Pathogenesis of pregnancy complications in systemic lupus erythematosus

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Purpose of review

In spite of the advances made in the management of pregnancies in women with systemic lupus erythematosus (SLE), maternal complications and adverse fetal outcomes still exceed the rate of pregnancy complications in the general population. An intriguing question relates to the observation that pregnancy loss, intrauterine growth restriction (IUGR), preterm birth, and preeclampsia remain major complications in SLE pregnancies, not substantially altered by improved therapy and monitoring.

Recent findings

From the review of the recent literature on the pathogenesis of pregnancy loss, IUGR, preeclampsia, and prematurity, it appears that clinical or subclinical inflammation, presence of autoantibodies, hormonal dysfunction, and immune alterations of lupus contribute to pregnancy complications. Impairment of early placenta development leads to poor vascularization, resulting in placental ischemia and subsequent endothelial damage. Depending on the extent of the pathological process, pregnancy loss, IUGR, and preeclampsia can develop.


Early recognition of pregnancy complications is desirable in order to prevent their development or to prompt intervention that improves the outcomes. Several biomarkers have been investigated for their ability to predict complications at an early stage of pregnancy. However, up to date only lupus anticoagulant has emerged as a consistent predictor for adverse pregnancy outcomes.

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