Alfredo Leaños-Miranda1, Inova Campos-Galicia2, María Guadalupe Berumen-Lechuga2, Carlos José Molina-Pérez2, Yolanda García-Paleta2, Irma Isordia-Salas2, Karla Leticia Ramírez-Valenzuela2. 1. From the Research Unit in Reproductive Medicine and Toco-Surgery Service, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala," Instituto Mexicano del Seguro Social (IMSS), and the Research Unit in Thrombosis, Hemostasia and Atherogenesis, H.G.R. No. 1 "Dr. Carlos Mac Gregor Sánchez Navarro," IMSS.A. Leaños-Miranda, MD, DSc; I. Campos-Galicia, MD; M.G. Berumen-Lechuga, MD; C.J. Molina-Pérez, MD; Y. García-Paleta, QBP, Research Unit in Reproductive Medicine, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala", IMSS; I. Isordia-Salas, MD, PhD, Research Unit in Thrombosis, Hemostasia and Atherogenesis, H.G.R. No. 1 "Dr. Carlos Mac Gregor Sánchez Navarro," IMSS; K.L. Ramírez-Valenzuela, MD, MSc, Toco-Surgery Service, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala," IMSS. alfredolm@yahoo.com. 2. From the Research Unit in Reproductive Medicine and Toco-Surgery Service, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala," Instituto Mexicano del Seguro Social (IMSS), and the Research Unit in Thrombosis, Hemostasia and Atherogenesis, H.G.R. No. 1 "Dr. Carlos Mac Gregor Sánchez Navarro," IMSS.A. Leaños-Miranda, MD, DSc; I. Campos-Galicia, MD; M.G. Berumen-Lechuga, MD; C.J. Molina-Pérez, MD; Y. García-Paleta, QBP, Research Unit in Reproductive Medicine, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala", IMSS; I. Isordia-Salas, MD, PhD, Research Unit in Thrombosis, Hemostasia and Atherogenesis, H.G.R. No. 1 "Dr. Carlos Mac Gregor Sánchez Navarro," IMSS; K.L. Ramírez-Valenzuela, MD, MSc, Toco-Surgery Service, Unidad Médica de Alta Especialidad-Hospital de Ginecología y Obstetricia "Luis Castelazo Ayala," IMSS.
Abstract
OBJECTIVE: To investigate whether angiogenic factors are associated with risk of developing preeclampsia in pregnant women with systemic lupus erythematosus (SLE). METHODS: We performed a nested case-control study within a cohort of SLE women with singleton pregnancies. The study included 42 patients with SLE who eventually developed preeclampsia and 75 normal SLE pregnancies. Serum samples were collected at 4-week intervals (from weeks 12 to 36). Serum samples were analyzed for soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng). RESULTS: Women destined to develop preeclampsia had lower PlGF levels and higher sFlt-1 and sEng levels, and a higher sFlt-1/PlGF ratio than normal pregnancies. These changes became significant at 12 weeks in patients destined to develop either early onset (< 34 weeks, p ≤ 0.003) or late-onset preeclampsia (≥ 34 weeks, p ≤ 0.02). The risk to develop preeclampsia was higher among patients with PlGF concentration values in the lowest quartile or with sFlt-1 and sEng levels, and sFlt-1/PlGF ratio, in the highest quartile of the normal SLE pregnancies distribution. The OR were higher and appeared earlier in patients destined to develop early onset preeclampsia (OR ≥ 16.2, from Week 12 onward) than in patients who presented preeclampsia later (OR ≥ 8.9, from Week 24 onward). CONCLUSION: Changes in circulating concentrations of sFlt-1, PlGF, sEng, and the sFlt-1/PlGF ratio precede the onset of preeclampsia in SLE pregnancies. The risk profile of circulating angiogenic factors for developing preeclampsia distinctly evolves depending on whether this condition is manifested earlier or later.
OBJECTIVE: To investigate whether angiogenic factors are associated with risk of developing preeclampsia in pregnant women with systemic lupus erythematosus (SLE). METHODS: We performed a nested case-control study within a cohort of SLEwomen with singleton pregnancies. The study included 42 patients with SLE who eventually developed preeclampsia and 75 normal SLE pregnancies. Serum samples were collected at 4-week intervals (from weeks 12 to 36). Serum samples were analyzed for soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng). RESULTS:Women destined to develop preeclampsia had lower PlGF levels and higher sFlt-1 and sEng levels, and a higher sFlt-1/PlGF ratio than normal pregnancies. These changes became significant at 12 weeks in patients destined to develop either early onset (< 34 weeks, p ≤ 0.003) or late-onset preeclampsia (≥ 34 weeks, p ≤ 0.02). The risk to develop preeclampsia was higher among patients with PlGF concentration values in the lowest quartile or with sFlt-1 and sEng levels, and sFlt-1/PlGF ratio, in the highest quartile of the normal SLE pregnancies distribution. The OR were higher and appeared earlier in patients destined to develop early onset preeclampsia (OR ≥ 16.2, from Week 12 onward) than in patients who presented preeclampsia later (OR ≥ 8.9, from Week 24 onward). CONCLUSION: Changes in circulating concentrations of sFlt-1, PlGF, sEng, and the sFlt-1/PlGF ratio precede the onset of preeclampsia in SLE pregnancies. The risk profile of circulating angiogenic factors for developing preeclampsia distinctly evolves depending on whether this condition is manifested earlier or later.
Authors: Norma C Serrano; Doris Cristina Quintero-Lesmes; Silvia Becerra-Bayona; Elizabeth Guio; Mónica Beltran; María C Paez; Ricardo Ortiz; Wilmar Saldarriaga; Luis A Diaz; Álvaro Monterrosa; Jezid Miranda; Clara M Mesa; José E Sanin; German Monsalve; Frank Dudbridge; Aroon D Hingorani; Juan P Casas Journal: PLoS One Date: 2018-12-06 Impact factor: 3.240