Doupis John, Lyons Thomas E, Wu Szuhuei, Gnardellis Charalambos, Dinh Thanh, Veves Aristidis
Microcirculation Laboratory, Joslin-Beth Israel Deaconess Foot Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston Massachusetts 02215, USA.
J Clin Endocrinol Metab. 2009 Jun;94(6):2157-63. doi: 10.1210/jc.2008-2385. Epub 2009 Mar 10.
We investigated the association between inflammation, microvascular reactivity, and the development of peripheral diabetic neuropathy.
We studied three groups: 55 healthy control subjects, 80 nonneuropathic patients, and 77 neuropathic diabetic patients. We also subdivided the neuropathic patients into a subgroup of 31 subjects with painless neuropathy and 46 with painful neuropathy. We measured the foot skin endothelium-dependent and -independent vasodilation, the nerve axon reflex-related vasodilation (NARV), and inflammatory cytokines and biochemical markers of endothelial function.
The endothelium-dependent and -independent vasodilation and NARV were lower in the neuropathic group (P < 0.05). NARV was further reduced in the subgroup of painless neuropathy when compared to painful neuropathy (P < 0.05). Compared to the other two groups, the neuropathic group also had higher serum levels of PDGF AA/BB (P < 0.05), RANTES (P < 0.01), leptin (P < 0.0001), osteoprotegerin (P < 0.01), G-CSF (P < 0.05), sE-Selectin (P < 0.01), sICAM (P < 0.0001), sVCAM (P < 0.001), CRP (P < 0.0001), TNFalpha (P < 0.05), and fibrinogen (P < 0.05). Patients with painful neuropathy had higher sICAM-1 (P < 0.05) and CRP levels (P < 0.01) when compared to painless neuropathy. No major changes in the above results were observed in 78 diabetic patients who were seen for a second visit 21 months after the first visit.
Peripheral diabetic neuropathy is associated with increased biochemical markers of inflammation and endothelial dysfunction. Painful neuropathy is associated with further increase in inflammation and markers of endothelial dysfunction and preservation of the nerve axon reflex.
我们研究了炎症、微血管反应性与糖尿病周围神经病变发生之间的关联。
我们研究了三组：55名健康对照者、80名非神经病变患者和77名神经病变糖尿病患者。我们还将神经病变患者细分为31名无痛性神经病变患者亚组和46名疼痛性神经病变患者亚组。我们测量了足部皮肤内皮依赖性和非内皮依赖性血管舒张、神经轴突反射相关血管舒张（NARV）以及内皮功能的炎性细胞因子和生化标志物。
神经病变组的内皮依赖性和非内皮依赖性血管舒张以及NARV较低（P<0.05）。与疼痛性神经病变相比，无痛性神经病变亚组的NARV进一步降低（P<0.05）。与其他两组相比，神经病变组的血清PDGF AA/BB（P<0.05）、RANTES（P<0.01）、瘦素（P<0.0001）、骨保护素（P<0.01）、G-CSF（P<0.05）、sE-选择素（P<0.01）、sICAM（P<0.0001）、sVCAM（P<0.001）、CRP（P<0.0001）、TNFα（P<0.05）和纤维蛋白原（P<0.05）水平也更高。与无痛性神经病变相比，疼痛性神经病变患者的sICAM-1（P<0.05）和CRP水平（P<0.01）更高。在首次就诊21个月后复诊的78名糖尿病患者中，上述结果未观察到重大变化。
糖尿病周围神经病变与炎症生化标志物增加和内皮功能障碍相关。疼痛性神经病变与炎症和内皮功能障碍标志物的进一步增加以及神经轴突反射的保留相关。
