Fernanda Spadotto Baptista1, Maria Rita de Figueiredo Lemos Bortolotto2, Fabiola Roberta Marim Bianchini3, Vera Lucia Jornada Krebs4, Marcelo Zugaib5, Rossana Pulcinelli Vieira Francisco6. 1. Divisao de Clinica Obstetrica, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: fernanda.spadotto@hc.fm.usp.br. 2. Divisao de Clinica Obstetrica, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: maria.bortolotto@hc.fm.usp.br. 3. Centro Neonatal do Instituto da Criança, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: fabiola.bianchini@hc.fm.usp.br. 4. Disciplina de Neonatologia, Departamento de Pediatria, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: vera.krebs@hc.fm.usp.br. 5. Disciplina de Obstetricia, Departamento de Obstetricia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: m.zugaib@hc.fm.usp.br. 6. Disciplina de Obstetricia, Departamento de Obstetricia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, Brazil. Electronic address: rossana.francisco@hc.fm.usp.br.
Abstract
OBJECTIVE: To evaluate whether thrombophilia worsens maternal and foetal outcomes among patients with severe preeclampsia (PE). METHOD: From October 2009 to October 2014, an observational retrospective cohort study was performed on pregnant women with severe PE diagnosed before 34 weeks of gestation and their newborns hospitalized at the Clinics Hospital, FMUSP. Patients who had no heart disease, nephropathies, pre-gestational diabetes, gestational trophoblastic disease, foetal malformation, or twin pregnancy and who underwent thrombophilia screening during the postnatal period were included. New pregnancies of the same patient; cases of foetal morphological, genetic, or chromosomal abnormalities after birth; and women who used heparin or acetylsalicylic acid during pregnancy were excluded. Factor V Leiden, G20210A prothrombin mutation, antithrombin, protein C, protein S, homocysteine, lupus anticoagulant, and anticardiolipin IgG and IgM antibodies were analysed. The groups with and without thrombophilia were compared regarding their maternal clinical and laboratory parameters and perinatal outcomes. RESULTS: Of the 127 patients selected, 30 (23.6%) had thrombophilia (hereditary or acquired). We found more white patients in thrombophilia group (p = .036). Analysis of maternal parameters showed a tendency of thrombophilic women to have more thrombocytopenia (p = .056) and showed worsening of composite laboratory abnormalities (aspartate aminotransferase ≥ 70 mg/dL, alanine aminotransferase ≥ 70 mg/dL, platelets < 100,000/mm3, serum creatinine ≥ 1.1 mg/dL; p = .017). There were no differences in foetal perinatal outcomes. CONCLUSION: The presence of thrombophilia leads to worsening of maternal laboratory parameters among patients with severe forms of PE but without worsening perinatal outcomes.
OBJECTIVE: To evaluate whether thrombophilia worsens maternal and foetal outcomes among patients with severe preeclampsia (PE). METHOD: From October 2009 to October 2014, an observational retrospective cohort study was performed on pregnant women with severe PE diagnosed before 34 weeks of gestation and their newborns hospitalized at the Clinics Hospital, FMUSP. Patients who had no heart disease, nephropathies, pre-gestational diabetes, gestational trophoblastic disease, foetal malformation, or twin pregnancy and who underwent thrombophilia screening during the postnatal period were included. New pregnancies of the same patient; cases of foetal morphological, genetic, or chromosomal abnormalities after birth; and women who used heparin or acetylsalicylic acid during pregnancy were excluded. Factor V Leiden, G20210A prothrombin mutation, antithrombin, protein C, protein S, homocysteine, lupus anticoagulant, and anticardiolipin IgG and IgM antibodies were analysed. The groups with and without thrombophilia were compared regarding their maternal clinical and laboratory parameters and perinatal outcomes. RESULTS: Of the 127 patients selected, 30 (23.6%) had thrombophilia (hereditary or acquired). We found more white patients in thrombophilia group (p = .036). Analysis of maternal parameters showed a tendency of thrombophilic women to have more thrombocytopenia (p = .056) and showed worsening of composite laboratory abnormalities (aspartate aminotransferase ≥ 70 mg/dL, alanine aminotransferase ≥ 70 mg/dL, platelets < 100,000/mm3, serum creatinine ≥ 1.1 mg/dL; p = .017). There were no differences in foetal perinatal outcomes. CONCLUSION: The presence of thrombophilia leads to worsening of maternal laboratory parameters among patients with severe forms of PE but without worsening perinatal outcomes.