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women without RA (12). Pre-eclampsia and caesarean section rates have been shown to be higher in mothers with RA (7, 9). Having increased RA activity and using disease-modifying anti-rheumatic drugs (DMARDs) and steroid medications increases the risks for these complications (13). Both clinical experience and the reports of over 500 patients in clinical studies demonstrate that RA activity decreases for many women. Studies show that an estimated 75% of women experienced improvement in their disease during pregnancy (range 54–86%) and 90% of women reported a relapse in disease within 3 months of delivery (14, 15). Two prospective studies have examined disease activity during pregnancy in the current era of expanded treatment options (16, 17). In the first, Barrett et al recruited 140 pregnant women [95 satisfied the American College of Rheumatology (ACR) criteria for RA and 45 women had definite synovitis observed by a physician] and followed them prospectively from the last trimester until 6 months postpartum (16). Retrospectively, 65% of the women reported that they had improvement in disease activity during pregnancy compared to pre-pregnancy. By the third trimester, 16% of women achieved remission, defined as using no anti-rheumatic drugs and having no swollen or painful joints. Ninety women (66%) reported worsening in joint swelling by 6 months postpartum, with the majority of deterioration occurring during the first month. In the second study, de Man et al prospectively followed 84 women with RA according to the ACR criteria and measured the Disease Activity Score in 28 joints (DAS28) and medication use pre-pregnancy (if possible), during each trimester, and at weeks 6, 12, and 26 postpartum (17). The percentage of women with moderate RA during pregnancy decreased from 70% before pregnancy to approximately 40% during pregnancy. During the third trimester, 27% of women were in complete remission (DAS28 < 2.6) and had a significant decrease in medication use. The largest decrease in DAS28 was seen among women with the most active disease. Postpartum, 40% of women had increased disease activity but only 4% had a severe flare. The majority of women restarted DMARD therapy in the first 6 weeks after delivery. The data and patient reports support a decrease in RA activity with pregnancy, but how does pregnancy suppress disease activity? The answer remains a mystery; however, the key may be regulatory T cells (Tregs). RA activity is partially driven by the T-cell production of tumour necrosis factor (TNF)α and interferon (IFN)-γ left unchecked by poorly functioning Tregs (18, 19). During pregnancy and particularly in the second trimester, Tregs increase in both number and suppressive activity (20, 21). In women with RA, this rise in Tregs leads to an increase in the anti-inflammatory interleukin (IL)-10 and a decline in TNFα and IFN-γ production, coinciding with the reduction in clinical RA symptoms (20). Maternal tolerance seems to be stronger when the mother and foetus are more genetically different. A study published in 1993 showed that 75% of women with RA improved during pregnancy when the mother and foetus were human leucocyte antigen (HLA) mismatched but only 25% improved when the foetus had a very similar HLA pattern to the mother (22). Ankylosing spondylitis (AS) Compared to pregnant women with RA, women with AS generally experience unchanged or increased disease activity including increased morning stiffness, spinal tenderness, pain at night, and need for non-steroidal medications during pregnancy (23–27). Of the 20% of woman in one study who had a marked improvement in their symptoms, all had AS
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