Multiple changes in thyroid function in patients with chronic active HCV hepatitis treated with recombinant interferon-alpha

Roti, Elio; Minelli, Roberta; Giuberti, T.; Marchelli, S.; Schianchi, Claudia; Gardini, E.; Salvi, Mario; Fiaccadori, F; Ugolotti, G; Neri, Tauro Maria; Braverman, Lewis E.

doi:10.1016/s0002-9343(96)00259-8

Cited by 172 publications

(149 citation statements)

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“…Also contributing to the variation in the frequency of clinical disease are differences in its definition-some authors define clinical IIT as abnormal thyroid functions requiring therapy, 30,31 while others include subclinical disease not requiring therapy in the definition of IIT. 13,32,33 In our view only individuals developing thyroiditis requiring therapy should be defined as having clinical IIT.…”

Section: Autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

“…In addition, in individuals who had positive TAb's prior to IFN␣ therapy several studies reported an increase in the level of antibodies during therapy. 13,14,[34][35][36] Thus, it seems IFN␣ can induce thyroid autoimmunity de novo, as well as exacerbate preexisting thyroid autoimmunity. However, it is possible that even in individuals in whom IFN␣ therapy induced TAb's "de novo" a genetic predisposition already existed for thyroid autoimmunity.…”

Section: Autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

“…14 Roti et al calculated that positive TPO antibodies before IFN␣ therapy had a positive predictive value of 67% for the development of thyroid dysfunction. 13 Therefore, screening for TAb's should be performed prior to the initiation of interferon therapy in order to assess the risk of developing HT (see Therapeutic Considerations in Interferon Induced Thyroiditis below).…”

Section: Autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

“…9,10 Since then, numerous studies have reported a high incidence of thyroid disease in patients treated with IFN␣. 11,12 Prospective studies have shown that up to 15% of patients with hepatitis C receiving IFN␣ developed clinical thyroid disease, 13 and up to 40% developed thyroid antibodies. 14 Thyroid abnormalities following interferon therapy have also been described in children receiving interferon for hepatitis C infection.…”

mentioning

confidence: 99%

“…14 Thyroid abnormalities following interferon therapy have also been described in children receiving interferon for hepatitis C infection. 15 Some of these complications of IFN␣ therapy, especially thyrotoxicosis, can be severe and may interfere with adequate interferon therapy in patients with hepatitis C. 13,[16][17][18] Moreover, because the symptoms of hypothyroidismsuch as fatigue, hair loss, myalgia, and weight gain-may be attributable to hepatitis C or IFN␣ therapy, 8 the diagnosis of hypothyroidism in these patients may be delayed. This delay may lead to development of further complications.…”

mentioning

confidence: 99%

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The clinical and physiological spectrum of interferon-alpha induced thyroiditis: Toward a new classification

et al. 2006

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Interferon-alpha (IFN␣) is a major treatment modality for several malignant and nonmalignant diseases, especially hepatitis C. Prospective studies have shown that up to 15% of patients with hepatitis C receiving IFN␣ develop clinical thyroid disease, and up to 40% were reported to develop thyroid antibodies. Some of these complications may result in discontinuation of interferon therapy. Thus, interferon induced thyroiditis (IIT) is a major clinical problem for patients receiving interferon therapy. IIT can be classified as autoimmune type and non-autoimmune type. I nterferons were discovered in the 1950Јs and were immediately recognized for their ability to render cells resistant to virus infection. 1 Interferons have been classified into two major groups, type I interferons and type II interferons, based on their capacity to bind to common receptor types. Type I interferons bind to a type I interferon receptor and include interferon-␣, interferon-␤, interferon-, and interferon-. 2 Type II interferons bind to a distinct type II receptor and include interferon-␥. 2 In addition to their antiviral properties, interferons have immunomodulatory, antiangiogenic, antiproliferative and antitumor activity, and act as important regulators of growth and differentiation. 3 Interferons work by directly binding to either type I or type II receptors. The cytoplasmic domains of the transmembrane glycoproteins are associated with members of the JAK family of kinases. They activate various signaling pathways, including the JAK-STAT pathway, the Crk-pathway, the IRS signaling pathway, and the MAP kinase pathway, which leads to signal transduction and subsequent activation or repression of specific genes. 3,4 More than twenty interferon-induced proteins have been identified. 5 Interferon-alpha (IFN␣) was the first cytokine to be reproduced by recombinant DNA technology and has emerged as a major therapeutic modality for several malignant and nonmalignant diseases. Among the diseases treated by IFN␣ are melanoma, renal cell carcinoma, hairy cell leukemia, Kaposi's sarcoma, and hepatitis B and C. 5 However, the most common prescription for IFN␣

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