Antiphospholipid Syndrome in Pregnancy
Section snippets
Pathogenesis
Several mechanisms have been proposed to explain the occurrence of recurrent thrombosis and pregnancy losses in patients with APS, including interference with the prostacyclin/thromboxane balance at the endothelial level, inhibition of annexin V (a natural placental anticoagulant), inhibition of antithrombin, protein C and protein S, and activation of platelets [1]. The pathologic findings in placentas of women with APS reinforce the role of thrombosis leading to placental insufficiency as the
Pharmacologic management of pregnancy losses in antiphospholipid syndrome
Historically, prednisone, aspirin, heparin, and immunoglobulins have been used in the treatment of pregnancy losses in women with APS. In the above-mentioned recent review by Petri and Qazi [7], the final recommendation for women with APS and one fetal loss or multiple first trimester losses is aspirin plus heparin, either unfractionated heparin (UFH) or low-molecular weight heparin (LMWH). Also in 2006, a Cochrane collaboration review on the therapy of miscarriage in women with aPL has been
Thromboprophylaxis in antiphospholipid syndrome during pregnancy
This group has been excluded systematically from clinical trials. However, good clinical sense indicates that all women with APS and previous thrombosis should maintain antithrombotic treatment throughout their entire pregnancy and during the postpartum period [36]. Therefore, combined treatment with low-dose aspirin and full antithrombotic doses of LMWH should be given to these patients. Moreover, postpartum LMWH is also mandatory in all women with purely obstetric APS and is also recommended
Hypertensive disorders
Hypertension is a cause of major complications in both the mother and the baby [42]. This is defined as a systolic or diastolic blood pressure of 140/90 mm Hg or higher, which can be present before or develop as a complication of pregnancy, usually after 20 weeks' gestation [42]. Preeclampsia is defined as the presence of pregnancy-induced hypertension plus proteinuria of at least 300 mg/d [42].
Positivity for aPL has been shown to be one of the most significant risk factors for preeclampsia in
Pulmonary hypertension
Connective tissue diseases, particularly systemic sclerosis, mixed connective tissue disease, SLE, and APS [51], can be a direct cause of pulmonary hypertension (PHT)—class 1.3.1 of the World Health Organization classification for PHT. In addition, chronic thromboembolic disease—classes 4.1 and 4.2—can be the consequence of hypercoagulability states, including APS [51].
The prognosis of untreated PHT is poor, with median survival rate less than 3 years after diagnosis [51]. Fortunately, several
Pregnancy, heparin, and osteoporosis
The complex relationship between pregnancy, osteoporosis, and heparin treatment has been recently reviewed [54]. Calcium demands rise during pregnancy. This may result in an increased turnover from bone, especially during the first and second trimesters. However, the process usually reverses during the third trimester, resulting in only minor reductions of bone mineral density (BMD) after normal pregnancy. Lactation may result in a delayed recovery of BMD. Although the risk for symptomatic
General care of pregnancy in women with antiphospholipid syndrome
Ideally, preconceptual counseling should be performed to explain the risks of pregnancy within the specific context of each patient. In general, women with APS should know that, under correct management, the likelihood of a live birth is around 75% to 80%. However, they must also be informed that there is an increased risk of serious complications (eg, hypertension/preeclampsia, prematurity, or thrombosis) that can take place during pregnancy and the puerperium. A complete aPL profile,
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