Zakareia Faten A
Department of Clinical Physiology, King Saud University, and King Khalid University Hospital, PO Box 2925, Riyadh 11461, Kingdom of Saudi Arabia. Tel/Fax. +966 (1) 4786798. E-mail:
Neurosciences (Riyadh). 2008 Oct;13(4):374-9.
To evaluate the electrophysiological changes, blood flow index, vascular endothelial growth factor (VEGF), soluble fatty acid synthase (s-FAS), and intercellular adhesion molecule (I-CAM) in diabetic neuropathy.
This study was conducted from March 2004 to November 2007 on 60 type II diabetic patients and 30 controls, recruited from the Diabetic Research Center of King Abdul-Aziz University Hospital, Riyadh, Kingdom of Saudi Arabia. Electrophysiological studies were carried out in the Clinical Physiology Laboratory. Patients and controls were of the same age, gender, and weight.
The study included 30 controls (group I), 30 diabetics type II without complications (group II), and 30 with peripheral neuropathy (group III). There was a significant decrease of motor conduction velocity, prolongation of F wave response of median, ulnar, peroneal nerves, significant decrease of median and ulnar sensory conduction velocity, sural nerve conduction velocity and sensory amplitude, showed significant decrease, ankle/brachial index (A/BI) showed insignificant change, also there was a significant increase of plasma VEGF, s-FAS, and ICAM all in group III compared to groups I and II. The results revealed that VEGF and s-FAS are good predictors for median nerve motor conduction velocity, also VEGF is a good predictor of sural nerve sensory conduction velocity in diabetic neuropathy.
The rise of VEGF in diabetic neuropathy may be protective to preserve the nerve blood flow, the significant rise of s-FAS may be causative in advancement of neuropathy, I-CAM high levels suggest its leading role in interaction between endothelium, blood elements, and peripheral nerves. The results showed that human neuropathy is the result of multiple factors, thus, it may be optimistic to believe that reversing one of them, such as s-FAS will halt, or reverse nerve damage. Targeting multiple mechanisms simultaneously, by administering combination treatments of VEGF, and anti-apoptotic drugs may be prospective.
评估糖尿病性神经病变中的电生理变化、血流指数、血管内皮生长因子(VEGF)、可溶性脂肪酸合酶(s-FAS)及细胞间黏附分子(I-CAM)。
本研究于2004年3月至2007年11月在沙特阿拉伯王国利雅得阿卜杜勒-阿齐兹国王大学医院糖尿病研究中心招募的60例II型糖尿病患者及30例对照者中进行。电生理研究在临床生理实验室开展。患者和对照者年龄、性别及体重相同。
研究纳入30例对照者(I组)、30例无并发症的II型糖尿病患者(II组)及30例伴有周围神经病变的患者(III组)。正中神经、尺神经、腓总神经的运动传导速度显著降低,F波反应延长,正中神经和尺神经感觉传导速度、腓肠神经传导速度及感觉波幅显著降低,踝肱指数(A/BI)变化不显著,与I组和II组相比,III组血浆VEGF、s-FAS及ICAM均显著升高。结果显示,VEGF和s-FAS是正中神经运动传导速度的良好预测指标,VEGF也是糖尿病性神经病变中腓肠神经感觉传导速度的良好预测指标。
糖尿病性神经病变中VEGF升高可能对维持神经血流具有保护作用,s-FAS显著升高可能是神经病变进展的原因,I-CAM高水平表明其在内皮细胞、血液成分及周围神经相互作用中起主导作用。结果表明,人类神经病变是多种因素导致的,因此,认为逆转其中之一(如s-FAS)将阻止或逆转神经损伤可能过于乐观。同时针对多种机制,联合应用VEGF及抗凋亡药物进行治疗可能具有前景。