Endocrine Abstracts

Objective: The MAB, alemtuzumab has been demonstrated to reduce the relapse and the risk of accumulation of sustained disability in multiple sclerosis when compared to β-interferon. The development of autoimmune diseases, including thyroid disease has been reported in the literature with a frequency of 15–25%.

Methods: We reviewed the case notes of 39 patients with multiple sclerosis initiated on alemtuzumab in our hospital from 2006 to 2012 and studied the clinical course of the patients who subsequently developed thyroid dysfunction.

Results: Of the 38 patients reviewed (25 females and 13 males) 15 patients (40%) developed thyroid dysfunction (ten females and five males). Nine patients developed symptoms of thyrotoxicosis (seven females and two males) five patients developed hypothyroidism (three males and two females) and one patient initially developed hypothyroidism and was commenced on thyroxine replacement and subsequently developed symptoms of thyrotoxicosis after withdrawal of thyroxine. Of the thyrotoxic patients (n=10) seven patients had TRAB positive antibodies (70%). The mean duration of development of abnormal thyroid function tests was 31 months after administration of 1st cycle of alemtuzumab. All patients with thyrotoxicosis were started initially on antithyroid medications and on further relapse four patients were offered radioiodine therapy with complete resolution and LT₄ replacement for post RAI hypothyroidism.

Conclusion: Graves’ disease is a common complication of alemtuzumab use. The mechanism of thyroid autoimmunity after alemtuzumab treatment is likely related to the loss of self tolerance in the homeostatic proliferation which occurs following profound lymphopenia. Ophthalmopathy may occur in some patients. Close monitoring of serum TSH levels is essential and an early response to a relative fall in levels that remain within the normal range in the form of more frequent monitoring is warranted. Monitoring must be maintained for many years.