Pregnancy and Rheumatic Diseases

M. Gayed; C. Gordon

Disclosures

Rheumatology. 2007;46(11):1634-1640. 

In This Article

Rheumatoid Arthritis

In contrast to SLE, RA has been known to improve during pregnancy for many years. Several studies have shown significant improvement in 75–95% of pregnant women with RA. The improvement commences in the first trimester and improves maximally in the last semester.[34,35] The discrepancy between RA and SLE in pregnancy is thought to be due to the differences in autoimmune response. Part of the mechanism for the induction of remission during pregnancy is likely to be mediated by the effect of endogenous female hormones on cytokines influencing disease activity.[36] SLE is characterized by a predominantly humoral response (Th2 type) response whereas RA is thought to be provoked by a more cellular response (Th1 type).[37] It is known that in pregnancy there is a raised Th2 type response, in comparison with the non-pregnant state, leading to over expression of Th2 cytokines, such as IL-4 and IL-10. IL-10 is believed to increase autoantibody response in SLE but to be immunosuppressive in RA.[38] There is recent evidence that not only is there a Th2 type of response in pregnancy, but in fact complex immunomodulation at the maternal–fetal interface occurs. This has systemic effects in the maternal circulation, dependent on the stage of pregnancy.[35,39] Another contributing cause to the remission of RA in pregnancy may be the depression of polymorph nuclear neutrophil function in the synovial fluid by alpha fetoprotein, which reduces the degree of synovial fluid inflammation.[40]

During the postpartum period it is common for RA to flare. In addition, new-onset RA has been reported to be 3–5 times more frequent at this time.[41,42] The precise aetiology for this phenomenon is unknown. It has been suggested that it may due to the increase of prolactin levels associated with breast-feeding as this hormone is pro-inflammatory, but there is conflicting views on this and the loss of pregnancy related immunomodulatory hormones may be sufficient to explain the observation. It has also been demonstrated that the long-term outcome of RA in terms of joint damage and disability, is minimally affected by pregnancy and oral contraceptive use, which is important when counselling women regarding pregnancy and contraception.[36] It has also been found that there is an increased risk of RA developing in women who have had adverse pregnancy outcomes, miscarriage, termination or stillbirth. These complications may increase the risk of RA, but conversely there is no reported increase of adverse pregnancy outcomes in RA.[34] However, a link has been found between miscarriage and the severity of RA. Women with at least one miscarriage have been found to have had an increased rate of joint damage.[43]

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