Autoimmune thyroiditis due to treatment with beta interferon-1b for Multiple sclerosis

Abstract

Introduction. Since introduction of IFN-β1b for treatment of multiple sclerosis (MS), it was identified that beta interferon-1b can induce multiple alterations in thyroid function; though thyroid dysfunction is generally subclinical and often transient. The frequency of biological thyroid dysfunction has been studied in patients treated with IFN-β1b and was evaluated between 8.3 and 33%. On the other hand, autoimmune thyroid disease, as well as other autoimmune diseases, can occur in MS patients not receiving interferon-β therapy. It is unclear whether the occurrence of these diseases is increased in MS patients. Case report. A 52-year-old female was diagnosed with a relapsing-remitting multiple sclerosis in 2012 in Lithuania. Beta interferon-1b was initiated. In 2014, after 2 years of treatment, the patient referred for evaluation of hyperthyroidism. Thyroid function tests revealed a TSH of 0.01 μIU/ml (normal range: 0.27-4.2), fT4 of 7.3 pmol/L (normal range: 12.0-22.0) and with positive TPO and TG antibodies. The patient was commenced on carbimazole 60 mg daily. After a month, because of the high level of TSH (45.3 μIU/ml), the dose of carbimazole was roughly decreased to 5 mg daily. Since then the dose of carbimazole varied from 2.5 to 10 mg daily according to the TSH levels. In September 2015 patient attended our clinic. Thyroid function tests demonstrated a TSH of 5.12 μIU/ml (normal range: 0.4-4.0), fT4 of 0.76 (normal range: 0.89-1.76) with positive TPO antibodies. An ultrasonographic study of the thyroid gland revealed multinodular goiter with decreased echogenicity. For the time being, patient was receiving 5 mg of carbimazole daily. The anti-thyroid drug was stopped and after 2 months the thyroid function tests were within normal ranges and, in addition, the patient showed no signs of either hypothyroidism or hyperthyroidism. Certainly, further follow-up of the thyroid function is required. Conclusion It is now not arguable that among patients treated with IFN-β1b a thyroid dysfunction could be expected. This side effect is sometimes severe. Furthermore, MS itself may be an additional risk factor for developing an autoimmune thyroid disease. So it is crucial to systematically assess thyroid function in MS patients receiving IFN-β1b for treatment.