Antiphospholipid Antibody Syndrome

Author Information

Chakre Shila*, Pardeshi Sachin*, Mayadeo NM**, Shah S.
(* Assistant Professor, ** Professor, *** Third Year Resident. Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


Antiphospholipid  antibody syndrome in obstetric is clinically defined by  repeated unexplained abortion before 10th weeks, unexplained fetal loss at or after 10th week, premature birth before 34 weeks due to preeclampsia.[1] In Antiphospholipid antibody syndrome placental mediated complications such as mild to severe pregnancy induced hypertension, intrauterine growth restriction, intrauterine fetal demise, missed abortion, antepartum hemorrhage and threatened abortion are high and hence the rate of cesarean section is also high.[2] Antiphospholipid  antibody syndrome  management is based on combined medical-obstetric high risk management and treatment with aspirin and injection heparin but still there are refractory cases to treatment in which there are obstetric complications. We present a case report of different obstetric outcomes in a same patient with two separate pregnancy, one year apart in a treated Antiphospholipid antibody syndrome.


Antiphospholipid antibody syndrome is defined by the presence of pregnancy morbidity and thromboembolic complications in presence of persistently increased titers of Antiphospholipid antibodies.[3] There are subtypes of antibodies in Antiphospholipid antibody syndrome. These are antibody against lupus anticoagulant, anticardiolipin antibody and anti β2 glycoprotein-1 antibodies. In Antiphospholipid antibody syndrome, pathogenesis for thrombosis is binding of Antiphospholipid antibodies to endothelial cells which stimulate an up regulation of adhesion molecule increasing leucocyte adhesions and thus thrombosis.[2] Anticardiolipin antibodies interfere with anticoagulation pathway. Lupus anticoagulant lead to thromboembolic event rather than clinical bleeding.[3]

Case Report

A 28 years old gravida 7, abortion 5, IUFD1, presented to antenatal OPD, with one and half month of amenorrhea with urine pregnancy test positive. Patient previous records were checked. She had consecutive five missed abortion before 10 weeks of gestation. She was evaluated for recurrent pregnancy loss. When she was pregnant for 6th time, 2 years back her thrombophilia profile showed lupus anticoagulant positive. During that pregnancy, she was started on low dose aspirin 75 mg OD and low molecular weight heparin 40 mg subcutaneous daily in prophylactic doses as there was no history of thrombotic events. Patient was monitored throughout pregnancy for Antiphospholipid antibody syndrome related complications. There was no complication noticed. At around 35 weeks of gestation there was sudden intrauterine fetal demise despite of being on treatment. The cause of intrauterine fetal demise was not explained. Patient delivered vaginally, 2.6 kg, female baby. Placenta was sent for histopathology which revealed no obvious placental thrombosis. Patient was advised to repeat lupus anticoagulant after 6 weeks which again was positive. Patient conceived seventh time after one year. Again she was started on low dose aspirin 75mg OD and low molecular weight injection heparin 40 mg subcutaneous 24 hourly from 8 weeks of gestation after cardiac activity was documented on ultrasonography. She was monitored again for Antiphospholipid antibody syndrome complications by daily fetal kick count, non stress test and obstetric Doppler. Obstetric Doppler at 32 weeks of gestation was suggestive of mild uteroplacental but no fetoplacental insufficiency. Patient was followed up with Doppler after four weeks which was showing the same changes.
Patient delivered by cesarean section in view of precious pregnancy with baby weight of 2.7 kg, male child. Patient was discharged and was advised to continue low molecular weight heparin for 6 weeks at dose of 40 mg subcutaneous 24 hourly. The postpartum period was uneventful.


Antiphospholipid antibodies causes activation of endothelial cells, monocytes and platelets causing overproduction of tissue factor, thromboxane A2 and complement activation.[2] All these lead to change in hemostatic system during normal pregnancy which results in hypercoagulable state. This leads to thrombosis and then to pregnancy complications associated with Antiphospholipid antibody syndrome. Antiphospholipid antibody trigger inflammatory response leading to trophoblast damage and so abnormal placentation.[4] Abnormal placentation which leads to  obstetric complication such as recurrent miscarriage, preterm delivery, oligohydramnios, prematurity, intrauterine growth restriction, fetal distress, fetal or neonatal thrombosis, preeclampsia, eclampsia, HELLP syndrome, arterial or venous thrombosis and placental insufficiency.[2] Obstetric Antiphospholipid antibody syndrome without thrombosis is currently managed by giving low dose aspirin and heparin.[5] Unfractionated heparin and low molecular heparin act by binding to antithrombin, to catalyze the molecule binding and altering the activity of serine protease procoagulants. There are more adverse outcomes with antibody against lupus anticoagulant.[6] Anticardiolipin antibody is associated with clinical bleeding. In our patient lupus anticoagulant was positive which might have lead to sudden intrauterine death even on treatment with low molecular heparin. There is continued occurrence of late pregnancy complications like preeclampsia, intrauterine growth restriction, prematurity and intrauterine fetal  demise despite treatment which suggest the need for strict monitoring of the disease and treatment-related complications throughout pregnancy.[7] In this pregnancy there was only uteroplacental insufficiency on low molecular weight heparin.
Lastly to conclude that severity of obstetric complications and thrombosis can be reduced by giving thromboprophylaxis with heparin, a close watch should be kept in the late pregnancy to prevent adverse outcomes though on heparin treatment. There might be a need of more dose effective regimen of heparin treatment.


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Chakre S, Pardeshi S, Mayadeo NM, Shah S.  Antiphospholipid Antibody Syndrome. JPGO 2014 Volume 1 Number 9 Available from: