Non-genetic and genetic risk factors for adult cerebral venous thrombosis

Abstract Introduction 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. Materials and methods 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. Results 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. Conclusions 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.