Oral Contraceptives Are a Risk Factor for Cerebral Vein Thrombosis

1996 ◽  
Vol 76 (03) ◽  
pp. 477-478 ◽  
Author(s):  
I Martinelli ◽  
F R Rosendaal ◽  
J P Vandenbroucke ◽  
P M Mannucci
1980 ◽  
Vol 25 (3) ◽  
pp. 243-244 ◽  
Author(s):  
M. L. Stirling ◽  
R. J. Lenton ◽  
M. D. Sumerling

A young woman who developed a cerebral venous thrombosis shortly after commencement of an oral contraceptive preparation was subsequently found to have paroxysmal nocturnal haemoglobinuria. The aetiology of thrombotic complications in this condition is discussed, with particular reference to the additional risk factor of the contraceptive pill in this case.


Blood ◽  
2006 ◽  
Vol 107 (7) ◽  
pp. 2766-2773 ◽  
Author(s):  
Francesco Dentali ◽  
Mark Crowther ◽  
Walter Ageno

AbstractRecent 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.


The Lancet ◽  
1998 ◽  
Vol 352 (9124) ◽  
pp. 326 ◽  
Author(s):  
I Martinelli ◽  
E Taioli ◽  
D Palli ◽  
PM Mannucci

1999 ◽  
Vol 81 (06) ◽  
pp. 991-992 ◽  
Author(s):  
K. Paciaroni ◽  
P. Chiusolo ◽  
I. Casorelli ◽  
E. Rossi ◽  
L. Teofili ◽  
...  

1998 ◽  
Vol 338 (25) ◽  
pp. 1793-1797 ◽  
Author(s):  
Ida Martinelli ◽  
Elisabetta Sacchi ◽  
Gianluca Landi ◽  
Emanuela Taioli ◽  
Francesca Duca ◽  
...  

2013 ◽  
Vol 110 (07) ◽  
pp. 197-199 ◽  
Author(s):  
Antonella Tufano ◽  
Assunta Nardo ◽  
Carlo Bonfanti ◽  
Silvia Crestani ◽  
Anna Cerbone ◽  
...  

2017 ◽  
Vol 75 (12) ◽  
pp. 858-861 ◽  
Author(s):  
Aníbal Chertcoff ◽  
Lucrecia Bandeo ◽  
Fátima Pantiu ◽  
Luciana León Cejas ◽  
Sol Pacha ◽  
...  

ABSTRACT Nontraumatic convexity subarachnoid hemorrhage is an increasingly recognized subtype of subarachnoid bleeding. Objective: Our aim was to describe the etiology and clinical features of a cohort of patients with convexity subarachnoid hemorrhage. Methods: We retrospectively analyzed all cases of convexity subarachnoid hemorrhage admitted to our hospital between January 2012 and April 2017. Demographic features, clinical characteristics, complementary investigations, etiology and mortality were assessed. Twenty patients (65% females) were identified. Mean age: 53 years (range, 15-86 years). Results: Symptoms on admission: headache (65%), sensory and/or motor symptoms (50%) and seizures (35%). Commonest causes: cerebral vein thrombosis (20%), reversible cerebral vasoconstriction syndrome (20%) and cerebral amyloid angiopathy (20%). Two patients died. Conclusion: Convexity subarachnoid hemorrhage may be related to a wide spectrum of etiologies. In our patients, an increased prevalence of cerebral vein thrombosis was observed. Mortality was low and not related to the bleeding itself.


Sign in / Sign up

Export Citation Format

Share Document