Increased Risk of Autoimmune Thyroid Disease in Hepatitis C vs Hepatitis B Before, During, and After Discontinuing Interferon Therapy

Fernandez-Soto, Luisa; Gonzalez, Amalia; Escobar-Jiménez, Fernándo; R, Vázquez; Ocete, Esther; Olea, Nicolás; Salmerón, Javier

doi:10.1001/archinte.158.13.1445

Cited by 176 publications

(122 citation statements)

References 24 publications

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“…[16][17][18][19] Our data demonstrated that TPOAb-positive patients had a higher chance of developing hypothyroidism; however, females were not more prone, similarly to the findings reported by Muratori et al 20 and Stefanova-Petrova et al 21 The prevalence of hypothyroidism in HCV patients is approximately 9% (0-13%) vs. 3% (0.5-4%) in healthy subjects. 19,[22][23][24] Thyroid autoimmunity was demonstrated in 15% (5-28%) of the HCV patients and in 12% (0-11%) of healthy subjects, indicating a slight though significantly higher risk.…”

Section: Discussionsupporting

confidence: 89%

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: Discussionsupporting

confidence: 89%

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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“…49 On the other hand, other studies have shown a significant correlation between hepatitis C infection and thyroid disorders (Table 2). 14,[52][53][54][55] In two studies from France of patients with hepatitis C infection who had not received interferon therapy, the incidence of TAb's and/or thyroid dysfunction was significantly higher in the patients than in the controls. 52,53 Another study from France in patients with hepatitis C who have not received interferon revealed that 13.6% had positive TAb's.…”

Section: The Hepatitis C Connectionmentioning

confidence: 99%

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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“…IFN-α therapy is associated with development of thyroid dysfunction in chronic hepatitis C (CHC) patients, usually exposing preexisting subclinical thyroid abnormalities [2]. The prevalence of anti-thyroid antibodies (anti-thyroid peroxidase antibody, TPOAb; anti-thyroglobulin antibody, TGAb; anti-thyroid microsomal antibody, ATMA) varied markedly, from 2% to 48% in IFN-α treated CHC patients [3][4][5]. However, some studies suggested that the prevalence of thyroid disease was also increased in CHC patients after exclusion of J Gastrointestin Liver Dis, June 2016 Vol.…”

Section: Introductionmentioning

confidence: 99%

Thyroid Disturbance in Patients with Chronic Hepatitis C Infection: A Systematic Review and Meta-analysis

Shen

Wang

Xie

et al. 2016

JGLD

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Background & Aims: The involvement of thyroid autoimmunity and dysfunction in patients with chronichepatitis C virus (HCV) infection before interferon-α (IFN-α) therapy remains controversial. We performedthis meta-analysis to evaluate the association of HCV infection with the presence of anti-thyroid antibodiesand dysthyroidism. Methods: A literature search was carried out to collect articles dated up to August 2015 to identify observationalstudies which compared the prevalence of anti-thyroid antibodies and thyroid dysfunction in IFN-α naïvechronic HCV-infected subjects with non-HCV infected controls. Random-effect or fixed-effect meta-analyseswere applied and results reported as odds ratios (ORs) with 95% confidence intervals (CIs). Results: Twelve studies were included, involving 1,735 HCV-infected and 1,868 non-HCV infected subjects.Pooled anti-thyroid antibody prevalence tended to be higher in HCV-infected subjects. The prevalence ofanti-thyroglobulin antibody (TGAb), anti-thyroid peroxidase antibody (TPOAb), anti-thyroid microsomalantibody (ATMA) were 2.40-fold, 1.96-fold and 1.86-fold higher in HCV-infected subjects than in controls,respectively. The prevalence of hypothyroidism also differed by HCV infection status, with a pooled risk of3.10 (95%CI: 2.19-4.40) in HCV-infected subjects. However, the results did not show a significant differencein the prevalence of hyperthyroidism between the two groups.Conclusion: Chronic HCV infection may be an independent risk factor for thyroid disturbance. It is advisablefor the clinicians to monitor both thyroid antibodies and function in the course of chronic HCV infection,independent of IFN-α treatment. Abbreviations: AITD: autoimmune thyroid disease; ATMA: anti-thyroid microsomal antibody; CHC:chronic hepatitis; GD: Graves’ disease; HCV: hepatitis C virus; HT: Hashimoto’s thyroiditis; IFN-α: interferonalpha;NOS: Newcastle-Ottawa quality assessment scale; T3: triiodothyronine; T4: thyroxine; TGAb: antithyroglobulinantibody; TPOAb: anti-thyroid peroxidase antibody.

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Increased Risk of Autoimmune Thyroid Disease in Hepatitis C vs Hepatitis B Before, During, and After Discontinuing Interferon Therapy

Cited by 176 publications

References 24 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: Toward a new classification

Thyroid Disturbance in Patients with Chronic Hepatitis C Infection: A Systematic Review and Meta-analysis

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