Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.13/808737
- The natural history of interferon-2b-induced thyroiditis and its exclusivity in a cohort of patients with chronic hepatitis C infection
Tran, H. A.;
Reeves, G. E. M.;
Jones, T. L.
- The University of Newcastle. Faculty of Health, School of Biomedical Sciences and Pharmacy
- Background: Interferon-α2b (IFN-α2b) is well known to cause both hyper- and hypo-thyroidism. In the former, the commonest aetiology is thyroiditis. As there is no previous data to fully characterize the entity of IFN-related thyroiditis, the aim of this study is to document in detail its evolution in a cohort of hepatitis C patients treated with pegylated IFN-α2b and Ribavirin (RBV). Methods: A prospective observational study was conducted in patients who developed thyroid diseases whilst receiving combination of pegylated IFN-α2b and RBV for hepatitis C. The patients were followed with monthly thyrotropin (TSH). Where TSH was undetectable, free tetra- (fT4) and tri-iodothyronine (fT3) were added. Anti-thyroperoxidase (TPO), anti-thyroglobulin (Tg) and thyroid stimulating immunoglobulin (TSI) levels were also performed at diagnosis, during and at the end of IFN therapy. All patients were assessed and followed up closely with monthly TSH, fT4 and fT3 levels until the completion, after 6 and 12 months of treatment. Results: There were seven females and four males over a 30-month period. All patients were found to have thyroiditis. On average, the time to the development of thyroid disease was 10 weeks and duration of disease 9 weeks. All patients eventually recovered normal biochemical thyroid function although two required short-term supplementation. Conclusions: Thyroiditis was found exclusively in our patients. Both the hyper- and hypo-thyroid phase can be short lived, extreme and transient in nature which warrants strict monthly TSH monitoring. Careful follow-up of all patients is mandatory as complete recovery is expected.
- QJM: An International Journal of Medicine Vol. 102, Issue 2, p. 117-122
- Publisher Link
- Oxford University Press
- Resource Type
- journal article