reaction.

RESULTS: Levels of Vit D and its active form were significantly lower in advanced liver disease (hepatic cirrhosis and/or carcinoma) patients, compared to those with bright hepatomegaly and perihepatic fibrosis. IL-17, IL-23 and PIIINP levels were markedly increased in HCV patients and correlated with the progression of hepatic damage. The decrease in Vit D and active Vit D was concomitant with an increase in viral load, as well as levels of IL-17, IL-23 and PIIINP among all subgroups of HCV-infected patients, compared to normal healthy controls. A significant negative correlation was evident between active Vit D and each of IL-17, IL-23 and PIIINP (r = -0.679, -0.801 and -0.920 at P < 0.001, respectively). HCV-infected men and women showed no differences with respect to Vit D levels. The viral load was negatively correlated with Vit D and active Vit D (r = -0.084 and -0.846 at P < 0.001, respectively), and positively correlated with IL-17, IL-23 and PIIINP (r = 0.951, 0.922 and 0.94 at P < 0.001, respectively). Whether the deficiency in Vit D was related to HCV-induced chronic liver disease or was a predisposing factor for a higher viral load remains to be elucidated.

CONCLUSION: The negative correlations between Vit D and IL-17, IL-23 and PIIINP highlight their involvement in the immune response in patients with HCV-4-related liver diseases in Egypt.

Keywords: Vitamin D, Interleukin-17, Interleukin-23, N-terminal propeptide of type III pro-collagen, Hepatitis genotype 4