Balkan Journal of Medical Genetics

RISK FACTORS OF VENOUS THROMBOEMBOLISM IN SUDANESE PREGNANT WOMEN
Abdalhabib EK, Alfeel A, Ali EI, Ibrahim IK, Mobarki AA, Dobie G, Hamali HA, Saboor M,
*Corresponding Author: Dr. Muhammad Saboor, Department of Medical Laboratory Technology, Faculty of Applied Medical Science, Jazan University, Jazan, Saudi Arabia. Tel.: +966-54-495-9029. E-mail: msaboor@ jazanu.edu.sa
page: 49

INTRODUCTION

Venous thromboembolism (VTE), manifested as deep vein thrombosis (DVT) and/or pulmonary embolism (PE), is one of the major causes of pregnancy-related mortality and morbidity [1]. The annual incidence of VTE ranges from one to five per 1000 individuals; however, its diagnosis remains challenging and difficult [2]. Venous thromboembolism may occur due to inherited disorders or be associated with acquired clinical condition(s). The prominent etiologies of VTE in pregnancy are inherited thrombophilias, which include deficiencies of protein C (PC), protein S (PS) and antithrombin (AT). Factor V Leiden (FVL G1691A) polymorphism, prothrombin G20210A, and methylenetetrahydrofolate reductase gene mutations also cause VTE in pregnancy [3,4]. Acquired clinical conditions that may result in VTE in pregnancy include autoimmune and inflammatory disorders, increased body mass index (BMI), obesity, prolonged immobilization, miscarriages, surgical intervention, contraceptive use and multiparity [4-6]. During pregnancy, which is a physiological hypercoagulable state, there is also increased activity of coagulation factors I, II, VII, VIII, IX and X and tissue factor [7]. Plasma level of PS, activated PC levels, and plasminogen activator inhibitor levels decrease in pregnancy [7]. Thrombophilia further aggravates the preexisting hypercoagulable state in pregnancy [3]. In pregnant women, the risk of VTE has been reported to be 5- to 6-fold compared with that in nonpregnant age-matched controls [1,8]. This risk further increases from 3.7- to 8.5-fold in women with a family history of VTE and up to 34-fold in women with hereditary thrombophilia [1]. The clinical manifestations associated with the FVL G1691A polymorphism in pregnant women include severe placental abruption, fetal growth disturbances, placental infarction, stillbirth, increased risk for gestational hypertension, hemolysis, elevated liver enzymes, and low platelet syndrome [9]. Considering the clinical manifestations of thrombophilia, this study aimed to determine the frequencies of FVL G1691A polymorphism and prothrombin G20210A mutations and measure the plasma levels of PC, PS and AT in pregnant women with VTE and healthy pregnant women.

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