We fully agree with Collins and Periquet that causes other than systemic vasculitis need to be ruled out before ascribing a polyneuropathy to vasculitic origin, especially in the absence of histological proof. In the cohort described in our article, we tried to exclude other disorders that could have caused the polyneuropathy. Specifically, blood glucose and glycosylated hemoglobin levels were checked in every patient, and folate and vitamin B12 deficiencies were excluded. Only 1 patient with type 1 diabetes mellitus developed polyneuropathy, which occurred during a severe generalized relapse of his vasculitis. Another 2 patients developed type 2 diabetes mellitus while taking corticosteroid medication for their vasculitis, but this was well after the manifestation of their polyneuropathy. In addition, 6 patients were undergoing dialysis; in all of them, polyneuropathy developed prior to end-stage renal failure or at the same time as the renal relapse, ultimately leading to dialysis dependency. None of the patients with symmetric polyneuropathy had a history of alcoholism, a preceding admission to the intensive care unit, or exposure to explicitly neurotoxic medications. A family history of neuropathy was not always explored in depth.
de Groot K, Reinhold-Keller E. In reply. Arch Neurol. 2002;59(8):1333–1334. doi:https://doi.org/
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