الفهرس 
Review of literatureOnly 14 pages are availabe for public view
 |  | from | 210 |  |  |
| | | from | 210 | | |
Abstract
Purpose
Recurrent pregnancy loss (RPL) is an important clinical and stressful problem that has been studied tremendously but the causes and treatment have not been fully resolved. No unequivocal cause is currently available for more than half of the cases suffering from RPL. About 9- 13% of women in the reproductive age group experience one clinically recognized loss, 5% experience two or more losses, and 1 to 2% suffer three or more losses. Up to 50% of cases of RPL, still remain unexplained after standard gynecological, hormonal, and karyotypic investigations. RPL has many possible causes that can be categorized as genetic abnormalities, hormonal and metabolic disorders, uterine anatomic abnormalities, infectious causes, immune disorders and thrombophilic disorders. Thrombophilia is defined as a disorder of hemostasis that predisposes a person to a thrombotic event. Data suggest that at least 50% of cases of venous thromboembolism in pregnant women are associated with an inherited or acquired thrombophilia. Here, we sought to determine whether thrombophilic and hypofibrinolytic gene variations is associated with RPL.
Patients and methods
► A total of 200 women were recruited to this study, 150 women with ≥ 2 successive fetal losses prior to 24 weeks of gestation. In addition, 50 age-matched healthy women with at least two live births and no history of miscarriages.
► All women experienced RPL underwent a standard diagnostic workup to rule out other causes of recurrent miscarriage. Diagnostic procedures included ultrasonography or hysteroalpingography; a comprehensive hormonal profiling; autoantibody testing anti-nuclear antibodies [ANA], anti-double stranded DNA [anti-dsDNA] antibodies, antiphospholipid antibodies [lupus anticoagulants (LAs), anticardiolipin antibodies (ACA) and anti-β2 glycoprotein I antibody (anti-β2GP I)], thyroid autoantibodies (thyroid peroxidase antibodies [TPOAb], thyroglobulin antibodies [TgAb], and thyroid stimulating hormone receptor antibodies [TRAb])); screening for TORCH infections; and karyotyping.
► A total of 13 genetic variants (FV G1691A [FVLeiden], FV A4070G [FVR2], F2 G20210A, F13A1 G103T, FGB
− 455G > A, PAI-1 − 675 4G/5G, ITGB3 T1565C, MTHFR C677T, MTHFR A1298C, ACE I/D, APOB G10708A, APOE T388C, and APOE C526T) were
genotyped using the ViennaLab CVD StripAssay (REF 4–240, ViennaLab Diagnostics GmbH, Vienna, Austria).
Results
► The genotype distributions and allele frequencies of F5 1691G > A, F5 4070A > G, F2 20210G > A, PAI-1 − 675
4G/5G, MTHFR 677C > T, MTHFR 1298A > C, ACE I/D, APOB 10708G > A, APOE 388 T > C, and APOE
526C > T genetic variants did not differ significantly between the study groups.
► There were statistically significant differences in the allelic and genotypic distribution of the F13A1 103G>T, FGB−455G>A, and ITGB3 1565 T>C genetic variants between control women and those with RPL.
► the distribution of the F5 1691G > A/4070A > G haplotypes (GA, GG, and AA), MTHFR 677C > T/1298A > C haplotypes (CA, CC, and TA), and APOE 388 T > C/526C > T haplotypes (TC [ε3], CC [ε4], TT
[ε2], and CT [ε1]) did not differ significantly between control women and those with RPL.
Conclusion
► Our data provide further support to the earlier idea that F13A1 103 T, FGB − 455A, and ITGB3 1565C alleles
may represent a potential genetic susceptibility factor for RPL.
► Our findings further strengthen prior data suggesting a potential involvement of thrombophilic and hypofibrinolytic defects in RPL pathophysiology.