Endocrine Abstracts

Alemtuzumab, a humanized anti-CD52 monoclonal antibody is effective in treating multiple sclerosis. However, it has been associated with thyroid disorder in up to 30–40% patients. While Graves’ disease is the most common disorder (70%), thyroiditis has been reported up to 4.9% cases.

Case 1: 34 year old woman with the background of multiple sclerosis and autoimmune hypothyroidism (on levothyroxine 50 mcg OD) was given Alemtuzumab infusion in July 2017. As part of surveillance, her TFTs were checked regularly. She developed thyrotoxicosis in July (TSH <0.01, FT4 84) before her next Alemtuzumab infusion in August 2018. Her GP stopped levothyroxine and she was seen in the endocrine clinic urgently. She was found to be mildly thyrotoxic (Heart rate 100/min, no sweating or tremors). There were no features to suggest Graves’ eye disease. Her repeat blood test showed TSH <0.01, FT3 10.1 and FT4 30. Her TPO antibodies were 148 (positive) and TSH receptor antibodies were 1.3 (positive). In view of improving biochemistry, anti-thyroid medications were not initiated. Subsequently, her ultrasound thyroid showed increased vascularity throughout normal size thyroid suggestive of thyroiditis and no nodules were identified. Her technetium scan showed reduced uptake on right suggestive of recovering thyroiditis\. She received Alemtuzumab infusion in August and her thyroid function tests were closely monitored which improved initially. However, she became thyrotoxic (TSH 0.01.FT3 6.7, FT4 19.2, TSH receptor antibodies 17.5) after 3–4 months. She was therefore, started on Carbimazole with the plan to monitor thyroid function test closely.

Case 2: 37 year old woman was admitted for autologous stem cell transplant for treatment of multiple sclerosis. She was previously treated with Alemtuzumab in February 2016 and October 2017. During admission, She was found to be clinically thyrotoxic and her thyroid function test showed TSH was 0.00, FT3 >46, FT4 47.9 and TSH receptor antibodies >30. However, as she was pancytopenic with neutrophils of 0, she was started on beta-blocker initially and Carbimazole was initiated once her neutrophilia resolved. She responded well to treatment and repeat TFTs showed TSH<0.01, FT3 10.6 and FT4 17.5 after 3 weeks. She is being closely monitored. We have presented two cases of Alemtuzumab-induced thyroid disorders with different clinical presentations and clinical courses. As these disorders can present unique challenges, it is extremely important to properly investigate and closely monitor such patients.