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associated with small joint disease, psoriasis, or ulcerative colitis (27). Postpartum flares are also common, especially during the first 3 months after delivery. The postpartum flare is independent of level of disease activity during pregnancy, period of lactation, or the return of menses. Disease activity during the year following delivery seems to return to the same level as before conception (24). There appears to be no increase in frequency of miscarriage, premature labour, or delivery complications in this population of women (25). Of note, women with AS experience a similar increase in Tregs during pregnancy as women with RA. However, Tregs in pregnant woman with AS secrete less IL-10 and have lower suppression of INF-γ and TNFα secretion by effector T cells (28). This may account for the difference in disease activity experienced during pregnancy among women with AS and RA. SLE Although the majority of women with SLE will have no or mild disease activity during pregnancy, a small but significant proportion will have more severe disease. The risk for severe disease during pregnancy is increased in women with active SLE in the 6 months prior to conception, in those with repeated flares in the years prior to conception, and in those who discontinue needed medications due to pregnancy (29, 30). For women with quiescent SLE in the 6 months prior to conception, less than 10% will have moderate to severe SLE during pregnancy (29). In my clinical experience, I find many women with relatively quiet SLE prior to pregnancy comment on how good they feel during pregnancy; it seems that, for some women, pregnancy may in fact ameliorate the arthritis, rashes, and fatigue of mild SLE activity. Almost 60% of women with increased SLE activity prior to conception continue to have SLE activity in pregnancy (29). Whether SLE is active or not, women with SLE are at increased risk for medical complications in pregnancy. Pregnancy itself is a hypercoagulable state, increasing the risk of thrombosis two- to threefold (31). For a non-pregnant woman with SLE without APS, the risk of thrombosis is estimated at 3/100 patient years (32). Therefore, 5–10 of every 100 pregnant women with SLE can be expected to develop a thrombosis during pregnancy; these can include deep vein thromboses, pulmonary embolisms, strokes, or heart attacks. The risk for thrombosis extends for 6 weeks following delivery. The maternal mortality rate for women with SLE is an estimated 20-fold higher than for average women (33). The rate of maternal mortality with SLE is 325/100 000 pregnancies. When compared to the annual death rate for women with SLE (estimated at 1000/100 000 patient years), it appears that pregnancy probably does not increase the risk of death for a women with SLE (34). There are particular women, however, who may be at higher risk for death. These include women with prior arterial thrombosis, a weakened heart from myocarditis, prior myocardial infarction or valve disease, uncontrolled hypertension, pulmonary hypertension, or a prior severe SLE flare during pregnancy. Ideally, prior to pregnancy a woman with SLE should have low lupus activity for at least 6 months and have medications adjusted. The benefits of maintaining low SLE activity in pregnancy is twofold: it improves the health of the mother and increases the chances of the delivery of a healthy baby. Increased SLE activity is a primary cause of preterm birth and pregnancy loss in this population. The risk for pregnancy loss is increased three- to fivefold if SLE is active or platelet counts are low in the first trimester (44% pregnancy loss with active SLE) (35). Women with active SLE are at twice the risk for a
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