Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, the Netherlands.
J Thromb Haemost. 2010 May;8(5):971-8. doi: 10.1111/j.1538-7836.2010.03819.x. Epub 2010 Feb 19.
It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization.
We determined whether the following mechanisms were involved: hypoxia, stress, inflammation or viral infection.
PATIENTS/METHODS: In a case crossover setting in 71 healthy volunteers who were exposed to an 8-h flight, 8-h movie marathon and 8 h of regular activities, we compared markers for several hypothetical pathways: plasminogen activator inhibitor-1 (PAI-1), stress, plasma factor (F)VIII coagulant activity (FVIIIc), soluble P-selectine (sP-selectine), interleukin-8 (IL-8) and neutrophil elastase. We reported earlier an activated clotting system, as evidenced by thrombin generation, in 17% of volunteers after the flight.
PAI-1 increased by 4.2 ng mL(-1) (CI95:-49.5 to 6.5) in volunteers with an activated clotting system whereas it decreased in those without (-20.0 ng mL(-1), CI95:-33.2 to -14.0). FVIIIc levels rose more in individuals with clotting activation (18.0%, CI95:-1.0 to 33.0) than in those without (2.0%, CI95:-2.0 to 5.0). The increases in FVIIIc were not associated with stress, which appeared unrelated to clotting activation. sP-selectin increased in those with clotting activation (3.5 microg L(-1), CI95: -3.0 to 10.0), but decreased in those without (-0.5 microg L(-1), CI95: -2.0 to 2.0). Changes in levels of neutrophil elastase or IL-8 were not different between the subjects with and without clotting activation.
Our results do not support the hypotheses that stress, infection or air pollution are involved in the development of a prothrombotic state in air travellers. After long haul air travel, this state is more pronounced in patients with risk factors and may be caused by hypoxia, triggering systemic inflammation and platelet activation, leading to coagulation induction and degranulation of platelets.
长距离航空旅行后发生静脉血栓是否完全由固定不动引起尚不清楚。
我们旨在确定是否涉及以下机制：缺氧、应激、炎症或病毒感染。
患者/方法：在 71 名健康志愿者中进行病例交叉研究，这些志愿者在暴露于 8 小时飞行、8 小时电影马拉松和 8 小时常规活动后，我们比较了几种假设途径的标志物：纤溶酶原激活物抑制剂-1（PAI-1）、应激、血浆因子（F）VIII 凝血活性（FVIIIc）、可溶性 P-选择素（sP-选择素）、白细胞介素-8（IL-8）和中性粒细胞弹性蛋白酶。我们之前报道过，在 17%的志愿者中，在飞行后出现了凝血系统激活的证据，即凝血酶生成。
在凝血系统激活的志愿者中，PAI-1 增加了 4.2ng/ml（95%CI：-49.5 至 6.5），而在没有凝血系统激活的志愿者中则下降了 20.0ng/ml（95%CI：-33.2 至-14.0）。在凝血系统激活的个体中，FVIIIc 水平升高（18.0%，95%CI：-1.0 至 33.0）比没有凝血系统激活的个体（2.0%，95%CI：-2.0 至 5.0）更多。FVIIIc 的增加与应激无关，应激似乎与凝血系统激活无关。在凝血系统激活的志愿者中，sP-选择素增加（3.5μg/L（95%CI：-3.0 至 10.0），而在没有凝血系统激活的志愿者中则下降（0.5μg/L（95%CI：-2.0 至 2.0）。在凝血系统激活和无凝血系统激活的受试者之间，中性粒细胞弹性蛋白酶或 IL-8 水平的变化没有差异。
我们的结果不支持应激、感染或空气污染与航空旅行者发生血栓前状态有关的假设。在长途航空旅行后，这种状态在有危险因素的患者中更为明显，可能是由缺氧引起的，触发全身炎症和血小板激活，导致凝血诱导和血小板脱颗粒。
