Thyroid autoimmunity and dysfunction associated with type I interferon therapy

Monzani, Fabio; Caraccio, N; Dardano, Angela; Ferrannini, Eleuterio

doi:10.1007/s10238-004-0026-3

Cited by 61 publications

(53 citation statements)

References 50 publications

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“…13,30,43 IFN␣ induced non-autoimmune thyroiditis exists in two forms, destructive thyroiditis and hypothyroidism.…”

Section: Non-autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

“…Indeed, several studies have shown patients infected with HCV are more susceptible to develop thyroid autoimmunity and interferon induce thyroiditis compared to patients infected with hepatitis B virus (HBV). 14,30,43,55 However, in these studies shorter regimens were being used to treat hepatitis B infection and it is possible that with the newer longer regimens the frequency of IIT in patients infected with HBV may be higher than originally reported.…”

Section: Non-genetic Factorsmentioning

confidence: 99%

“…13 It remains unclear if the above findings are related to a direct toxicity of IFN␣ on thyroid cells or to induction of an abnormal expression and/or function of specific enzymes involved in iodine uptake. 43 Therapeutic Considerations in Interferon Induced Thyroiditis (Fig. 1) Given that IIT is a major clinical problem for patients receiving interferon therapy, we suggest some basic therapeutic guidelines and stress the importance of close collaboration between hepatologists and endocrinologists in the care of these patients.…”

Section: Direct Effects Of Ifn␣ On the Thyroidmentioning

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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“…13,30,43 IFN␣ induced non-autoimmune thyroiditis exists in two forms, destructive thyroiditis and hypothyroidism.…”

Section: Non-autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

Section: Non-genetic Factorsmentioning

confidence: 99%

Section: Direct Effects Of Ifn␣ On the Thyroidmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2006

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“…20,21 Bir derlemede de, MS hastalarında anti-TPO pozitifliğinin %4-22 arasında olduğu belirtilmiştir. 22 Tiroid hormonları; beynin normal gelişimi, oligodendrosit matürasyonu ve miyelinizasyon için gereklidir. 23 Tiroid hormon eksikliğinin hipomiyelinizasyona yol açabildiği in vivo ortamda gösteril-miştir.…”

Section: Discussionunclassified

The Prevalence of Thyroid Autoantibodies in Multiple Sclerosis Patients

Gençer¹,

Türkoğlu²,

Çetinkaya³

et al. 2015

Turkiye Klinikleri J Neur

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“…Levesque et al 1999;Alsalameh et al 1998], type I diabetes [Burdick et al 2009;Fabris et al 2003], and autoimmune hepatitis [Duchini, 2002;Heathcote, 1995]. Thyroid dysfunction is also a relatively common side effect of IFN treatment, particularly in patients with pre-existing thyroid autoimmunity [Monzani et al 2004]. As in the case of SLE, polymorphisms in the genes encoding proteins involved in the activation or activity of type I IFNs are also associated with a predisposition to develop certain of these diseases.…”

Section: Therapeutic Advances In Drug Safety 2 (3)mentioning

confidence: 99%

Immunogenicity and other problems associated with the use of biopharmaceuticals

Tovey¹,

Lallemand

2011

Therapeutic Advances in Drug Safety

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Biopharmaceuticals are used widely for the treatment of cancer, chronic viral hepatitis, inflammatory, and autoimmune diseases. Biopharmaceuticals such as interferons are well tolerated for the most part with the most common adverse events observed being 'flu-like' symptoms that resolve rapidly after initial treatment. Prolonged treatment is associated, however, with more serious adverse events including leucopenia, thrombocytopenia, and neuropsychiatric effects, which may necessitate dose reduction or even cessation of treatment in some patients. Recombinant growth factors, such as erythropoietin (EPO), granulocyte colony-stimulating factor, or granulocyte macrophage colony-stimulating factor, are for the most part well tolerated, although severe complications have been reported in patients with cancer or chronic kidney disease treated with EPO. Similarly, treatment of patients with cancer with high doses of interleukin-2 is associated with significant toxicity. Treatment of chronic inflammatory diseases, such as rheumatoid arthritis, psoriasis, and Crohn's disease, with antitumor necrosis factor-alpha monoclonal antibodies is associated with an increased risk of granulomatous infections and, in particular, tuberculosis. The monoclonal antibody, natalizumab, that targets alpha4 integrins is effective in the treatment of multiple sclerosis but is associated with the activation of JC virus and development of progressive multifocal leukoencephalopathy. Repeated administration of recombinant proteins can cause a break in immune tolerance in some patients resulting in the production of a polyclonal antibody response that can adversely affect pharmacokinetics and clinical response. In addition, neutralizing antibodies that cross react with nonredundant essential proteins such as EPO can cause severe autoimmune reactions.

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Thyroid autoimmunity and dysfunction associated with type I interferon therapy

Cited by 61 publications

References 50 publications

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

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

The Prevalence of Thyroid Autoantibodies in Multiple Sclerosis Patients

Immunogenicity and other problems associated with the use of biopharmaceuticals

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