
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
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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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