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P79 Predictors of adverse neonatal outcome during the pregnancy of women with antiphospholipid syndrome in the French GR2 prospective study
  1. Anne Murarasu1,
  2. Gaëlle Guettrot-Imbert1,
  3. Véronique Le Guern1,
  4. Francois Maurier2,
  5. Patrick Jego3,
  6. Estibaliz Lazaro4,
  7. Alban Deroux5,
  8. Maëlle Le Besnerais6,
  9. Odile Souchaud-Debouverie7,
  10. Pauline Orquevaux8,
  11. Catherine Deneux-Tharaux9,
  12. Nathalie Costedoat-Chalumeau1,
  13. the GR2 study group
  1. 1Internal Medicine Dept., Hôpital Cochin AP-HP, Paris
  2. 2Internal Medicine Dept., Hôpital Belle-Isle, Metz
  3. 3Internal Medicine Dept., CHU de Rennes, Rennes
  4. 4Internal Medicine Dept., CHU de Bordeaux, Bordeaux
  5. 5Internal Medicine Dept., CHU de Grenoble, La Tronche
  6. 6Internal Medicine Dept., CHU de Rouen, Rouen
  7. 7Internal Medicine Dept., CHU de la Milétrie, Poitiers
  8. 8Internal Medicine Dept., CHU Robert Debré, Reims
  9. 9EPOPé Team, University of Paris, Epidemiology and Statistics Research Center/CRESS, INSERM, INRA F-75004, Paris, France


Introduction Data about the predictors of adverse neonatal outcome in pregnant women with antiphospholipid syndrome (APS) are sparse. The main study on this subject is the prospective American study PROMISSE on 144 carriers of antiphospholipid antibodies.1 We report the first results of the French study, GR2.

Methods Inclusion criteria were: (1) an ongoing pregnancy at 12 weeks of gestation (WG), (2) conceived before May 2018, (3) of a woman with APS.2 Exclusion criteria were proteinuria (ratio >1 g/g), serum creatinine >100 µmol/L, and multifetal pregnancy.

The composite primary outcome included an intrauterine fetal death (IUFD), a neonatal death, placental insufficiency (fetal growth restriction, preeclampsia, HELLP syndrome, and/or placental abruption) leading to a delivery ≤34 WG, and/or a small for gestational age (SGA) ≤3rd percentile.

Results We analysed 119 pregnancies in 119 patients: 53% thrombotic and 47% obstetric only APS; 60% had lupus anticoagulant (LA) and 26% associated SLE. Treatment included aspirin (99%), heparin (98%, in the therapeutic range for 50%), and hydroxychloroquine (62%).

The primary outcome was observed in 14% of pregnancies: 3% IUFD, 8% delivery ≤34WG due to placental insufficiency and/or 5% of SGA (and no neonatal death). It was observed in 20% of the pregnancies with LA compared with 7% for women negative for LA (P=0.096). This outcome did not differ according to anticardiolipin or antiβ2GP1 antibody status, or prior thrombosis (14%, versus 14% for women with only obstetric APS). There was a trend toward more adverse neonatal outcomes in case of prior arterial thrombosis (29% versus 12%, P=0.07). The rate of adverse neonatal outcomes did not differ among the women with or without associated SLE (29% versus 26%, P=0.77).

In multivariate analysis, independent features associated with pregnancy failure were: in a serological model, LA positive status (ORa=8.5, 95%CI[1.0–71.5]) and in a serological and clinical model, ‘non-white’ skin colour (ORa=6.1, 95%CI[1.1–34.7]).

Conclusion The rate of adverse neonatal outcomes tended to be lower than in the PROMISSE study (14% versus 19%), although the women included here were theoretically more severe (definite APS). One potential explanation might be that our patients were all treated. In keeping with the PROMISSE study, LA and skin colour were the main predictors of neonatal outcome.

Acknowledgement Fondation pour la Recherche Médicale (M2R201806006403)


  1. Lockshin MD, et al. Arthritis Rheum. 2012; 64;2311–8.

  2. Miyakis S, et al. J Thromb Haemost. 2006; 4 ;295–306.

  3. Andreoli L, et al. Ann Rheum Dis. 2017; 76; 476–85.

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