Sural nerve injury in Behçet's disease patients treated with thalidomide.

INTRODUCTION

Thalidomide has shown exceptional results in the management of Behçet's disease. Despite its efficacy, thalidomide is associated with a number of adverse effects, including peripheral neuropathy. This study aims to characterize the pathologic features of neuropathy in Behçet's disease patients who received thalidomide therapy.

MATERIALS AND

METHODS

Consecutive adult Behçet's disease patients who received thalidomide and developed neuropathy were collected. Clinical manifestations, electrophysiologic evaluations, and pathologic findings were studied.

RESULTS

Three patients who met the inclusion criteria were collected. Sensory deficits, particularly in the lower extremities, emerged in a length-dependent manner 6 - 12 months after initiation of thalidomide therapy. Symptoms remained unchanged after discontinuation of thalidomide for 2 years. Electrophysiologic evaluations showed sensory axonal polyneuropathy in all 3 patients who also received sural nerve biopsy. Histological findings confirmed axonal degenerations. A noteworthy finding was neurofilament accumulation in both myelinated and unmyelinated axons.

DISCUSSION: Sensory fibers, particularly in the lower extremities, were susceptible to thalidomide therapy. The features of thalidomide-induced neuropathy are characterized as axonal degeneration.

CONCLUSION

Earlier recognition of thalidomide-induced sensory axonal neuropathy should be carried out in patients with Behçet's disease during the thalidomide therapy.