他克莫司相关格林-巴利综合征。

IF 0.6 Q3 MEDICINE, GENERAL & INTERNAL
Archive of clinical cases Pub Date : 2025-05-22 eCollection Date: 2025-01-01 DOI:10.22551/2025.47.1202.10317
Abdulrahman Nasiri, Tamam Alshammari, Alanood Alsolaihim, Huda Alfattah, Ali Alahmri
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引用次数: 0

摘要

吉兰-巴罗综合征(GBS)是一种在造血干细胞移植受者中罕见但严重的神经病变。免疫抑制剂,特别是他克莫司,被认为是潜在的诱因。我们报告了一名27岁的男性bcr - abl阳性急性髓性白血病患者,他在移植后发展为急性脱髓鞘多神经病变,可能与他克莫司治疗有关,突出了诊断挑战和管理注意事项。患者在接受hla匹配的同胞供体异体干细胞移植58天后出现进行性上升性无力、反射性松弛、感觉丧失和球症状。脑脊液(CSF)分析显示蛋白升高(1,900 mg/L),伴淋巴细胞增多(51个细胞/μL),为GBS的非典型表现。磁共振成像显示细微的神经根增强,神经传导研究显示传导速度明显减慢,远端潜伏期延长,与急性炎性脱髓鞘性多发性神经病一致。广泛的感染检查(包括病毒PCR板和培养)为阴性,脑脊液中未见白血病细胞。停用他克莫司(谷底水平3.1 ng/mL,低于治疗范围),并开始静脉注射免疫球蛋白(5天内总计2 g/kg)。病人的神经功能缺损迅速改善,四周内几乎完全康复。值得注意的是,停用他克莫司免疫抑制并没有引发移植物抗宿主病,患者的急性白血病在单药治疗下仍处于缓解期。本病例描述了移植后患者急性脱髓鞘性多神经病变,与他克莫司相关。它强调了对移植受者GBS进行仔细诊断评估的重要性,包括考虑非典型CSF发现和其他诊断。及时识别和管理——包括免疫抑制剂调整和免疫治疗——可以在不影响移植结果的情况下实现神经系统的完全恢复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tacrolimus associated Guillain-Barre syndrome.

Guillain-Barré syndrome (GBS) is a rare but serious neuropathy in hematopoietic stem cell transplant recipients. Immunosuppressants, particularly tacrolimus, have been implicated as potential triggers. We present a 27-year-old man with BCR-ABL-positive acute myeloid leukemia who developed an acute demyelinating polyneuropathy possibly related to tacrolimus therapy post-transplantation, highlighting diagnostic challenges and management considerations. The patient developed progressive ascending weakness, areflexia, sensory loss, and bulbar symptoms 58 days after an allogeneic stem cell transplant from an HLA-matched sibling donor. Cerebrospinal fluid (CSF) analysis showed elevated protein (1,900 mg/L) with lymphocytic pleocytosis (51 cells/μL), an atypical finding for GBS. Magnetic resonance imaging revealed subtle nerve root enhancement, and nerve conduction studies demonstrated markedly slowed conduction velocities and prolonged distal latencies consistent with an acute inflammatory demyelinating polyneuropathy. Extensive infectious work-up (including viral PCR panels and cultures) was negative, and no leukemic cells were seen in CSF. Tacrolimus was discontinued (trough level 3.1 ng/mL, below therapeutic range) and intravenous immunoglobulin (2 g/kg total over five days) initiated. The patient's neurological deficits improved rapidly, with near-complete recovery within four weeks. Notably, withdrawal of tacrolimus immunosuppression did not precipitate graft-versus-host disease, and the patient's acute leukemia remained in remission on ponatinib monotherapy. This case illustrates an acute demyelinating polyneuropathy in a post-transplant patient, associated with tacrolimus. It underscores the importance of careful diagnostic assessment of GBS in transplant recipients, including consideration of atypical CSF findings and alternative diagnoses. Prompt recognition and management - including immunosuppressant adjustment and immunotherapy - can achieve full neurological recovery without compromising transplant outcomes.

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