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Background: Active Systemic Lupus Erythematosus (SLE) during pregnancy is associated with poor obstetrical outcome but it is still not clear if remission, lupus low disease activity state (LLDAS) is the best target to achieve at conception. Besides, the effect of damage on pregnancy outcome has not been studied.
Objectives: Our aim was to determine the 1 st trimester risk factors for adverse pregnancy outcome (APO).
Methods: Inclusion criteria were: 1) women≥18 years enrolled in the prospective GR2 study; 2) with SLE (SLICC criteria); 3) and an ongoing singleton pregnancy at 12 weeks (only 1 pregnancy per patient). We used the following definitions: DORIS 1 , DORIA 2 , clinical SLEDAI-2K=0, LLDAS 3 (for SLE activity), SFI 4 (for flares), and SLICC-damage index 5 (for damage). APO included: foetal death, neonatal death, placental insufficiency with premature delivery<37 weeks, and small for gestational age (SGA:≤3 rd percentile).
Results: 238 patients were included. 234 (98.3%) women were on hydroxychloroquine (HCQ) and 206 (86.5%) had a clinical SLEDAI-2K=0. Regarding pregnancy outcome, 230 (96.6%) patients had a live birth (mean term 37.7 weeks). Thirty-four (14.3%) patients developed at least 1 APO: placental insufficiency (n=22), foetal death (n=7), neonatal death (n=1), and SGA (n=5). Two different regression logistic models were assessed, one for DORIA and one for LLDAS. We found that only SLICC-Damage index and lupus anticoagulant (LAC) were associated with APO (p=0.02, OR 1.8, 95% CI: 1.1-2.9; p=0.001, OR 4.2, 95% CI: 1.8-9.7 respectively for DORIA model; p=0.03, OR 1.7, 95% CI:1.1-2.8; p=0.002, OR 3.7, 95% CI: 1.6-8.7 respectively for LLDAS model).
Conclusion: We confirmed that LAC predicts APO. We found for the first time that chronic damage at 1 st trimester also predicted APO. No effect of remission/LLDAS was observed in this cohort of patients on HCQ with a stable and well-controlled SLE.
REFERENCES:
[1]van Vollenhoven R, et al. ARD 2017.
[2]Zen M, et al. ARD. 2015.
[3]Franklyn, K. et al. ARD 2016.
[4]Petri M, et al. NEJM 2005.
[5]Gladman DD, et al. Arthritis Rheum, 1997.
| Univariate analysis for APO | ||||
| Maternal features | Total (N=238 ) | APO (N=34 ) | Non-APO (N=204 ) | P value |
| Age, mean (SD) | 31.6(4.5) | 30.7(4.8) | 31.7(4.4) | 0.22 |
| Secondary APS | 34(14.3) | 10(29.4) | 24(11.8) | 0.01 |
| Previous renal phenotype | 67(28.2) | 13(38.2) | 54(26.5) | 0.16 |
| At least 1 flare during pregnancy | 37(15.5) | 6(17.4) | 31(15.2) | 0.80 |
| Positive anti-DNA (N=222) | 104(46.8) | 21(67.7) | 83(43.5) | 0.01 |
| Hypocomplementemia (N=216) | 57(26.4) | 13(40.6) | 44(23.9) | 0.05 |
| LAC (N=232) | 41(17.7) | 15(44.1) | 26(13.1) | <0.001 |
| Triple aPL (N=232) | 17(7.3) | 5(14.7) | 12(6.1) | 0.08 |
| 24h-proteinuria>0.5g/day | 9(3.8) | 3(8.8) | 6(2.9) | 0.12 |
| Activity/Damage | ||||
| SLEDAI-2K, median (IQR) (N=212) | 2(0-3) | 2(2-4) | 2(0-2) | 0.01 |
| SLICC-DI, median (IQR) (N=236) | 0(0-0) | 0(0-0) | 0(0-0) | 0.007 |
| PGA, median (IQR)(N=235) | 0.1(0-0.2) | 0.1(0-0.41) | 0.1(0-0.2) | 0.06 |
| DORIA remission* | 154(64.7) | 17(50.0) | 137(67.2) | 0.05 |
| DORIS remission** | 147(61.8) | 17(50.0) | 130(63.4) | 0.13 |
| LLDAS (N=219) | 157(71.7) | 19(57.6) | 138(74.2) | 0.05 |
| Clinical SLEDAI-2K=0 | 206(86.5) | 28(82.4) | 178(87.3) | 0.44 |
| Treatment | ||||
| Prednisone (PDN) | 119(50.0) | 23(67.7) | 96(47.1) | 0.03 |
| PDN (mg/day) median (IQR) | 7(5-10) | 0(0-6) | 5(0-10) | 0.007 |
| Immunosuppressants | 57(24.0) | 13(38.2) | 44(21.6) | 0.04 |
| Hydroxychloroquine | 234(98.3) | 34(100.0) | 200(98.0) | 1.00 |
| Low dose aspirin | 165(69.3) | 29(85.3) | 136(66.7) | 0.03 |
| Low molecular weight heparin | 61(25.6) | 15(44.1) | 46(22.6) | 0.01 |
Legend: APS: antiphospholipid syndrome; aPL: antiphospholipid; PGA: Physician global assessment. *: DORIA definition of remission = clinical SLEDAI=0 and prednisone ≤5 mg/day; **: DORIS definition of remission = clinical SLEDAI=0, prednisone ≤5 mg/day, and PGA<0.5.
Disclosure of Interests: None declared.