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Thalidomide is an “old” drug with new indications in many immune-related and neoplastic diseases. In addition to teratogenicity, peripheral neurotoxicity is the main adverse effect limiting its therapeutic use. The incidence of thalidomide-induced neuropathy is variable, ranging from 1% in leprosy to 70% in prurigo nodularis.1 Clinical features include sensory axonal polyneuropathy with early distal tingling followed by impairment of all modalities of sensation, which may remit after immediate drug withdrawal. Mild motor involvement and severe proprioceptive sensory failure have been reported in severe cases. Prospective neurophysiological studies performed every 3 to 6 months, or after a cumulative dose of 10 g, have shown a sensory nerve action potential (SNAP) amplitude decrease, less than 40% or 50% from baseline, to be the most useful parameter for detecting early nerve damage.1,2⇓
Case report.
In a 67-year-old man with a 4-year history of biopsy-proven prurigo nodularis unresponsive to steroids and cyclosporine, treatment with thalidomide (100 mg/d) led to complete remission of cutaneous manifestations. Five months after therapy onset, the patient had tingling in hands and feet, followed …
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