Recurrent miscarriage (RM), unlike sporadic pregnancy loss, necessitates additional attention, monitoring, and follow-up in subsequent pregnancies to be successful [1, 2]. RM is a disappointing experience that negatively impacts couples’ psychological status and worsens their social discomfort [3]. RM is classified into primary and secondary: primary RM is the repeated miscarriage without viable previous babies, but secondary RM is the repeated pregnancy loss with a live birth at some time [3]. Secondary RM has a better prognosis than primary RM, in fact, primary RM is a poorly understood condition, which affects 1–3% up to 5% of couples trying to have children worldwide [3,4,5,6,7,8,9,10,11,12,13,14]. RM is defined by the American Society of Reproductive Medicine (ASRM) and the European Society for Human Reproductive and Embryology (ESHRE) as the loss of two or more consecutive pregnancies from conception to 24 weeks of gestation [1, 4,5,6,7,8,9, 11, 13,14,15,16,17]. While the World Health Organization (WHO) and the Royal College of Obstetricians and Gynecologists (RCOG) define RM as three or more miscarriages verified by ultrasonography or histology up to 24 weeks of gestation [2, 4, 5, 15, 16, 18,19,20]. As a result, several measurements and recommendations were developed and implemented to reach standardization for appropriate inquiry and treatment approaches [1, 15].

In normal pregnancy, the hemostatic system is modified to a hypocoagulable condition to preserve oxygen and nutrition transmission via the placenta for fetal survival, then changed to a hypercoagulable state to prevent excessive bleeding following birth [2, 6, 10, 21,22,23]. Because of the interaction of various risk factors that play a role in RM such as maternal age, lifestyle behaviors (stress, smoking, and excessive alcohol consumption), history of miscarriage, antiphospholipid syndrome, uterine malformation, endometritis, endocrinological, abnormal parental karyotypes, obesity, genetic factors, and thrombophilia with other unknown factors, RM is considered a multifactorial condition [1,2,3,4,5, 7,8,9, 11, 12, 14, 15, 17, 19, 24, 25]. Inherited thrombophilia (IT) is a hypercoagulopathy state that increases the risk of thrombosis. The combination of physiological alterations in hemostatic systems with IT in pregnancy has been reported to increase the risk of pregnancy complications in 40–50% [6, 24] or even 80% of cases [12].

RM is a multi-etiological syndrome with more than 50% of cases remaining unexplained, with the underlying processes remaining unknown, limiting the diagnosis and treatment protocols, and creating a challenge to patients and doctors [1, 3, 4, 6,7,8, 12, 14,15,16, 18, 20, 24, 26]. RM demonstrates significant causative variability in known and unknown etiology groups [15, 16]. Despite substantial research on the subject, studies are still limited, suffer from population selection bias, use diverse diagnostic criteria, and yield conflicting conclusions [4].

Inherited or acquired thrombophilia causes irregular blood coagulation and an increased risk of venous thromboembolism (VTE). IT is caused by mutations that affect gene function in the anticoagulant mechanism, causing the hemostatic system to become thrombotic [11, 21]. Thrombophilia affects about 5% of the general population [3]. Prothrombin gene (FII) mutation (G20210A) and factor V Leiden (FVL) were detected in around 50–70% of VTE cases diagnosed with inherited thrombophilia [21]. Pregnancy is associated with around 20% of thrombotic events; additionally, pregnancy raises the incidence of VTE by 5 times [12, 18, 21]. It is estimated that around 40–50% of VTE caused by IT occurs during pregnancy [3, 12, 21]. The association between thrombophilia and RM has been investigated by many studies with controversial conclusions [3, 11, 12]. Therefore, in cases of RM, a panel of laboratory tests belonging to hemostatic, and IT are usually recommended [3].

Clinically, most carriers of thrombophilia mutations will not show symptoms and will go untreated, but exposure to additional risk factors such as pregnancy may raise the likelihood of life-threatening complications to become clinically clear [12, 26]. IT panel includes FVL R506Q mutation, FII gene G20210A mutation, Methyltetrahydrofolate Reductase gene mutations (MTHFR C1677T; A1298C), B-fibrinogen gene − 455G > A, Plasminogen activator inhibitor 1 (PAI1) 5G/4G, Factor XIIIA (FXIIIA) V34L, and FV HR2 A4070G. FII G20210A, FVL and MTHFR C677T and A1298C are the most extensively studied thrombophilia mutations in RM, and most studies reported wide ranges of prevalence for each mutation among the respective study population with controversial findings [6, 10,11,12,13,14,15,16, 24, 26,27,28,29,30].

In the past 13 years, eight studies have been conducted regarding RM among Palestinian women in Palestine (West Bank and Gaza) [6,7,8,9,