Vitamin D deficiency showed no causative effect in the development of autoimmune disease after treatment with alemtuzumab, a lytic monoclonal antibody used as a high-efficacy therapy in multiple sclerosis (MS), according to a new retrospective case-control study published in Multiple Sclerosis and Related Disorders.

“Relative vitamin D deficiency is a risk factor for MS and this has also been noted for a number of other autoimmune diseases. This has led some to speculate that vitamin D deficiency might be a potentially modifiable factor in the development of autoimmune disease following alemtuzumab for MS,” Arnett et al wrote.

According to their analysis, the mean vitamin D level from 6 months pretreatment to the onset of autoimmune disease or last follow-up was not associated with the risk of autoimmunity.


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However, they did find an association between the risk of autoimmunity and sex, with female patients being more likely to develop autoimmune disease sooner. They also found a higher risk of autoimmunity in patients with higher Expanded Disability Status Scale (EDSS) scores during treatment.

The study included clinical data and vitamin D levels from 113 patients with MS who were treated with alemtuzumab. The median follow-up period was 4.4 years. Most (68%) patients had vitamin D levels below 75 nmol/L.

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Alemtuzumab has been associated with the development of autoimmune diseases in MS patients in the first 5 years following the initial dose. These include, but are not limited to, Graves’ disease, idiopathic thrombocytopenia, and nephropathy.

“Risk of autoimmune disease following alemtuzumab, which appears to be unique to people with MS being treated with this agent, has been noted to be associated with elevated serum levels of IL21,” Arnett et al explained.

Reference

Arnett S, Sanchez SJ, Downing J, Boggild M, Sun J, Broadley SA. Low vitamin D levels do not predict risk of autoimmune disease following alemtuzumab treatment for multiple sclerosis. Mult Scler Relat Disord. Published online January 10, 2022. doi:10.1016/j.msard.2022.103511