title: Prothrombin G20210A mutation and oral contraceptive use increase upper-extremity deep vein thrombotic risk.
abstract: The role played by a hypercoagulable state, either inherited or acquired, in the pathogenesis of upper-extremity deep vein thrombosis (UEDVT) remains a question of debate. We performed a case-control study including 79 patients with a first objectively confirmed episode of UEDVT, 31 secondary and 48 primary, and 165 healthy controls. Nine patients (11.4%) with UEDVT were carriers of the prothrombin G20210A mutation vs. six (3.7%) in controls; P = 0.025, OR: 3.39 (95% CI 1.16 to 9.88). No statistical difference was observed between cases and controls for the factor V Leiden mutation, AT, protein C or protein S deficiency and anticardiolipin antibodies (ACAs). Thirteen (35.1%) UEDVT patients were oral contraceptive (OC) users vs. 12 (16%) controls; P = 0.020, OR: 2.89 (95% CI 1.16-7.21). When secondary UEDVT patients were compared with controls, no differences were observed in any of the risk factors analysed. On the other hand, when primary UEDVT was considered, six (12.5%) patients were carriers of the prothrombin G20210A mutation vs. six (3.7%) controls; P = 0.031, OR: 3.76 (95% CI 1.15-12.26). Regarding ACAs, a borderline statistical significance was observed when primary UEDVT was compared with controls, P = 0.048; OR: 4.88 (95% CI 1.05-22.61). In primary UEDVT, 52% of the fertile women were OC users vs. 16% of controls; P = 0.001, OR: 5.78 (95% CI 2.13-15.67). When the interaction of both factors, i.e. prothrombin G20210A mutation and OC intake, were considered, the risk increased markedly, indicating a synergistic effect as observed with other thrombotic locations. In patients with primary UEDVT screening for antithrombin, protein C and protein S deficiency and APC resistance would not be justified, although it might be reasonable to determine the carrier status of the prothrombin G20210A mutation only in OC users.
authors.affiliation: Thrombosis and Hemostasis Unit, Department of Clinical Pathology, La Fe University Hospital, Valencia, Spain. vaya_amp@gva.e
authors.forename: Amparo
authors.initials: A
authors.lastname: Vayá
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Mira
authors.forename: Jose
authors.initials: J
authors.lastname: Mateo
authors.forename: Cristina
authors.initials: C
authors.lastname: Falco
authors.forename: Piedad
authors.initials: P
authors.lastname: Villa
authors.forename: Amparo
authors.initials: A
authors.lastname: Estelles
authors.forename: Dolores
authors.initials: D
authors.lastname: Corella
authors.forename: Jordi
authors.initials: J
authors.lastname: Fontcuberta
authors.forename: Justo
authors.initials: J
authors.lastname: Aznar
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000991:Antithrombins / Q000172:deficiency; D001132:Arm; D016022:Case-Control Studies; D003276:Contraceptives, Oral / Q000009:adverse effects*; D005165:Factor V / Q000235:genetics; D005260:Female; D006579:Heterozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D017354:Point Mutation; D020151:Protein C Deficiency / Q000097:blood / Q000150:complications / Q000235:genetics; D018455:Protein S Deficiency / Q000097:blood / Q000150:complications / Q000235:genetics; D011516:Prothrombin / Q000235:genetics*; D012307:Risk Factors; D020246:Venous Thrombosis / Q000097:blood / Q000209:etiology* / Q000235:genetics
chemical_list: D017153:Antibodies, Anticardiolipin; D000991:Antithrombins; D003276:Contraceptives, Oral; C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin