June 15, 2007 Disease activity in patients with rheumatoid arthritis (RA) is significantly reduced during pregnancy, according to new data. In the study, RA improved significantly from the first trimester to the third trimester of the participants' pregnancy and this effect extended into the postpartum stage.
This is the first prospective study to confirm the relationship between RA and pregnancy, tracking 124 female RA patients throughout their pregnancy and at 6, 12 and 26 weeks postpartum. The RA improvement was seen in 40% of patients. Furthermore, 64% of patients remained relatively stable or improved postpartum. Only a third of patients (36%) experienced flares (periods of worsened symptoms), 5% severely.
Dr Yaël de Man of Erasmus MC University Medical Center, Rotterdam, The Netherlands, who performed this research, said: "Whilst previous literature has suggested an improvement of RA in pregnancy, this is the first prospective study to put a figure to this. The percentage of patients experiencing flares was much lower than previous studies, which we attribute to adequately-used DMARDs and biologicals to suppress disease activity postpartum. It is also interesting to note the existence of a complex interaction between female hormones during pregnancy and the epidemiology of RA, which may contribute to the development of new prevention and treatment approaches."
In the study, patients were assessed according to medication use, the Disease Activity Score DAS28 and the level of inflammation marker C-reactive protein (CRP). Disease activity was calculated with DAS28-CRP with 3 variables (DAS28-CRP-3). The change between the DAS28 at first and third trimester was used to categorise patients according to the EULAR response criteria into good, moderate and non-responders. The change between the DAS28 at 6 weeks and 12 or 26 weeks postpartum was used to determine if a severe or moderate flare was present.
The DAS28 decreased significantly during pregnancy from 3.7 (SD 1.1) in the first trimester to 3.4 (SD 1.1) in the third trimester (n=124, p=0.003). The mean DAS28 was 3.4 (SD 1.1) at six weeks postpartum. During pregnancy, 11% (49/124) were good responders, 40% were at least moderate responders (49/124) and 60% (75/124) were non-responders. The relapse of disease activity was present at twelve weeks postpartum with a mean DAS28 of 3.7 (SD 1.2) and was slightly lower at 26 weeks postpartum with a mean of 3.6 (SD 1.2). Postpartum, 5% (5/110) had a severe flare, 36% (40/110) had at least a moderate flare and 64% (70/110) remained relatively stable or improved.
During all trimesters, the percentages of DMARDs used were stable (sulfasalazine 32%, prednisone 35%, hydroxychloroquine 1% and gold i.m 1%), whilst DMARD use rose considerably postpartum (57% at the third trimester versus 82% post partum), mainly due to methotrexate (44%) and biologicals (8%).
This research was presented at EULAR 2007, the Annual European Congress of Rheumatology in Barcelona, Spain.
This study was supported by the Dutch Arthritis Association.
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