Institute of Cardiovascular Research, Royal Holloway, University of London (ICR2UL), Egham, United Kingdom.
Department of Medicine, Imperial College London, London, United Kingdom.
Thromb Res. 2018 Sep;169:15-22. doi: 10.1016/j.thromres.2018.07.005. Epub 2018 Jul 6.
A wide variety of non-genetic and genetic factors have been shown to associate with increased risk for cerebral venous thrombosis (CVT). However, there is a paucity of risk factor data and conclusions about their impact are often conflicting. Herein, we quantified the associations of non-genetic and genetic risk factors for CVT in adults.
Electronic databases were searched up to January 2017. Meta-analyses were performed (RevMan v5.3) to determine pooled odds ratios (ORs and 95% CIs) for risk factors, interstudy heterogeneity and publication bias.
Twenty non-genetic (n = 2314) and 33 genetic (n = 2117) studies up to January 2017 met the selection criteria. For non-genetic factors, CVT risk increased in the presence of glucocorticosteroid therapy by 18.3-fold (3.3-102.6), alcohol consumption 2.7-fold (1.8-3.9), infection 7.5-fold (2.6-21.6), surgery 9.6-fold (1.1-83.5), hypercholesterolaemia 2.4-fold (1.3-4.4), hyperhomocysteinaemia 3.1-fold (2.1-4.6), antiphospholipid antibodies 7.0-fold (2.1-23.6), autoimmune diseases 5.6-fold (2.3-13.6), anaemia 4.0-fold (2.1-7.9), malignancy 3.2-fold (1.4-7.1) and pregnancy/puerperium 11.4-fold (5.7-24.3). Smoking, hypertension and diabetes did not associate with CVT risk. For genetic factors, CVT risk increased in the presence of factor V Leiden (G1691A) by 2.5-fold (1.9-3.3), protein C deficiency 10.7-fold (3.1-37.7), protein S deficiency 5.7-fold (1.4-22.4), antithrombin deficiency 3.8-fold (1.0-13.8), prothrombin (G20210A) 5.5-fold (4.0-7.27) and TAFI gene variant (C1040T) 1.6-fold (1.0-2.4). Prothrombin G20210A and factor V Leiden polymorphisms tended to have higher ORs for CVT than for ischaemic stroke.
We provide quantitative data supporting a strong basis for genetic and non-genetic risk factors in CVT. Its genetic liability seems higher when compared with sporadic ischaemic stroke.
大量非遗传和遗传因素已被证明与脑静脉血栓形成（CVT）风险增加相关。然而，有关危险因素的数据仍然缺乏，并且关于其影响的结论往往存在冲突。在此，我们定量评估了成人 CVT 的非遗传和遗传危险因素的关联。
截至 2017 年 1 月，我们检索了电子数据库。采用 Meta 分析（RevMan v5.3）来确定危险因素的汇总比值比（OR 和 95%CI）、研究间异质性和发表偏倚。
截至 2017 年 1 月，共纳入了 2314 项非遗传（n=2314）和 2117 项遗传（n=2117）研究。对于非遗传因素，皮质类固醇治疗使 CVT 风险增加 18.3 倍（3.3-102.6），饮酒使 CVT 风险增加 2.7 倍（1.8-3.9），感染使 CVT 风险增加 7.5 倍（2.6-21.6），手术使 CVT 风险增加 9.6 倍（1.1-83.5），高胆固醇血症使 CVT 风险增加 2.4 倍（1.3-4.4），高同型半胱氨酸血症使 CVT 风险增加 3.1 倍（2.1-4.6），抗磷脂抗体使 CVT 风险增加 7.0 倍（2.1-23.6），自身免疫性疾病使 CVT 风险增加 5.6 倍（2.3-13.6），贫血使 CVT 风险增加 4.0 倍（2.1-7.9），恶性肿瘤使 CVT 风险增加 3.2 倍（1.4-7.1），妊娠/产褥期使 CVT 风险增加 11.4 倍（5.7-24.3）。吸烟、高血压和糖尿病与 CVT 风险无关。对于遗传因素，因子 V Leiden（G1691A）使 CVT 风险增加 2.5 倍（1.9-3.3），蛋白 C 缺乏使 CVT 风险增加 10.7 倍（3.1-37.7），蛋白 S 缺乏使 CVT 风险增加 5.7 倍（1.4-22.4），抗凝血酶缺乏使 CVT 风险增加 3.8 倍（1.0-13.8），凝血酶原（G20210A）使 CVT 风险增加 5.5 倍（4.0-7.27），血栓调节蛋白基因变体（C1040T）使 CVT 风险增加 1.6 倍（1.0-2.4）。凝血酶原 G20210A 和因子 V Leiden 多态性似乎比缺血性脑卒中具有更高的 CVT OR。
我们提供了定量数据，为 CVT 的遗传和非遗传危险因素提供了强有力的依据。与散发性缺血性脑卒中相比，CVT 的遗传易感性似乎更高。
