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神经莱姆病所致周围神经病:对CXCL13作为早期诊断标志物不敏感。

Peripheral neuropathy due to neuroborreliosis: Insensitivity for CXCL13 as early diagnostic marker.

作者信息

Gubanova Kristina, Lang Julia, Latzko Juliane, Novotna Bianka, Perneczky Julian, Pingitzer Stefan, Purer Petra, Wuchty Bianca, Waiß Christoph, Sellner Johann

机构信息

Department of Neurology, Landesklinikum Mistelbach-Gänserndorf, Mistelbach, Austria.

Institute for Hygiene and Microbiology, University Hospital of St Pölten, Karl Landsteiner University of Health Sciences, St Pölten, Austria.

出版信息

Int J Infect Dis. 2021 Apr;105:460-462. doi: 10.1016/j.ijid.2021.02.050. Epub 2021 Mar 5.

Abstract

The case of a 69-year-old woman with peripheral neuropathy caused by Lyme neuroborreliosis (LNB) in an endemic region in Eastern Austria is reported. The patient had noticed transient numbness of her left leg. On initial examination, she had patchy sensory disturbances of the left lower leg, but ancillary examinations of nerve conduction and cerebrospinal fluid (CSF), including the B-cell chemokine CXCL13, were normal. A re-tap performed 54 days later, following clinical progression with foot drop, widespread lower leg paresthesia, and pain, revealed an increased cell count, autochthonous IgM production, synthesis of Borrelia-specific IgM, and elevated CXCL13. Neurophysiological examinations disclosed an incomplete conduction block, mixed axonal and demyelinating sensorimotor neuropathy, and subacute neurogenic damage of muscles innervated by the peroneal nerve. This case study presents rare evidence of very early diagnostic findings in peripheral neuropathy caused by LNB. These are characterized by insensitivity of CXCL13 in CSF to aid earlier diagnosis and the development of an intrathecal immune response against Borrelia at a later stage. These findings reinforce the need for a re-tap to confirm the diagnosis and facilitate appropriate treatment in this rare manifestation of LNB.

摘要

报告了一名69岁女性的病例,该患者在奥地利东部的一个流行地区患有莱姆神经疏螺旋体病(LNB)引起的周围神经病变。患者注意到左腿有短暂麻木感。初次检查时,她左小腿有片状感觉障碍,但神经传导和脑脊液(CSF)的辅助检查,包括B细胞趋化因子CXCL13,均正常。54天后,随着病情进展出现足下垂、广泛的小腿感觉异常和疼痛,再次进行腰椎穿刺,结果显示细胞计数增加、自身IgM产生、伯氏疏螺旋体特异性IgM合成以及CXCL13升高。神经生理学检查发现不完全性传导阻滞、混合性轴索性和脱髓鞘性感觉运动性神经病变以及腓总神经支配肌肉的亚急性神经源性损伤。本病例研究提供了LNB所致周围神经病变非常早期诊断结果的罕见证据。其特点是脑脊液中的CXCL13对早期诊断不敏感,且后期会出现针对伯氏疏螺旋体的鞘内免疫反应。这些发现强化了再次进行腰椎穿刺以确诊并促进对这种罕见的LNB表现进行适当治疗的必要性。

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