Development of thyroid disease during therapy of chronic viral hepatitis with interferon alfa

Lisker‐Melman, Mauricio; Bisceglie, Adrian M. Di; Usala, Stephen J.; Weintraub, Bruce D.; Murray, Linda; Hoofnagle, Jay H.

doi:10.1016/0016-5085(92)90348-3

Cited by 206 publications

(115 citation statements)

References 16 publications

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“…Several studies found even lower prevalence of hyperthyroidism, ranging from 0.9% to 1.1%. 16,27,29,44 Destructive thyroiditis occurred in 5.1% of our patients and approximately 70% developed permanent hypothyroidism. Almost 50% of non-autoimmune IFN-α-induced thyroiditis manifests such a destructive thyroiditis, a self-limited inflammatory disorder characterized by three phases of six to eight weeks each: thyrotoxicosis, hypothyroidism and resolution to euthyroidism or definitive hypothyroidism in less than 5% of the cases.…”

Section: Discussionmentioning

confidence: 70%

“…[29][30][31] In our patients, the presence of thyroid dysfunction did not lead to changes in the dose or therapy withdrawal.…”

Section: Discussionmentioning

confidence: 96%

“…Previous studies have reported that thyroid dysfunction induced by IFN-α could develop in the first week or after a few months, during and after therapy, with a possible contribution of cumulative dose. 17,29,32 Nevertheless, the underlying mechanism remains unclear. The immunomodulatory action of IFN-α in susceptible patients 38,40-42 could affect the thyroid hormone syn-thesis and secretion in vitro.…”

Section: Discussionmentioning

confidence: 99%

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Virus C genotype predisposes to primary hypothyroidism during interferon-α treatment for chronic hepatitis C

Pavan¹,

Pavin²,

Gonçales³

et al. 2011

Braz J Infect Dis

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Objective: The treatment of the chronic hepatitis C (HCV) with α-interferon is associated with thyroid dysfunction (TD). The aim of this study was to evaluate thyroid function outcome among patients with chronic HCV under treatment with conventional interferon (IFN) or peguilated interferon (PEG-IFN) in association with ribavirin. Patients and Methods: We studied 293 patients with chronic HCV, submitted to drug therapy for 24 or 48 weeks. Initially, we evaluated FT4, TSH, TPOAb, TgAb, and continued to monitor FT4 and TSH every three months during therapy and six months thereafter. Results: At baseline, TD prevalence was 6.82% (n = 20); 6.14% hypothyroidism; 0.68% hyperthyroidism. TPOAb was present in 5.46% of euthyroid patients. Out of 273 euthyroid patients at baseline, 19% developed TD: 17.2% hypothyroidism; 1.8% hyperthyroidism; 5.1% destructive thyroiditis (DT). 90% of TPOAb-positive patients at baseline developed hypothyroidism vs 14.5% of TPOAb-negative patients (p < 0.001). On average, TD occurred after 25.8 ± 15.5 weeks of treatment. 87.2% of patients who developed hypothyroidism did so during the first therapeutic cycle (p = 0.004; OR = 3.52; 95% CI = 1.36-9.65). Patients infected with genotype 1 virus were 2.13 times more likely to develop hypothyroidism (p = 0.036; 95% CI = 1.04-4.38). Hypothyroid and DT patients presented higher TSH levels before-treatment than patients who had remained euthyroid (p < 0.001; p = 0.002, respectively). DT patients presented lower qALT (p = 0.012) than euthyroid patients. Conclusion: Hypothyroidism was the most frequent TD, especially during the first cycle of α-interferon. Genotype 1 virus was associated with a risk two times higher for developing the illness. There was no need to interrupt or to change HCV treatment. Therefore, approximately 34% of TD was transient.

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Section: Discussionmentioning

confidence: 70%

“…[29][30][31] In our patients, the presence of thyroid dysfunction did not lead to changes in the dose or therapy withdrawal.…”

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Virus C genotype predisposes to primary hypothyroidism during interferon-α treatment for chronic hepatitis C

Pavan¹,

Pavin²,

Gonçales³

et al. 2011

Braz J Infect Dis

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“…30 In another large multicenter study 3 of 237 patients receiving IFN␣ developed GD, and required definitive treatment. 31 In most reported cases of GD developing secondary to IFN␣ therapy the disease did not go into remission after completion of interferon therapy and the patients required treatment even after interferon therapy ended. 30,31,34 This outcome may suggest that in these cases interferon triggered the development of GD in individuals already predisposed to the disease.…”

Section: Autoimmune Interferon Induced Thyroiditismentioning

confidence: 99%

“…The same factors likely contributed to the wide variations in the frequency of reported clinical thyroid disease in patients with hepatitis C receiving interferon therapy (Table 1). 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%

The clinical and physiological spectrum of interferon‐alpha induced thyroiditis

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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Incidence of Thyroid Dysfunction During Interferon Alfa-2b and Ribavirin Therapy in Men With Chronic Hepatitis C

Bini¹,

Mehandru²

2004

Arch Intern Med

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Development of thyroid disease during therapy of chronic viral hepatitis with interferon alfa

Cited by 206 publications

References 16 publications

Virus C genotype predisposes to primary hypothyroidism during interferon-α treatment for chronic hepatitis C

Virus C genotype predisposes to primary hypothyroidism during interferon-α treatment for chronic hepatitis C

The clinical and physiological spectrum of interferon‐alpha induced thyroiditis

Incidence of Thyroid Dysfunction During Interferon Alfa-2b and Ribavirin Therapy in Men With Chronic Hepatitis C

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