Article PDF :

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Article type :

Original Article

Author :

Vasanthy Nagarajan*, Sarah Andrea Wilson, Asha G K, Kaveri Krishansamy, Banumathi Radhika, Anupama C P

Volume :

9

Issue :

4

Abstract :

Background: Autoimmune thyroid disease (AITD) is the result of a complex interaction between genetic and environmental factors, which leads to failure of one or more mechanisms responsible for controlling thyroid-reactive T and B cells. The most frequently occurring clinical forms of autoimmune thyroiditis include Hashimoto’s thyroiditis and Grave’s disease. Viruses have been implicated in the onset of autoimmune disorders. This study aims to investigate the association between Hepatitis C virus, Parvovirus B19 and Enteroviruses in autoimmune thyroiditis by assessing virologic and immunologic parameters of cases with clinical indication of AITD. Materials and Methods: Anti-thyroid peroxidase (TPO) and Anti-thyroglobulin (TG) antibodies were evaluated using ELISA. The presence of Hepatitis C virus (HCV) IgG antibodies and Parvovirus B19 IgM antibodies were evaluated using ELISA. The presence of Enterovirus RNA was investigated by RT-PCR.  Results: A total of sixty study subjects were involved in this study. Sixteen male patients (26.66%) and forty-four female patients (68.33%) were positive for Anti-TPO antibodies. Four male patients (6.66%) and twenty-five female patients (41.66%) were positive for Anti-TG antibodies. Four male patients (6.66%) and twenty-two female patients (36.66%) were positive for both Anti-TPO and Anti-TG antibodies. One female patient tested positive for HCV IgG antibodies. Sixteen patients (26.66%) were positive for Parvovirus B19 IgM by ELISA of which 3 patients (5%) were male and 13 patients (21.66%) were female. None of the samples were positive for enterovirus RNA. Conclusion: We conclude that viral infection may be involved in triggering autoimmune mechanisms. Further studies with a larger population are necessary to establish an association between HCV, Parvovirus B19 and Enteroviruses in the pathogenesis of autoimmune thyroid disorders.