Daily high-dose biotin has been suggested to improve disability in patients with progressive multiple sclerosis (P-MS) in a small controlled trial conducted in France.1 The supposed mechanisms of action supporting high-dose biotin are (1) the support of myelin repair through acetyl-CoA carboxylase activation by enhancing fatty acid synthesis and (2) the protection against axonal degeneration related to hypoxia through enhanced energy production.2 In the trial, safety was good, with incidence of adverse events similar in both groups, and few serious adverse events (SAE).1 Here, we report a detailed SAE: a transient myopathy resembling multiple acyl-coenzyme A dehydrogenase deficiency (MADD) or riboflavin transporter defects, reversible upon biotin withdrawal.

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