The patient consulted to our clinic due to medical history of miscarriages of 16 times with unexplained recurrent miscarriages on the first trimester. Her general condition was good with pale appearance, and the systemic evaluations were normal. No any genetic, metabolic, morphological, or anatomical problems were diagnosed at pregnancy. She had no history of hypertension, hyperlipidemia, smoking cigarette, and small vascular thrombotic signs such as skin purpura. Also, she had no any medical treatment during the pregnancies. Liver enzymes, renal, thyroid function tests, coagulation analysis and immunological markers were negative. Serologically infections by HIV, HCV cytomegaly virus, Epstein-Barr-virus and Toxoplasma were also negative except for HBV. HBsAg was positive since 2 years. There was no liver cirrhosis. The laboratory tests for thrombophilia revealed homozigotous factor V leiden gene mutation, and the presence of β2 glycoprotein-I IgM for two times (22.6 U/ml and 34.1 U/ml, respectively). As clinical and laboratuary findings, patient was diagnosed with APS, factor V Leiden mutation and chronic viral hepatitis B.

In APS, blood clot as a result of thrombosis in artery or vein may affect many organs, and cause clinical manifestations such as stroke, myocardial infarction, deep vein thrombosis or pregnancy morbidity (recurrent early miscarriage, fetal death, preeclampsia, placental insufficiency) [1]. Otherwise, at least one of three laboratory test positivity (anticardiolipin antibodies, anti-β2 glycoprotein-I or lupus anticoagulant IgG/M) required with clinical findings [1,2]. In our patient, anti-β2 glycoprotein-I antibodies were positive with recurrent fetal death. Higher prevalence for anticardiolipin antibodies have been described in HBV (24%), HCV (20%), and in HIV (49.8%) [3]. However, the prevalence of β2 glycoprotein-I antibodies is lower than anticardiolipin antibodies in viral infections (HBV: 3.3%, HCV: 1.7%, HIV: 5.6%, respectively) [3]. The receptor for HBV called apolipoprotein H and viral phospholipids would provide the immunogenic stimulus for antiphospholipid synthesis [4]. The mechanisms of APS by infection are still unclear. Both APL and factor V Leiden mutation as thrombophilic disorders increase hypercoagulabity and thrombotic events. The association of factor V Leiden mutation with APS has not been proven, although all of us have seen patients having both, factor V Leiden mutation and anti-phospholipid antibodies. It’s believed that this coexistence occur by chance. The combination of APL antibodies and Factor V Leiden is a very high risk condition for the pregnancy. These coexistences with the clinical presentations such as thalamo-mesencephalic infarction, Libman-Sacks endocarditis with stroke, myocardial infarction, and unexplained recurrent fetal and embryo loss were reported rarely in literature [5-8].

The clinicians should be careful for antiphospholipid syndrome and factor V Leiden mutation in patients with chronic viral hepatitis. And also, should keep in mind about the differential diagnosis of numerous recurrent miscarriages [9].