Preeclampsia: Fisiopatología, Marcadores Bioquímicos, su vía común hacia la Restricción de Crecimiento Intrauterino y estrategias preventivas-terapéuticas.
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sep 26, 2025
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https://doi.org/10.36677/medicinainvestigacion.v13i2.24487
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Ilse Guadalupe Yarce Gómez
Gerardo Lorca Jiménez
http://orcid.org/0009-0004-1481-2058
http://orcid.org/0009-0004-1481-2058
Resumen
La Preeclampsia es un tema de suma importancia en la salud pública, debido a que es una de las causas más comunes de complicaciones en el embarazo, teniendo importantes consecuencias materno-fetales durante y después del embarazo, afectando la calidad de vida de quienes la padecen. Se ha hablado del origen de la Preeclampsia en la hipoxia tisular y la disfunción endotelial causados por una mala implantación placentaria secundario a una falla en la remodelación de las arterias espirales, y la conexión que esto tiene con un desequilibrio entre los agentes vasoconstrictores como la endotelina 1 (ET-1) y vasodilatadores como el óxido nítrico (ON), así como la elevación del Factor de Crecimiento Endotelial Vascular (VEGF) y del receptor 1 del Factor de Crecimiento Vascular (sFLT-1), con una marcada disminución del Factor de Crecimiento Placentario (PIGF) en su patogenia. En este texto se hace una revisión de los cambios bioquímicos descritos en el desarrollo de la enfermedad y abordaremos la manera en la que este conocimiento podría ayudar a estrategias terapéuticas oportunas
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YARCE GÓMEZ, Ilse Guadalupe; LORCA JIMÉNEZ, Gerardo.
Preeclampsia: Fisiopatología, Marcadores Bioquímicos, su vía común hacia la Restricción de Crecimiento Intrauterino y estrategias preventivas-terapéuticas..
Medicina e Investigación Universidad Autónoma del Estado de México, [S.l.], v. 13, n. 2, p. 140-147, sep. 2025.
ISSN 2594-0600.
Disponible en: <https://medicinainvestigacion.uaemex.mx/article/view/24487>. Fecha de acceso: 04 dic. 2025
doi: https://doi.org/10.36677/medicinainvestigacion.v13i2.24487.
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Esta obra está bajo licencia internacional Creative Commons Reconocimiento-NoComercial-SinObrasDerivadas 4.0.
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Rana, S., Lemoine, E., Granger, J. P., & Karumanchi, S. A. (2019). Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circulation research, 124(7), 1094–1112. https://doi.org/10.1161/CIRCRESAHA.118.313276.
De Jesús-García A, Jiménez-Baez MV, González-Ortiz DG, De la Cruz-Toledo P, Sandoval-Jurado L, Kuc-Peña LM. Características clínicas, epidemiológicas y riesgo obstétrico de pacientes con preeclampsia-eclampsia. (2018). Rev Enferm Inst Mex Seguro Soc. 2018;26(4):256-62.
Bokslag, A., van Weissenbruch, M., Mol, B. W., & de Groot, C. J. (2016). Preeclampsia; short and long-term consequences for mother and neonate. Early human development, 102, 47–50. https://doi.org/10.1016/j.earlhumdev.2016.09.007.
Ives, C. W., Sinkey, R., Rajapreyar, I., Tita, A. T. N., & Oparil, S. (2020). Preeclampsia-Pathophysiology and Clinical Presentations: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 76(14), 1690–1702. https://doi.org/10.1016/j.jacc.2020.08.014.
Wang, Y., Li, B., & Zhao, Y. (2022). Inflammation in Preeclampsia: Genetic Biomarkers, Mechanisms, and Therapeutic Strategies. Frontiers in immunology, 13, 883404. https://doi.org/10.3389/fimmu.2022.883404.
Lu, H. Q., & Hu, R. (2019). Lasting Effects of Intrauterine Exposure to Preeclampsia on Offspring and the Underlying Mechanism. AJP reports, 9(3), e275–e291. https://doi.org/10.1055/s-0039-1695004.
Granger, J. P., Alexander, B. T., Llinas, M. T., Bennett, W. A., & Khalil, R. A. (2002). Pathophysiology of preeclampsia: linking placental ischemia/hypoxia with microvascular dysfunction. Microcirculation (New York, N.Y. : 1994), 9(3), 147–160. https://doi.org/10.1038/sj.mn.7800137.
Tomimatsu, T., Mimura, K., Matsuzaki, S., Endo, M., Kumasawa, K., & Kimura, T. (2019). Preeclampsia: Maternal Systemic Vascular Disorder Caused by Generalized Endothelial Dysfunction Due to Placental Antiangiogenic Factors. International journal of molecular sciences, 20(17), 4246. https://doi.org/10.3390/ijms20174246.
