Session Type: ACR Concurrent Abstract Session
Session Time: 4:30PM-6:00PM
Background/Purpose: Early preeclampsia is a serious pregnancy complication characterized by abnormal placentation and diffuse maternal endothelial cell dysfunction, and requires emergent delivery which may be very premature. SLE has been shown to increase the risk of preeclampsia, but little is known about the risks of early onset preeclampsia – a pregnancy morbidity associated with stroke, placental abruptions, and perinatal death.
Methods: Using national population-based Swedish registers we identified women with SLE (≥2 visits with corresponding ICD codes) and without SLE who gave birth to singleton infants 2001-2012 in the Swedish Medical Birth Register. Comparators without SLE were drawn from the general population. Preeclampsia was defined using date of first corresponding diagnosis during pregnancy to define early onset (<34 weeks). The association between early preeclampsia and maternal SLE was estimated by multivariable-adjusted modified Poisson models for first, subsequent, and all births. BMI, age, smoking, and pregestational hypertension and diabetes were included as potential confounders. We used ICD-10- coded visit and heparin dispensing during pregnancy from the Prescribed Drug Register (2006-2012) as a proxy for antiphospholipid syndrome (APS).Preeclampsia history was adjusted for in analyses of subsequent and all births. We investigated effect modification by pregestational hypertension, examined residual confounding by APS and misclassification of preeclampsia due to lupus nephritis.
Results: There were 742 births to women with SLE (343 first births) and 10484 births to women from the general population (4443 first births). Compared to the general population, SLE was associated with a significantly increased risk of early preeclampsia for all, first, and subsequent births [RR=7.3, (95% CI=4.5, 11.9), mvar-adj, all births]. Adjustment for APS proxy attenuated the association (RR=3.7, 95% CI=1.7, 7.9), but SLE remained significantly associated with early preeclampsia. Findings were similar among women without pregestational hypertension, a strong risk factor for early preeclampsia, as well as in the absence of recent nephrology care. RRs for early preeclampsia were smaller, but significant, for subsequent births compared to first and all births [RR=2.8, (95% CI=1.2, 6.4) subsequent].
Conclusion: Women with SLE are at increased risk of preeclampsia before 34 weeks gestation, and importantly, this increased risk may be independent of pregestational hypertension, APS, BMI, or smoking. Traditional risk factors alone may not explain the increased risk of early preeclampsia among women with SLE for first, subsequent, or any birth. Women with SLE during pregnancy should continue to be monitored carefully for early preeclampsia and future research is needed to identify what non-traditional preeclampsia factors might be causing this serious outcome.
To cite this abstract in AMA style:Simard JF, Arkema EV, Nguyen C, Svenungsson E, Wikstrom AK, Palmsten K, Salmon JE. Early Preeclampsia Risk in Lupus Pregnancy: A Swedish Population-Based Register Investigation [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/early-preeclampsia-risk-in-lupus-pregnancy-a-swedish-population-based-register-investigation/. Accessed October 17, 2021.
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