Coimbra J, Costa A P, Pita F, Rosado P, de Almeida L B
Serviço de Neurologia, Hospital Garcia de Orta, Almada.
Acta Med Port. 1995 Apr;8(4):253-7.
The association of a neuropathy and a paraproteinaemia such as Waldenström's macroglobulinaemia is frequent and not fortuitous. This paper reports a slowly progressive, predominantly sensory neuropathy, occurring in a 69-year-old man, as the first sign of a Waldenström's macroglobulinaemia. A saphenous [correction of sural] nerve biopsy revealed a mixed process of primary demyelination and axonal degeneration. Accumulations of immunoglobulin M were observed in the myelin sheets and the perineurium by immunocytochemistry. Infiltrations of inflammatory blood cells and accumulations of amyloid material were absent in the peripheral nerve. The axonal loss was most prominent in central areas of the nerve fascicles. This find supports the hypothesis of an ischemic mechanism for the axonal degeneration plus secondary demyelination, associated to a direct immunological attack against myelin. The various types of peripheral nerve involvement in Waldenström's macroglobulinaemia, as well as the admitted mechanisms of nerve lesion and the therapeutic approaches to this still unclear neuropathy are briefly reviewed.
神经病变与副蛋白血症(如华氏巨球蛋白血症)的关联很常见,并非偶然。本文报告了一名69岁男性出现的缓慢进展的、以感觉神经病变为主的神经病变,这是华氏巨球蛋白血症的首发症状。隐神经活检显示为原发性脱髓鞘和轴突变性的混合过程。通过免疫细胞化学观察到髓鞘板和神经束膜中有免疫球蛋白M的积聚。周围神经中未见炎性血细胞浸润和淀粉样物质积聚。轴突丢失在神经束的中央区域最为明显。这一发现支持了轴突变性加继发性脱髓鞘的缺血机制假说,该假说与针对髓鞘的直接免疫攻击有关。本文简要回顾了华氏巨球蛋白血症中周围神经受累的各种类型,以及公认的神经病变机制和针对这种仍不清楚的神经病变的治疗方法。