{"title":"Sural nerve injury in Behçet's disease patients treated with thalidomide.","authors":"Hui Wang, Jinjun Luo, Yun Yuan, Lingchao Meng","doi":"10.5414/NP301657","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Materials and methods: </strong>Consecutive adult Behçet's disease patients who received thalidomide and developed neuropathy were collected. Clinical manifestations, electrophysiologic evaluations, and pathologic findings were studied.</p><p><strong>Results: </strong>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.</p><p><strong>Discussion: </strong>Sensory fibers, particularly in the lower extremities, were susceptible to thalidomide therapy. The features of thalidomide-induced neuropathy are characterized as axonal degeneration.</p><p><strong>Conclusion: </strong>Earlier recognition of thalidomide-induced sensory axonal neuropathy should be carried out in patients with Behçet's disease during the thalidomide therapy.</p>","PeriodicalId":55251,"journal":{"name":"Clinical Neuropathology","volume":" ","pages":""},"PeriodicalIF":0.8000,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Neuropathology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5414/NP301657","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍:
Clinical Neuropathology appears bi-monthly and publishes reviews and editorials, original papers, short communications and reports on recent advances in the entire field of clinical neuropathology. Papers on experimental neuropathologic subjects are accepted if they bear a close relationship to human diseases. Correspondence (letters to the editors) and current information including book announcements will also be published.