Enhanced post-herpetic neuralgia by Bortezomib

Abstract

Bortezomib, a proteasome inhibitor, has been used for patients with refractory multiple myeloma. We present a 58-year old man who had IgG-λ-type multiple myeloma, refractory for MP (melphalan-predonisolone) and VAD (vincrisitine-doxorubicin-dexamethasone) therapy. He was complicated with reactivation of varicella-zoster virus (VZV) 4 weeks before bortezomib administration. Two weeks of consolidation treatment with standard dose valaciclovir caused VZV infection to settle down and, after a further 2 weeks, VZV remission was confirmed. Bortezomib was started at a dose of 1.3 mg/m² with prophylactic use of valaciclovir for VZV reactivation, post-herpetic neuralgia exacerbated the following day and grade 3 neuralgia developed the following week without recurrence of skin eruption. Neuralgia improved after the cessation of bortezomib with various supportive treatments and interventions. Although the reactivation of VZV was suspicious, no apparent skin lesions were observed. Although the mechanisms of post-herpetic neuralgia and chemotherapy-induced neuropathy are different, bortezomib might enhance post-herpetic neuralgia independent of the manner of viral reactivation.