Introduction Alemtuzumab (Campath-1H), the first humanised monoclonal antibody, is emerging as the most effective disease modifying treatment for multiple sclerosis (MS). One common side effect is thyroid gland disturbance. However, despite use in clinical trials and off-licence as a compassionate treatment, little is known about the spectrum, clinical aspects, and treatment requirements of Campath induced thyroid dysfunction.
Aim To characterise the thyroid complications of the Plymouth Hospitals Campath cohort.
Method Hospital notes from all people with MS treated with Campath, were examined in chronological order (since 2002). Thyroid complications were characterised clinically, biochemically and immunologically.
Results To date notes from 135 consecutive patients have been examined (2002–2011). There is a thyroid disturbance in 34.1%, in 5.2% the disturbance being only immunological (TPO positive), while 28.9% have a biochemical and/or clinical thyroid disturbance. Of these last group there have been 19 thyrotoxicosis cases (14.1%) with an onset date between 14 and 45 months after the 1st Campath dose, 1 thyroid eye disease (0.7%), eight transient hyperthyroidism (5.9%) and 13 hypothyroidism (9.6%). All the patients with thyrotoxicosis received Carbimazole and two radioiodine. Of note from the 25 TPO positive patients only seven haven't developed a biochemical or clinical thyroid complication.
Conclusion Campath induced thyroid disturbance in MS appears common and of a wide variety. Most people required treatment and have persistent thyroid dysfunction many years after treatment. The minority were severe. Careful pro-active surveillance is required to prevent and treat these complications promptly.
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