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pregnancy loss will occur in 45–90% of pregnancies with APS (55). Treatment, however, reduces the chance of pregnancy loss to less than 30% (56). There are several proposed mechanisms for pregnancy loss from APS, including aPL interaction with platelet membrane phospholipids, inhibition of annexin-V, a cell surface protein that inhibits tissue factor, direct inhibition of protein S, and, most recently discovered, altered regulation of the complement cascade (54, 57). Recent insights into the pathophysiology of the disease highlight that not only thrombosis but also inflammation via the complement cascade plays an important role in poor pregnancy outcomes. Although it was previously thought that heparin was particularly helpful because of its anticoagulant properties, recent studies show that it also inhibits complement formation and deposition in decidual tissues in vitro (58). There have been several trials evaluating different therapeutic regimens for women with APS. The most well-designed studies are in women with obstetric APS, defined as women with aPL and recurrent early pregnancy loss or at least one foetal loss, in the absence of SLE or previous thrombosis (see Table 5). The current recommendations, based on the best existing data and expert opinion, are: (i) no treatment or treatment with LDA in patients with aPL but no history of thrombosis or pregnancy complication; (ii) prophylactic dose of low molecular weight heparin (LMWH) with LDA in women with aPL and history of pregnancy complication; (iii) full-dose LMWH and LDA in women with aPL and history of vascular thrombosis (62). Given the increased risk of thrombosis in the postpartum period, treatment with anticoagulation for up to 6 weeks postpartum is also recommended for patients with APS (63). Although unfractionated heparin costs less than LMWH and has been used for anticoagulation in APS patients, LMWH is the recommended anticoagulant because of the decreased risk for osteoporosis, heparin-induced thrombocytopaenia, and bruising (64). Currently, there are no data to suggest that long-term anticoagulation following pregnancy with warfarin is indicated in APS patients with only obstetric complications, although there are some retrospective data that suggest aspirin provides protection against thrombosis (65). Medications in pregnancy The US Federal Drug Administration (FDA) has designated medications according to a pregnancy risk score. The assigned category can be misleading and is not always a good guide for discontinuing medications. The FDA is planning to eliminate the categories in favour of more data disclosure about pregnancy outcomes in the future. In the meantime, we have included the FDA pregnancy categories for general reference. According to the current FDA system, category A is assigned to drugs with extensive human safety data demonstrating no foetal risk. Category B includes drugs with reassuring animal studies and little or no human data OR animal studies demonstrating risk but good human data showing no foetal risk. Category C includes drugs in which animal studies show risk and no human data are available to refute this concern. Category D includes drugs with some evidence of adverse reactions in the foetus, but in which the potential benefit of the drug to the mother may outweigh these foetal risks. Category X includes drugs in which there is documented foetal harm and the benefits to the mother do not outweigh the foetal risks Treatment algorithms for SLE in pregnancy and inflammatory arthritis in pregnancy are presented in Tables 6 and 7, respectively. Corticosteroids are relatively safe in pregnancy and are the mainstay of rheumatic disease
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