Vital C, Vallat J M, Deminiere C, Loubet A, Leboutet M J
Cancer. 1982 Oct 15;50(8):1491-7. doi: 10.1002/1097-0142(19821015)50:8<1491::aid-cncr2820500808>3.0.co;2-q.
Peripheral nerve biopsies of 22 patients who were seen with a peripheral neuropathy were studied. On each occasion an ultrastructural study was performed and on 12 occasions an immunopathologic study was done. Ten patients had Waldenström's macroglobulinemia and 12 had multiple myeloma. Cellular infiltrates were observed in three cases of Waldenström's macroglobulinemia by light microscopy. A widening of the myelin sheath, corresponding to an accumulation of macroglobulin, was found in three cases of Waldenström's macroglobulinemia. The presence of abundant deposits of amyloid was noted in one case of multiple myeloma. These diverse features show the various possible mechanisms that can produce peripheral nerve damage during the course of malignant dysglobulinemias. The segmental demyelination is probably of immunologic origin. The axonal lesions cannot be explained satisfactorily except in those rare cases where amyloid deposits are present in the endoneurium.
对22例患有周围神经病变的患者进行了周围神经活检研究。每次均进行超微结构研究,其中12次还进行了免疫病理学研究。10例患者患有华氏巨球蛋白血症,12例患有多发性骨髓瘤。通过光学显微镜在3例华氏巨球蛋白血症患者中观察到细胞浸润。在3例华氏巨球蛋白血症患者中发现髓鞘增宽,对应于巨球蛋白的积聚。在1例多发性骨髓瘤患者中注意到有大量淀粉样蛋白沉积。这些不同的特征显示了在恶性球蛋白异常血症过程中可导致周围神经损伤的各种可能机制。节段性脱髓鞘可能源于免疫。除了那些在内神经膜中存在淀粉样蛋白沉积的罕见病例外,轴索性病变无法得到满意的解释。