Amsterdam UMC, Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma's Children's Hospital, VU University, Amsterdam, The Netherlands.
Neuroscience, Cellular & Molecular Mechanisms, VU University, Amsterdam, The Netherlands.
J Neurol. 2024 Jul;271(7):4028-4038. doi: 10.1007/s00415-024-12322-3. Epub 2024 Apr 2.
Metachromatic leukodystrophy (MLD) is a neuro-metabolic disorder due to arylsulfatase A deficiency, causing demyelination of the central and peripheral nervous system. Hematopoietic cell transplantation (HCT) can provide a symptomatic and survival benefit for pre-symptomatic and early symptomatic patients by stabilizing CNS disease. This case series, however, illustrates the occurrence of severely progressive polyneuropathy shortly after HCT in two patients with late-infantile, one with late-juvenile, and one with adult MLD, leading to the inability to walk or sit without support. The patients had demyelinating polyneuropathy before HCT, performed at the ages of 2 years in the first two patients and at 14 and 23 years in the other two patients. The myeloablative conditioning regimen consisted of busulfan, fludarabine and, in one case, rituximab, with anti-thymocyte globulin, cyclosporine, steroids, and/or mycophenolate mofetil for GvHD prophylaxis. Polyneuropathy after HCT progressed parallel with tapering immunosuppression and paralleled bouts of infection and graft-versus-host disease (GvHD). Differential diagnoses included MLD progression, neurological GvHD or another (auto)inflammatory cause. Laboratory, electroneurography and pathology investigations were inconclusive. In two patients, treatment with immunomodulatory drugs led to temporary improvement, but not sustained stabilization of polyneuropathy. One patient showed recovery to pre-HCT functioning, except for a Holmes-like tremor, for which a peripheral origin cannot be excluded. One patient showed marginal response to immunosuppressive treatment and died ten months after HCT due to respiratory failure. The extensive diagnostic and therapeutic attempts highlight the challenge of characterizing and treating progressive polyneuropathy in patients with MLD shortly after HCT. We advise to consider repeat electro-neurography and possibly peripheral nerve biopsy in such patients. Nerve conduction blocks, evidence of the presence of T lymphocytes and macrophages in the neuronal and surrounding nerve tissue, and beneficial effects of immunomodulatory drugs may indicate a partially (auto)immune-mediated pathology. Polyneuropathy may cause major residual disease burden after HCT. MLD patients with progressive polyneuropathy could potentially benefit from a more intensified immunomodulatory drug regime following HCT, especially at times of immune activation.
异染性脑白质营养不良(MLD)是一种由于芳基硫酸酯酶 A 缺乏导致的神经代谢疾病,会引起中枢和外周神经系统脱髓鞘。造血细胞移植(HCT)可以通过稳定中枢神经系统疾病为症状前和早期症状患者提供症状和生存获益。然而,本病例系列说明了两名晚婴型、一名晚青少型和一名成年型 MLD 患者在 HCT 后不久发生严重进行性多发性神经病,导致无法在没有支撑的情况下行走或坐下。这三名患者在 HCT 前均患有脱髓鞘性多发性神经病,前两名患者在 2 岁时进行 HCT,另两名患者分别在 14 岁和 23 岁时进行 HCT。骨髓清除性预处理方案包括白消安、氟达拉滨,以及在一名患者中还包括利妥昔单抗,用于 GvHD 预防的药物还有抗胸腺细胞球蛋白、环孢素、类固醇和/或霉酚酸酯。HCT 后多发性神经病与免疫抑制药物的逐渐减少平行进展,与感染和移植物抗宿主病(GvHD)的发作平行。鉴别诊断包括 MLD 进展、神经 GvHD 或其他(自身)炎症性原因。实验室、电神经图和病理学检查结果均无定论。在两名患者中,免疫调节药物治疗导致暂时改善,但多发性神经病没有持续稳定。一名患者恢复到 HCT 前的功能,除了一个可能为周围起源的霍姆斯样震颤外。一名患者对免疫抑制治疗有边缘反应,并在 HCT 后 10 个月因呼吸衰竭而死亡。广泛的诊断和治疗尝试突出了在 HCT 后不久的 MLD 患者中,对进行性多发性神经病进行特征描述和治疗的挑战。我们建议对这些患者考虑重复电神经图检查和可能的周围神经活检。神经传导阻滞、神经元和周围神经组织中 T 淋巴细胞和巨噬细胞的存在证据,以及免疫调节药物的有益效果可能表明存在部分(自身)免疫介导的病理。HCT 后多发性神经病可能导致严重的残留疾病负担。进行性多发性神经病的 MLD 患者在 HCT 后可能受益于更强化的免疫调节药物治疗方案,尤其是在免疫激活时。