Lozhnikova S M, Pirogov V N, Piradov M A, Sakharova A V, Liudkovskaia I G
Arkh Patol. 1997 Mar-Apr;59(2):11-7.
18 patients with grave DP treated with a long-term artificial pulmonary ventilation and feeding through a naso-gastric probe were studied. Biopsies of n. suralis taken at different periods after the appearance of the first signs of DP (from the 19th to the 69th day) were studied at light and electronic microscopy. The basis of DP is toxic myelopathy with paranodal demyelination mainly in the large myelinated neural fibers and a segmentary one in the smaller neural fibers. Axonal degeneration was observed in the gravest cases of DP and was secondary being the result of axon squeezing by a folded myelin and voluminous Schwann cell cytoplasm invaginated into the axon. In no case of DP inflammatory changes and(or) involvement of the immunocompetent cells were found. There was pronounced proliferation and activation of Schwann cells due to intensive utilization of the degradation products of myelin and remyelinization. Morphological signs of remyelinization were observed on the 35th day of DP in the presence of enhancing neurological symptoms. But remyelinization was not complete even on the 69th day of DP.
对18例接受长期人工肺通气并通过鼻胃管进食的严重糖尿病性周围神经病（DP）患者进行了研究。在DP首次出现症状后的不同时期（第19天至第69天）采集腓肠神经活检标本，进行光镜和电镜检查。DP的病理基础是中毒性脊髓病，主要在大的有髓神经纤维中出现节旁脱髓鞘，在较小的神经纤维中出现节段性脱髓鞘。在最严重的DP病例中观察到轴突变性，这是继发性的，是由于折叠的髓鞘和大量侵入轴突的施万细胞胞质挤压轴突所致。在任何DP病例中均未发现炎症变化和（或）免疫活性细胞的浸润。由于髓鞘降解产物的大量利用和髓鞘再生，施万细胞出现明显的增殖和活化。在DP第35天，在神经症状加重的情况下观察到髓鞘再生的形态学迹象。但即使在DP第69天，髓鞘再生也未完全完成。
