Solá Eva, Vayá Amparo, Contreras Teresa, Falcó Cristina, Corella Dolores, Hernández Antonio, Aznar Justo
Endocrinology Service, Dr. Peset Hospital, Valencia, Spain.
Clin Hemorheol Microcirc. 2004;30(3-4):415-8.
The association of hemorheological alterations with morbid obesity remains a question of debate. In order to ascertain whether morbid obese subjects show certain hemorheological alterations which might be involved in the higher thrombotic risk which characterizes these subjects, we determine glucose, plasma lipids, apolipoproteins, fibrinogen, hematocrit, blood viscosity (Brookfield DVIII viscosimeter), both at native and corrected hematocrit of 45%, plasma viscosity (Fresenius capillary viscosimeter), erythrocyte aggregation (Myrenne aggregometer), both at stasis and at 3 s(-1) at 45% hematocrit and erythrocyte indexes in 41 morbid obese subjects (32 female, 9 male aged 33+/-10 years), and in a well matched non-obese control group (40 female, 15 male, aged 32+/-10 years). Mean BMI in the morbid obese group was 44.9+/-6.7 kg/m2 vs 23.5+/-4.8 kg/m2 in the control group (p<0.001). Morbid obese subjects when compared with the control group showed a statistically higher glucose level (p<0.001), LDL-cholesterol (p=0.019), triglycerides (p<0.001), apoB (p=0.019), apoB/A1 (p<0.001), fibrinogen (p<0.001), erythrocyte aggregation (p<0.001), and a statistically lower HDL-cholesterol (p<0.001). No differences between both groups were observed regarding total-cholesterol, plasma viscosity, blood viscosity and hematocrit (p=0.109; p=0.690; p=0.510; p=0.950), respectively. After the adjustment for BMI, differences in glucose, LDL-cholesterol, triglycerides, apoB, apoB/A1, and erythrocyte aggregation did not reach the statistical significance, and differences in fibrinogen were borderline significant (p=0.051), showing a direct effect of BMI on the detected differences between obese and non-obese. Our results suggest that in morbid obese subjects the increased fibrinogen levels and the altered lipid profile associated with their higher BMI, could in addition to its known mechanisms on haemostasis, favour both venous and arterial thrombotic events by enhancing erythrocyte aggregation.
血液流变学改变与病态肥胖之间的关联仍是一个有争议的问题。为了确定病态肥胖受试者是否存在某些可能与这些受试者较高血栓形成风险相关的血液流变学改变,我们测定了41名病态肥胖受试者(32名女性,9名男性,年龄33±10岁)以及与之匹配良好的非肥胖对照组(40名女性,15名男性,年龄32±10岁)的血糖、血浆脂质、载脂蛋白、纤维蛋白原、血细胞比容、血液粘度(Brookfield DVIII粘度计)(包括自然状态下及血细胞比容校正至45%时)、血浆粘度(费森尤斯毛细管粘度计)、红细胞聚集性(Myrenne聚集仪)(包括血流停滞时及血细胞比容为45%时切变率为3 s-1时)以及红细胞指数。病态肥胖组的平均体重指数为44.9±6.7 kg/m2,而对照组为23.5±4.8 kg/m2(p<0.001)。与对照组相比,病态肥胖受试者的血糖水平(p<0.001)、低密度脂蛋白胆固醇(p=0.019)、甘油三酯(p<0.001)、载脂蛋白B(p=0.019)、载脂蛋白B/载脂蛋白A1(p<0.001)、纤维蛋白原(p<0.001)、红细胞聚集性(p<0.001)在统计学上显著更高,而高密度脂蛋白胆固醇在统计学上显著更低(p<0.001)。两组在总胆固醇、血浆粘度、血液粘度和血细胞比容方面未观察到差异(分别为p=0.109;p=0.69;p=0.510;p=0.950)。在对体重指数进行校正后,血糖、低密度脂蛋白胆固醇、甘油三酯、载脂蛋白B、载脂蛋白B/载脂蛋白A1和红细胞聚集性的差异未达到统计学显著性,纤维蛋白原的差异接近显著性(p=0.051),表明体重指数对肥胖与非肥胖者之间检测到的差异有直接影响。我们的结果表明,在病态肥胖受试者中,与其较高体重指数相关的纤维蛋白原水平升高和脂质谱改变,除了其已知的止血机制外,还可能通过增强红细胞聚集性,促进静脉和动脉血栓形成事件。