Interferon induced thyroiditis - PubMed (original) (raw)

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Interferon induced thyroiditis

Yaron Tomer et al. Best Pract Res Clin Endocrinol Metab. 2009 Dec.

Abstract

Interferon-alpha (IFNalpha) is used for the treatment of various disorders, most notable chronic hepatitis C virus (HCV) infection. One of the commonest side effects of IFNalpha therapy is thyroiditis, with up to 40% of HCV patients on IFNalpha developing clinical or subclinical disease. In some cases interferon induced thyroiditis (IIT) may result in severe symptomatology necessitating discontinuation of therapy. IIT can manifest as clinical autoimmune thyroiditis, presenting with symptoms of classical Hashimoto's thyroiditis or Graves' disease, or as non-autoimmune thyroiditis. Non-autoimmune thyroiditis can manifest as destructive thyroiditis, with early thyrotoxicosis and later hypothyroidism, or as non-autoimmune hypothyroidism. While the epidemiology and clinical presentation of IIT have been well characterized the mechanisms causing IIT are still poorly understood. It is likely that the hepatitis C virus (HCV) itself plays a role in the disease, as the association between HCV infection and thyroiditis is well established. It is believed that IFNalpha induces thyroiditis by both immune stimulatory effects and by direct effects on the thyroid. Early detection and therapy of this condition are important in order to avoid complications of thyroid disease such as cardiac arrhythmias.

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Figure 1

Figure 1

Postulated mechanism for the development of IIT. Both autoimmune and non-autoimmune effects of IFNα are involved. Immune effects of IFNα include activation of immune cells, switching the immune response to Th1 pathways, downregulation of Treg cells, and induction of cytokine release and MHC I expression. Direct thyroid toxic effects include upregulation of thyroid-specific proteins (TSHR, Tg, TPO, NIS) expression, as well as induction of heat shock proteins (Hsp) expression, and thyroid cell death. The combination of direct thyroid toxicity and immune stimulation can cause release of thyroid auto-antigens and their presentation to resident T-cells. This will initiate an autoimmune response by a bystander mechanism.

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References

    1. Pfeffer LM, Dinarello CA, Herberman RB, Williams BR, Borden EC, Bordens R, et al. Biological properties of recombinant alpha-interferons: 40th anniversary of the discovery of interferons. Cancer Res. 1998;58(12):2489–2499. - PubMed
    1. Parmar S, Platanias LC. Interferons: mechanisms of action and clinical applications. Curr Opin Oncol. 2003;15(6):431–439. - PubMed
    1. Jonasch E, Haluska FG. Interferon in oncological practice: review of interferon biology, clinical applications, and toxicities. Oncologist. 2001;6(1):34–55. - PubMed
    1. Baron S, Tyring SK, Fleischmann WR, Jr, Coppenhaver DH, Niesel DW, Klimpel GR, et al. The interferons. Mechanisms of action and clinical applications. JAMA. 1991;266(10):1375–1383. - PubMed
    1. Fried MW, Shiffman ML, Reddy KR, Smith C, Marinos G, Goncales FL, Jr, et al. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection. N Engl J Med. 2002;347(13):975–982. - PubMed

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