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Year : 2020  |  Volume : 5  |  Issue : 1  |  Page : 50-56

Thyroid dysfunction among chronic hepatitis C patients and its relation to Interferon therapy

Internal Medicine Department, Faculty of Medicine, Assiut University, Assiut, Egypt

Correspondence Address:
Marwa A Mohammed
Department of Internal Medicine, Faculty of Medicine, Assiut University, Assiut
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCMRP.JCMRP_122_18

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Background: Thyroid dysfunction (TD) represents an extrahepatic manifestation of chronic hepatitis C (CHC). Moreover, the currently approved treatment of CHC is often associated with TD. However, it remains debatable if TD is mainly virus or treatment related. The aim of this study was to assess the incidence of TD and to identify its predictors in treated and untreated CHC-infected patients. Patients and methods: A total of 1290 patients with CHC were evaluated for TD for 48 weeks: 200 were untreated (control group) and 1090 were treated with pegylated interferon α (PEG-IFN-α) plus ribavirin (treatment group). Results: The incidence of TD was more evident by the end of treatment (week 48); it was found to be 15.5%, mostly in the form of hypothyroidism (8.4%), whereas the least incidence was detected by week 12 (9.1%), mostly in the form of hyperthyroidism (5.2%). Generally, hyperthyroidism was higher than hypothyroidism in multiple folds, but in the end, hypothyroid cases became more dominant. Males were more affected, but the prevalence of hypothyroidism was more in females (10.1%) than males (8.0%). TD was not related to sex, age, BMI, pretreatment viral load, pretreatment laboratory characteristics, post-treatment biochemical tests, treatment duration, severity of hepatic inflammation and fibrosis, type of biopsy used, or virological outcome, but PEG-IFN formulation was related, particularly IFN-α-2a. TD did not lead to dose reduction or therapy withdrawal. Conclusion: Both hepatitis C virus and IFN-α therapy have been found to be inducing thyroid disorders in patients with CHC virus infection. Antiviral therapy of CHC possibly induces de novo or exacerbates pre-existing silent TD especially subclinical hypothyroidism. The role of CHC per se in TD remains to be determined.

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