Thrombophilic abnormalities, oral contraceptives, and risk of cerebral vein thrombosis: a meta-analysis

Abstract

Recent studies suggest that thrombophilic abnormalities and the use of oral contraceptives (OCs) are the leading causes of cerebral vein thrombosis (CVT). The purpose of this study was to assess the association between CVT and thrombophilic states, OCs, and their interaction. For data sources, we used the MEDLINE, EMBASE, and Cochrane Library databases (January 1994 to March 2005), reference lists of retrieved articles, and contact with content experts. We selected studies comparing the prevalence of OC use and the prevalence of prothrombitic abnormalities in patients with CVT compared with healthy controls. Two reviewers independently selected studies and extracted study characteristics, quality, and outcomes. Odds ratios (ORs) were calculated for each trial and pooled using the Mantel-Haenszel method. Seventeen studies were included. There was an increased risk of CVT in patients using OCs (OR 5.59; 95% confidence interval [CI] 3.95 to 7.91; P < .001), and in patients with factor V Leiden (OR 3.38; 95% CI 2.27 to 5.05; P < .001), with mutation G20 210A of prothrombin (OR 9.27; 95% CI 5.85 to 14.67; P < .001) and with hyperhomocysteinemia (OR 4.07; 95% CI 2.54 to 6.52; P < .001). We concluded that OC users, and patients with factor V Leiden, the prothrombin G20 120A mutation, and hyperhomocysteinemia are at a significantly increased risk of CVT. (Blood. 2006;

Familial risks of unusual forms of venous thrombosis: a nationwide epidemiological study in Sweden

“…Other studies have found an association between the prothrombin G2010A mutation and thrombosis of the cerebral and portal veins [13,20,21]. A genetic or familial contribution to migrating thrombophlebitis (Trousseau's syndrome when associated with malignancy) has not been demonstrated previously [7,8].…”

“…In some rare thrombotic conditions, an association has been made in case-control studies with factor V Leiden and prothrombin G20210A mutations reviewed by Martinelli et al [13]. These two mutations have been associated with an increased risk of cerebral vein [20] and portal vein thrombosis [21]. Budd-Chiari syndrome has been associated with factor V Leiden [22].…”

Cerebral Venous Sinus Thrombosis: Incidence and Hyperhomocysteinemia as a Risk Factor in Japanese Patients

“…Hyper-Hcy is confirmed as a risk factor for CVT [7,8], and its risk ratio is 4-fold compared to controls [26]. The prevalence of hyper-Hcy in CVT might exhibit racial differences [7][8][9]. Since we identified hyper-Hcy in 56.3% of our CVT patients, the prevalence of hyper-Hcy as a risk factor for CVT could be high in Japan.…”

“…Arterial and venous thromboses are potential complications [25]. Hyper-Hcy is confirmed as a risk factor for CVT [7,8], and its risk ratio is 4-fold compared to controls [26]. The prevalence of hyper-Hcy in CVT might exhibit racial differences [7][8][9].…”

“…Its incidence is about 0.5% to 1.0% among all types of stroke [1][2][3]. There are many risk factors of CVT [1][2][3]; genetic or acquired thrombophrenia and oral contraceptive use are the most common risk factors, and hyper-homocysteinemia (Hcy) is an additional risk factor [4][5][6][7][8]. A meta-analysis of 17 clinical studies showed that oral contraceptive use, Leiden mutation of Factor V, and hyperHcy were recognized as statistically significant risk factors 8).…”