Are you lucky to have autoimmunity with alemtuzumab


Development of autoimmune thyroid disease in multiple sclerosis patients post-alemtuzumab improves treatment response.Sovetkina A, Nadir R, Scalfari A, Tona F, Murphy K, Rigoni E, Dorsey R, Malik O, Nandoskar A, Singh-Curry V, Nicholas R, Martin N.J Clin Endocrinol Metab. 2020 Jul 15:dgaa453

Context: Alemtuzumab is an anti-CD52 monoclonal antibody used in the treatment of relapsing-remitting multiple sclerosis (MS). Between 20-40% of alemtuzumab-treated MS patients develop autoimmune thyroid disease (AITD) as a side effect.

Objective: To determine whether MS disease progression following alemtuzumab treatment differs in patients that develop AITD compared to those who do not.

Results: Twenty-six percent (33 out of 126, 25 female, 8 male) of alemtuzumab-treated patients developed AITD, 55% of which was Graves’ disease. EDSS score following alemtuzumab was reduced in patients who developed AITD compared to those who did not (median [IQR]; AITD: -0.25 [-1 – 0.5] vs non-AITD: 0 [1 – 0]. P=0.007]. Analysis confirmed that the development of AITD was independently associated with EDSS score improvement (p=0.011). Moreover, AITD patients had higher relapse-free survival following alemtuzumab (p=0.023). There was no difference in the number of new focal T2-lesions and contrast-enhancing MRI lesions developed following alemtuzumab between the two groups.

Conclusion: Graves’ disease was the most common form of AITD developed by MS patients following alemtuzumab. This study suggests that MS patients who develop AITD may have an improved response to alemtuzumab, as measured by reduced disability and lower relapse rate.

This is an interesting one, it suggests thats people wit thyroid auoimmunity do better. It should not take too long for either Cambridge or the manufacturer to confirm or refue this one.

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  • “There was no difference in the number of new focal T2-lesions and contrast-enhancing MRI lesions developed following alemtuzumab between the two groups.”

    In the hope they meant a big fat 0 new lesions for both groups….

  • So, in a similar manner, is it possible that people developing lymphopoenia with cladribine are doing/will do better with respect to the others?
    I was wondering that it could be a similar situation with alemtuzumab autoimmunity rising from a more profound depletion and subsequent loss of tolerance. With cladribine we would just have profound depletion identified by lymphopenia.
    If so, this would support ProfG idea that cladribine may be underdosed.

  • I read this paper with fascination when first published and I’m still struggling to understand the results. The immune system finds a new autoantigen following IRT. Tlink between thyroid problems, MS, and Alemtuzumab need to be examined closely as I suspect it may tell us something about the disease mechanism.

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