Citation Information :
Zakaria Gad Y, El-Bendary M, Mahmoud Arafa M, Fawzy Lotfy Z. HLA Status and Antithyroid Autoantibodies in Egyptian Patients with Chronic Hepatitis C Virus Infection. Euroasian J Hepatogastroenterol 2011; 1 (1):15-18.
Background/Aim: The role of hepatitis C virus (HCV) has been demonstrated in many autoimmune diseases, including the autoimmune
thyroid disease. However, there is paucity of information about the prevalence of extrahepatic autoimmune phenomenon in HCV-infected
patients from Egypt and developing countries. This study checked the prevalence of antithyroid autoantibodies in patients with chronic HCV
infection and their possible relation to the human leukocyte antigen (HLA) status.
Patients and methods: Sera from 147 consecutive patients (75 males and 72 females) with chronic HCV infection at the Mansoura University
Hospitals, Egypt during 2008 to 2009, were analyzed for antithyroid antibodies (group 1). A total of 126 anti-HCV positive patients without
antithyroid antibodies were enrolled as controls (group 2).
Thyroid microsomal and thyroglobulin autoantibodies were determined by the hemagglutination tests. IgG type anti-GOR were measured
using an ELISA assay. HLA-A,-B, -C and -DR were determined using the standard complement-dependent microdroplet lymphocyte cytotoxicity
Results: Antithyroid antibodies were detected in 21 HCV RNA positive patients (group 1; 18 females, 3 males) and remaining 126 patients
(group 2; 72 males and 54 females). The prevalence of anti-GOR antibodies was significantly higher in patients of group 1 compared to that
of group 2.
A statistically significant difference was observed regarding anti-GOR antibodies in group 1 (p < 0.001), antithyroid autoantibodies
among the females (p < 0.001). HLA-A2 antigen was prevalent in group 1 (p < 0.05).
Conclusion: Our data revealed that HLA-A2 may be regarded as an immunologic risk factor for the development of antithyroid autoantibodies
in patients with chronic HCV infection and these autoantibodies should be evaluated prior to initiating IFN-α therapy.