Nagamatsu, T., Fujii, T., Kusumi, M., Zou, L., Yamashita, T., Osuga, Y., Momoeda, M., Kozuma, S., & Taketani, Y. (2004). Cytotrophoblasts up-regulate soluble fms-like tyrosine kinase-1 expression under reduced oxygen: an implication for the placental vascular development and the pathophysiology of preeclampsia. Endocrinology, 145(11), 4838–4845. https://doi.org/10.1210/en.2004-0533.
Kwiatkowski, S., Dołegowska, B., Kwiatkowska, E., Rzepka, R., Marczuk, N., Loj, B., & Torbè, A. (2017). Maternal endothelial damage as a disorder shared by early preeclampsia, late preeclampsia and intrauterine growth restriction. Journal of perinatal medicine, 45(7), 793–802. https://doi.org/10.1515/jpm-2016-0178.
Alahakoon, T. I., Zhang, W., Trudinger, B. J., & Lee, V. W. (2014). Discordant clinical presentations of preeclampsia and intrauterine fetal growth restriction with similar pro- and anti-angiogenic profiles. The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 27(18), 1854–1859. https://doi.org/10.3109/14767058.2014.880882.
Levine, R. J., Maynard, S. E., Qian, C., Lim, K. H., England, L. J., Yu, K. F., Schisterman, E. F., Thadhani, R., Sachs, B. P., Epstein, F. H., Sibai, B. M., Sukhatme, V. P., & Karumanchi, S. A. (2004). Circulating angiogenic factors and the risk of preeclampsia. The New England journal of medicine, 350(7), 672–683. https://doi.org/10.1056/NEJMoa031884.
George, E. M., Palei, A. C., & Granger, J. P. (2012). Endothelin as a final common pathway in the pathophysiology of preeclampsia: therapeutic implications. Current opinion in nephrology and hypertension, 21(2), 157–162. https://doi.org/10.1097/MNH.0b013e328350094b.
Maynard, S. E., Min, J. Y., Merchan, J., Lim, K. H., Li, J., Mondal, S., Libermann, T. A., Morgan, J. P., Sellke, F. W., Stillman, I. E., Epstein, F. H., Sukhatme, V. P., & Karumanchi, S. A. (2003). Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. The Journal of clinical investigation, 111(5), 649–658. https://doi.org/10.1172/JCI17189.
Conrad, K. P., Miles, T. M., & Benyo, D. F. (1998). Circulating levels of immunoreactive cytokines in women with preeclampsia. American journal of reproductive immunology (New York, N.Y. : 1989), 40(2), 102–111. https://doi.org/10.1111/j.1600-0897.1998.tb00398.x.
Stark J. M. (1993). Pre-eclampsia and cytokine induced oxidative stress. British journal of obstetrics and gynaecology, 100(2), 105–109. https://doi.org/10.1111/j.1471-0528.1993.tb15203.x.
Sunderland, N. S., Thomson, S. E., Heffernan, S. J., Lim, S., Thompson, J., Ogle, R., McKenzie, P., Kirwan, P. J., Makris, A., & Hennessy, A. (2011). Tumor necrosis factor α induces a model of preeclampsia in pregnant baboons (Papio hamadryas). Cytokine, 56(2), 192–199. https://doi.org/10.1016/j.cyto.2011.06.003.
Shibuya M. (2001). Structure and function of VEGF/VEGF-receptor system involved in angiogenesis. Cell structure and function, 26(1), 25–35. https://doi.org/10.1247/csf.26.25.
Vuorela, P., Helske, S., Hornig, C., Alitalo, K., Weich, H., & Halmesmäki, E. (2000). Amniotic fluid--soluble vascular endothelial growth factor receptor-1 in preeclampsia. Obstetrics and gynecology, 95(3), 353–357. https://doi.org/10.1016/s0029-7844(99)00565-7.
