Interferon-α and Autoimmune Thyroid Disease

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Abstract
Interferon-α (IFNα) is the main therapeutic agent in patients infected with the hepatitis C virus (HCV). It is rather safe, but is known to induce the production of autoantibodies and can lead to the occurrence of autoimmune disease. This minireview focuses on the induction of autoimmune thyroid disease (AITD) in HCV-infected patients treated with IFNα. Females carry a higher risk to develop AITD upon IFNα treatment, with a relative risk of 4.4 (95% confidence interval 3.2-5.9). The presence of thyroid peroxidase antibodies before therapy has a relative risk for AITD of 3.9 (95% confidence interval 1.9-8.1). IFNα-associated AITD can consist of autoimmune primary hypothyroidism, Graves' hyperthyroidism, and destructive thyroiditis, with hypothyroidism being the most common side effect. The clear association between AITD and IFNα use suggests that high endogenous IFNα levels may also be associated with naturally occurring AITD. High endogenous IFNα levels are seen in patients infected with certain viruses. It is concluded that IFNα is one of the environmental factors capable of triggering the onset of AITD in genetically susceptible individuals.