Sural nerve pathology in diabetic patients with minimal but progressive neuropathy
Sural nerve pathology in diabetic patients with minimal but progressive neuropathy
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DOI：
10.1007/s00125-004-1663-5
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发表时间：
2005-03-01
期刊：
影响因子：
8.2
通讯作者：
Ward, JD
中科院分区：
文献类型：
--
作者：
Malik, RA;Tesfaye, S;Ward, JD
目的/假设：人类糖尿病神经病变的早期病理特征尚未明确。因此，我们对糖尿病患者的腓肠神经活检中的神经纤维和微血管病理进行了量化。方法：12例糖尿病患者在基线时进行了详细的神经病变评估和腓肠神经束支活检，并在8.7+/-0.6年后再次评估神经病变。结果：基线时，神经病变症状、神经功能缺失、定量感觉测试、心脏自主神经功能和周围神经电生理均表现为轻微异常，并在随访时恶化。有髓纤维密度、纤维和轴突面积以及G-比率正常，但梳理纤维检查显示结旁异常(P<；0.001)、节段性脱髓鞘(P<；0.01)和重新髓鞘形成(P<；0.01)，未见轴突变性。非相关雪旺细胞轮廓密度(p<；0.04)和无髓轴突密度(p<；0.001)增加，轴突直径减小(p<；0.007)。毛细血管表现为基底膜增厚(P<；0.006)，内皮细胞增生(P<；0.004)和管腔面积缩小(P<；0.007)。结论/解释：人类糖尿病神经病变的早期病理特征包括有髓纤维雪旺细胞异常和无髓纤维变性伴再生。这些改变伴随着一种显著的神经内膜微血管病变。
Aims/hypothesis: The early pathological features of human diabetic neuropathy are not clearly defined. Therefore we quantified nerve fibre and microvascular pathology in sural nerve biopsies from diabetic patients with minimal neuropathy. Methods: Twelve diabetic patients underwent detailed assessment of neuropathy and fascicular sural nerve biopsy at baseline, with repeat assessment of neuropathy 8.7 +/- 0.6 years later. Results: At baseline, neuropathic symptoms, neurological deficits, quantitative sensory testing, cardiac autonomic function and peripheral nerve electrophysiology showed minimal abnormality, which deteriorated at follow-up. Myelinated fibre density, fibre and axonal area, and g-ratio were normal but teased fibre studies showed paranodal abnormalities (p < 0.001), segmental demyelination (p < 0.01) and remyelination (p < 0.01) without axonal degeneration. Unassociated Schwann cell profile density (p < 0.04) and unmyelinated axon density (p < 0.001) were increased and axon diameter was decreased (p < 0.007). Endoneurial capillaries demonstrated basement membrane thickening (p < 0.006), endothelial cell hyperplasia (p < 0.004) and a reduction in luminal area (p < 0.007). Conclusions/interpretation: The early pathological features of human diabetic neuropathy include an abnormality of the myelinated fibre Schwann cell and unmyelinated fibre degeneration with regeneration. These changes are accompanied by a significant endoneurial microangiopathy.