Autoantibodies against EPCR are found in antiphospholipid syndrome and are a risk factor for fetal death

Verónica Hurtado, Ramón Montes, Jean Christophe Gris, María L. Bertolaccini, Álvaro Alonso, Miguel A. Martínez-González, Munther A. Khamashta, Kenji Fukudome, David A. Lane, José Hermida

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


The antiphospholipid syndrome (APS) is associated with thrombosis and fetal death but the pathologic mechanisms are poorly understood. Since endothellal protein C receptor (EPCR) plays a role in the anticoagulant system and in placental development, we hypothesized that anti-EPCR autoantibodies may be involved in clinical manifestations of APS and in fetal loss. The levels of immunoglobulin M (IgM) and IgG anti-EPCR autoantibodies were analyzed by enzyme-linked immunosorbent assay (ELISA) in 43 patients with APS and 43 controls. Anti-EPCR levels were higher in APS patients than in controls. Interestingly, one of the IgM anti-EPCR autoantibodies inhibited the generation of activated protein C on endothelium. Since markedly high anti-EPCR levels were found in women with fetal death, 87 patients with a first episode of unexplained fetal death were subsequently analyzed and their anti-EPCR levels were compared with 87 matched controls. We found that anti-EPCR autoantibodies constitute an independent risk factor for a first fetal death episode: the adjusted odds ratios (ORs) for anti-EPCR autoantibodies above the 95th percentile were 23.0 (95% confidence interval [CI], 2.0-266.3) for IgM and 6.8 (95% CI, 1.2-38.4) for IgG. Anti-EPCR autoantibodies can be detected in APS patients and are independent risk factors for fetal death.

Original languageEnglish (US)
Pages (from-to)1369-1374
Number of pages6
Issue number5
StatePublished - Sep 1 2004
Externally publishedYes


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