Lip P L, Blann A D, Hope-Ross M, Gibson J M, Lip G Y
Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, England, UK.
Ophthalmology. 2001 Apr;108(4):705-10. doi: 10.1016/s0161-6420(00)00663-1.
To investigate laboratory evidence of abnormal angiogenesis, hemorheologic factors, endothelial damage/dysfunction, and age-related macular degeneration (ARMD).
Comparative cross-sectional study.
We studied 78 subjects (26 men and 52 women; mean age 74 years; standard deviation [SD] 9.0) with ARMD attending a specialist referral clinic. Subjects were compared with 25 healthy controls (mean age, 71 years; SD, 11).
Levels of vascular endothelial growth factor (VEGF, an index of angiogenesis), hemorheologic factors (plasma viscosity, hematocrit, white cell count, hemoglobin, platelets), fibrinogen (an index of rheology and hemostasis), and von Willebrand factor (a marker of endothelial dysfunction) were measured.
Median plasma VEGF (225 vs. 195 pg/ml, P = 0.019) and mean von Willebrand factor (124 vs. 99 IU/dl, P = 0.0004) were greater in ARMD subjects than the controls. Mean plasma fibrinogen and plasma viscosity levels were also higher in the subjects (both P < 0.0001). There were no significant differences in other indices between cases and controls. When "dry" (drusen, atrophy, n = 28) and "exudative" (n = 50) ARMD subjects were compared, there was no significant differences in VEGF, fibrinogen, viscosity, or von Willebrand factor levels. There were no significant correlations between the measured parameters. Stepwise multiple regression analysis did not demonstrate any significant clinical predictors (age, gender, smoking, body mass index, history of vascular disease, or hypertension) for plasma VEGF or fibrinogen levels, although smoking status was a predictor of plasma von Willebrand factor levels (P < 0.05).
This study suggests an association between markers of angiogenesis (VEGF), hemorheologic factors, hemostasis, endothelial dysfunction, and ARMD. The interaction between abnormal angiogenesis and the components of Virchow's triad for thrombogenesis may in part contribute to the pathogenesis of ARMD.
研究异常血管生成、血液流变学因素、内皮损伤/功能障碍及年龄相关性黄斑变性（ARMD）的实验室证据。
比较性横断面研究。
我们研究了78例患有ARMD并在专科转诊诊所就诊的受试者（26名男性和52名女性；平均年龄74岁；标准差[SD]9.0）。将这些受试者与25名健康对照者（平均年龄71岁；SD，11）进行比较。
测量血管内皮生长因子（VEGF，血管生成指标）、血液流变学因素（血浆粘度、血细胞比容、白细胞计数、血红蛋白、血小板）、纤维蛋白原（流变学及止血指标）及血管性血友病因子（内皮功能障碍标志物）的水平。
ARMD受试者的血浆VEGF中位数（225对195 pg/ml，P = 0.019）及平均血管性血友病因子水平（124对99 IU/dl，P = 0.0004）高于对照组。受试者的平均血浆纤维蛋白原和血浆粘度水平也更高（均P < 0.0001）。病例组与对照组在其他指标上无显著差异。当比较“干性”（玻璃膜疣、萎缩，n = 28）和“渗出性”（n = 50）ARMD受试者时，VEGF、纤维蛋白原、粘度或血管性血友病因子水平无显著差异。所测参数之间无显著相关性。逐步多元回归分析未显示任何血浆VEGF或纤维蛋白原水平的显著临床预测因素（年龄、性别、吸烟、体重指数、血管疾病史或高血压），尽管吸烟状态是血浆血管性血友病因子水平的预测因素（P < 0.05）。
本研究提示血管生成标志物（VEGF）、血液流变学因素、止血、内皮功能障碍与ARMD之间存在关联。异常血管生成与血栓形成的魏尔啸三联征各成分之间的相互作用可能部分促成了ARMD的发病机制。
