Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, The University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK.
Diabetologia. 2014 Aug;57(8):1711-9. doi: 10.1007/s00125-014-3271-3. Epub 2014 May 28.
AIMS/HYPOTHESIS: We sought to establish the molecular and pathological changes predisposing diabetic and non-diabetic patients to the development of carpal tunnel syndrome (CTS).
The posterior interosseous nerve (PIN) was biopsied in 25 diabetic and 19 non-diabetic patients undergoing carpal tunnel decompression for CTS. Detailed morphometric and immunohistological analyses were performed in the nerve biopsy.
In diabetic patients median nerve distal motor latency was prolonged (p < 0.05 vs non-diabetic patients), PIN myelinated fibre density (p < 0.05), fibre area (p < 0.0001) and axon area (p < 0.0001) were reduced, the percentage of unassociated Schwann cell profiles (p < 0.0001) and unmyelinated axon density (p < 0.0001) were increased and the axon diameter was reduced (p < 0.0001). Endoneurial capillary basement membrane area was increased (p < 0.0001) in diabetic patients, but endothelial cell number was increased (p < 0.01) and luminal area was reduced (p < 0.05) in non-diabetic patients with CTS. There was no difference in the expression of hypoxia-inducible factor 1α between diabetic and non-diabetic patients with CTS. However, the expression of vascular endothelial growth factor A (VEGF) (p < 0.05) and its receptors VEGFR-1 (p < 0.01) and VEGFR-2 (p < 0.05) was significantly increased in diabetic patients, particularly those with type 1 diabetes, and related to the severity of nerve fibre pathology.
CONCLUSIONS/INTERPRETATION: This study demonstrates increased nerve fibre and microvascular pathology in relation to enhanced expression of VEGF and its receptors in a non-compressed nerve in diabetic compared with non-diabetic patients with CTS. It therefore provides a potential molecular and pathological basis for the predisposition of diabetic patients to the development of CTS.
目的/假设：我们旨在确定导致糖尿病和非糖尿病患者发生腕管综合征（CTS）的分子和病理变化。
对 25 例糖尿病和 19 例非糖尿病 CTS 患者进行腕管减压时，对其正中神经的后骨间神经（PIN）进行了活检。对神经活检进行了详细的形态计量学和免疫组织化学分析。
与非糖尿病患者相比，糖尿病患者的正中神经远端运动潜伏期延长（p<0.05），PIN 有髓纤维密度（p<0.05）、纤维面积（p<0.0001）和轴突面积（p<0.0001）降低，无相关雪旺细胞形态（p<0.0001）和无髓轴突密度（p<0.0001）增加，轴突直径减小（p<0.0001）。糖尿病患者的神经内膜毛细血管基底膜面积增加（p<0.0001），但 CTS 非糖尿病患者的内皮细胞数量增加（p<0.01），管腔面积减小（p<0.05）。CTS 糖尿病和非糖尿病患者之间缺氧诱导因子 1α 的表达没有差异。然而，血管内皮生长因子 A（VEGF）及其受体 VEGFR-1（p<0.01）和 VEGFR-2（p<0.05）的表达显著增加（p<0.05），尤其是 1 型糖尿病患者，且与神经纤维病变的严重程度相关。
结论/解释：与非糖尿病 CTS 患者相比，糖尿病患者的神经纤维和微血管病理变化更为严重，且 VEGF 及其受体的表达增强，这为糖尿病患者易发生 CTS 提供了潜在的分子和病理基础。
