Interferon-α and autoimmune thyroid disease

Interferon-alpha (IFNalpha) 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 IFNalpha. Females carry a higher risk to develop AITD upon IFNalpha 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). IFNalpha-associated AITD can consist of autoimmune primary hypothyroidism, Graves' hyperthyroidism, and destructive thyrolditis, with hypothyroidism being the most common side effect. The clear association between AITD and IFNalpha use suggests that high endogenous IFNalpha levels may also be associated with naturally occurring AITD. High endogenous IFNalpha levels are seen in patients infected with certain viruses. It is concluded that IFNalpha is one of the environmental factors capable of triggering the onset of AITD in genetically susceptible individuals.