[Vascular endothelium-related factors and atherosclerosis/arteriosclerosis: serum hepatocyte growth factor as a possible indicator of vascular lesions].
[Vascular endothelium-related factors and atherosclerosis/arteriosclerosis: serum hepatocyte growth factor as a possible indicator of vascular lesions].
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血管内皮相关因子与动脉粥样硬化/动脉硬化：血清肝细胞生长因子作为血管病变的可能指标。
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发表时间：
1998
期刊：
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通讯作者：
M. Yoshimura
中科院分区：
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作者：
M. Nishimura;M. Ushiyama;A. Nanbu;K. Ohtsuka;M. Yoshimura
为了探讨肝细胞生长因子（HGF）与血管病变的可能关系，我们研究了血清HGF浓度与视网膜动脉硬化程度、糖尿病患者视网膜冠状动脉粥样硬化增生性改变和系统性血管炎活动的关系。视网膜动脉病变程度越深的患者血清HGF值越高（0级，0.053 +/- 0.005 ng/ml ; 1级，0.144 +/- 0.022 ng/ml ; 2级，0.338 +/- 0.36 ng/ml ; 3级，0.526 +/- 0.051 ng/ml）。单支、双支和三支冠状动脉病变患者血清HGF浓度分别为0.200 ± 0.012ng/ml、0.334 ± 0.018ng/ml和0.379 ± 0.022ng/ml，而冠状动脉完整者血清HGF浓度为0.112 ± 0.008ng/ml。糖尿病无视网膜病变组血清HGF水平低于非糖尿病组（0.041 +/- 0.003 ng/ml vs 0.080 +/- 0.010 ng/ml，p < 0.05），但与其他背景视网膜病变的糖尿病受试者无差异（0.058 +/- 0.007 ng/ml）或增殖前视网膜病变（0.048 +/- 0.010 ng/ml）。无光凝的增生性视网膜病变患者血清HGF升高（0.213 ± 0.025 ng/ml，p < 0.01），但光凝患者血清HGF升高不明显（0.040 ± 0.008 ng/ml）。在Schönlein-Henoch紫癜（一种系统性血管炎）急性期，血清HGF浓度升高（p < 0.01）（0.31 ± 0.15 ng/ml），但在缓解期恢复到对照水平（0.11 ± 0.10 ng/ml）。血清HGF升高可能参与动脉硬化/动脉粥样硬化、视网膜新生血管或血管炎的发病机制，血清HGF的测量可能是预测这些血管病变的有用测试。
To investigate the possible involvement of hepatocyte growth factor (HGF) with vascular lesions, we studied the relationship between serum HGF concentrations and the grades of retinal arteriosclerosis, coronary atherosclerosis proliferative changes in the retina of diabetic subjects, and activities of systemic vasculitis. Individuals with more advanced grades of retinal arteriosclerotic change showed higher serum HGF values (grade 0, 0.053 +/- 0.005 ng/ml ; grade 1, 0.144 +/- 0.022 ng/ml ; grade 2, 0.338 +/- 0.36 ng/ml ; grade 3, 0.526 +/- 0.051 ng/ml). The serum HGF concentration was increased in subjects with single- (0.200 +/- 0.012 ng/ml, double- (0.334 +/- 0.018 ng/ml) or triple- (0.379 +/- 0.022 ng/ml) vessel coronary heart diseases, compared with that in subjects with intact coronary arteries (0.112 +/- 0.008 ng/ml). Serum HGF in diabetes without retinopathy was lower than that in nondiabetic subjects (0.041 +/- 0.003 ng/ml vs 0.080 +/- 0.010 ng/ml, p < 0.05), but did not differ from that in other diabetic subjects with background retinopathy (0.058 +/- 0.007 ng/ml) or preproliferative retinopathy (0.048 +/- 0.010 ng/ml). Serum HGF was increased in patients with proliferative retinopathy without photocoagulation (0.213 +/- 0.025 ng/ml, p < 0.01), but not in those with photocoagulation (0.040 +/- 0.008 ng/ml). Serum HGF concentration was increased (p < 0.01) during the acute phase of Schönlein-Henoch purpura (0.31 +/- 0.15 ng/ml), a systemic vasculitis, but it returned to control levels during the remission phase (0.11 +/- 0.10 ng/ml). Increased serum HGF may be involved in the pathogenesis of arteriosclerosis/atherosclerosis, retinal neovascularization, or vasculitis, and measurement of serum HGF may be a useful test for predicting these vascular lesions.