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Pregnancy Outcome in Juvenile Systemic Lupus Erythematosus: A Brazilian Multicenter Cohort Study CLOVIS A.A. SILVA, MARIA O. HILARIO, MARILIA V. FEBRONIO, SHEILA K. OLIVEIRA, ROZANA G. ALMEIDA, ADRIANA R. FONSECA, EDSON M. YAMASHITA, MARCOS V. RONCHEZEL, LUCIENE L. CAMPOS, SIMONE APPENZELLER, MARIA V. QUINTERO, ANA B. SANTOS, ANA C. MEDEIROS, LUCIANA M. CARVALHO, TERESA C. ROBAZZI, SILVANA P. CARDIN, and ELOISA BONFA
ABSTRACT. Methods. A total of 315 female patients with JSLE followed in 12 Brazilian pediatric rheumatology centers were consecutively selected. Menarche was observed in 298 (94.6%) patients. Patients' medical records were reviewed for pregnancy outcomes and demographic, clinical, and therapeutic data. Results. A total of 24 unplanned pregnancies occurred in 298 (8%) patients. The outcomes were 5 (21%) early fetal losses (prior to 16 wks gestation), 18 (75%) live births, and 1 (4%) death due to preeclampsia and premature birth. The frequencies of active diffuse proliferative glomerulonephritis, proteinuria ≥ 0.5 g/day, and arterial hypertension at the beginning of pregnancy were higher in pregnancies resulting in fetal losses than in live births [60% vs 5% (p = 0.02), 60% vs 5% (p = 0.02), 60% vs 5% (p = 0.02), respectively]. JSLE pregnancies with fetal losses had a significantly higher mean SLE Disease Activity Index 2000 (SLEDAI-2K) at the start of pregnancy compared with those with live births (9.40 ± 7.47 vs 3.94 ± 6.00; p = 0.049). Four pregnancies were inadvertently exposed to intravenous cyclophosphamide therapy for renal involvement despite contraceptive prescriptions, resulting in fetal loss in 3 (p = 0.02). In multivariate analysis only intravenous cyclophosphamide use at start of pregnancy (OR 25.50, 95% CI 1.72-377.93, p = 0.019) remained as an independent risk factor for fetal loss. Conclusion. We identified immunosuppressive therapy as the major contributing factor for fetal loss in JSLE, reinforcing the importance of contraception. (J Rheumatol First Release April 1 2008) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Paediatric Rheumatology Units of the University of São Paulo, Federal University of São Paulo, Federal University of Rio de Janeiro, Santa Casa of São Paulo, State University of Rio de Janeiro, State University of Campinas, Santa Casa of Belo Horizonte; Division of Rheumatology, Federal University of Rio de Janeiro; Division of Rheumatology, University of São Paulo; University of São Paulo-Ribeirão Preto, Hospital São Rafael-Bahia, State University of São Paulo-Botucatu, Brazil. Supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico-CNPQ (grants 302469/2005-2 to C.A.A. Silva, 302313/2004-4 to M.O. Hilario, and 305468/2006-5 to E. Bonfa) and a Federico Foundation Grant to E. Bonfa. C.A.A. Silva, MD, PhD, University of São Paulo; M.O. Hilario, MD, PhD, Federal University of São Paulo; M.V. Febronio, MD, PhD, University of São Paulo; S.K. Oliveira, MD, PhD; R.G. Almeida, MD; A.R. Fonseca, MD, Federal University of Rio de Janeiro; E.M. Yamashita, MD, Federal University of São Paulo; M.V. Ronchezel, MD, PhD, Santa Casa of São Paulo; L.L. Campos, MD, State University of Rio de Janeiro; S. Appenzeller, MD, PhD, State University of Campinas; M.V. Quintero, MD, Santa Casa of Belo Horizonte; A.B. Santos, MD, Division of Rheumatology, Federal University of Rio de Janeiro; A.C. Medeiros, MD, Division of Rheumatology, University of São Paulo; L.M. Carvalho, MD, University of São Paulo-Ribeirão Preto; T.C. Robazzi, MD, Hospital São Rafael-Bahia; S.P. Cardin, MD, State University of São Paulo-Botucatu; E. Bonfa, MD, PhD, Division of Rheumatology, University of São Paulo. Address reprint requests to Dr. C.A.A Silva, Rua Senador César Lacerda Vergueiro, 494/82 - Vila Madalena, São Paulo-SP, Brazil, CEP 05435-010. E-mail: clovisaas@icr.hcnet.usp.br Accepted for publication December 3, 2007. |