Robinson, E. S., Khankin, E. V., Karumanchi, S. A., & Humphreys, B. D. (2010). Hypertension induced by vascular endothelial growth factor signaling pathway inhibition: mechanisms and potential use as a biomarker. Seminars in nephrology, 30(6), 591–601. https://doi.org/10.1016/j.semnephrol.2010.09.007
Baksu, B., Davas, I., Baksu, A., Akyol, A., & Gulbaba, G. (2005). Plasma nitric oxide, endothelin-1 and urinary nitric oxide and cyclic guanosine monophosphate levels in hypertensive pregnant women. International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics, 90(2), 112–117. https://doi.org/10.1016/j.ijgo.2005.04.018
Nishikawa, S., Miyamoto, A., Yamamoto, H., Ohshika, H., & Kudo, R. (2000). The relationship between serum nitrate and endothelin-1 concentrations in preeclampsia. Life sciences, 67(12), 1447–1454. https://doi.org/10.1016/s0024-3205(00)00736-0
Verdonk, K., Saleh, L., Lankhorst, S., Smilde, J. E., van Ingen, M. M., Garrelds, I. M., Friesema, E. C., Russcher, H., van den Meiracker, A. H., Visser, W., & Danser, A. H. (2015). Association studies suggest a key role for endothelin-1 in the pathogenesis of preeclampsia and the accompanying renin-angiotensin-aldosterone system suppression. Hypertension (Dallas, Tex. : 1979), 65(6), 1316–1323. https://doi.org/10.1161/HYPERTENSIONAHA.115.05267
Rath, G., Aggarwal, R., Jawanjal, P., Tripathi, R., & Batra, A. (2016). HIF-1 Alpha and Placental Growth Factor in Pregnancies Complicated With Preeclampsia: A Qualitative and Quantitative Analysis. Journal of clinical laboratory analysis, 30(1), 75–83. https://doi.org/10.1002/jcla.21819
Caniggia, I., Mostachfi, H., Winter, J., Gassmann, M., Lye, S. J., Kuliszewski, M., & Post, M. (2000). Hypoxia-inducible factor-1 mediates the biological effects of oxygen on human trophoblast differentiation through TGFbeta(3). The Journal of clinical investigation, 105(5), 577–587. https://doi.org/10.1172/JCI8316
Chappell, L. C., Seed, P. T., Briley, A. L., Kelly, F. J., Lee, R., Hunt, B. J., Parmar, K., Bewley, S. J., Shennan, A. H., Steer, P. J., & Poston, L. (1999). Effect of antioxidants on the occurrence of pre-eclampsia in women at increased risk: a randomised trial. Lancet (London, England), 354(9181), 810–816. https://doi.org/10.1016/S0140-6736(99)80010-5
Rana, S., Lemoine, E., Granger, J. P., & Karumanchi, S. A. (2019). Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circulation research, 124(7), 1094–1112. https://doi.org/10.1161/CIRCRESAHA.118.313276.
De Jesús-García A, Jiménez-Baez MV, González-Ortiz DG, De la Cruz-Toledo P, Sandoval-Jurado L, Kuc-Peña LM. Características clínicas, epidemiológicas y riesgo obstétrico de pacientes con preeclampsia-eclampsia. (2018). Rev Enferm Inst Mex Seguro Soc. 2018;26(4):256-62.
Bokslag, A., van Weissenbruch, M., Mol, B. W., & de Groot, C. J. (2016). Preeclampsia; short and long-term consequences for mother and neonate. Early human development, 102, 47–50. https://doi.org/10.1016/j.earlhumdev.2016.09.007.
Ives, C. W., Sinkey, R., Rajapreyar, I., Tita, A. T. N., & Oparil, S. (2020). Preeclampsia-Pathophysiology and Clinical Presentations: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 76(14), 1690–1702. https://doi.org/10.1016/j.jacc.2020.08.014.
Wang, Y., Li, B., & Zhao, Y. (2022). Inflammation in Preeclampsia: Genetic Biomarkers, Mechanisms, and Therapeutic Strategies. Frontiers in immunology, 13, 883404. https://doi.org/10.3389/fimmu.2022.883404.
Lu, H. Q., & Hu, R. (2019). Lasting Effects of Intrauterine Exposure to Preeclampsia on Offspring and the Underlying Mechanism. AJP reports, 9(3), e275–e291. https://doi.org/10.1055/s-0039-1695004.
Granger, J. P., Alexander, B. T., Llinas, M. T., Bennett, W. A., & Khalil, R. A. (2002). Pathophysiology of preeclampsia: linking placental ischemia/hypoxia with microvascular dysfunction. Microcirculation (New York, N.Y. : 1994), 9(3), 147–160. https://doi.org/10.1038/sj.mn.7800137.
Tomimatsu, T., Mimura, K., Matsuzaki, S., Endo, M., Kumasawa, K., & Kimura, T. (2019). Preeclampsia: Maternal Systemic Vascular Disorder Caused by Generalized Endothelial Dysfunction Due to Placental Antiangiogenic Factors. International journal of molecular sciences, 20(17), 4246. https://doi.org/10.3390/ijms20174246.
Nagamatsu, T., Fujii, T., Kusumi, M., Zou, L., Yamashita, T., Osuga, Y., Momoeda, M., Kozuma, S., & Taketani, Y. (2004). Cytotrophoblasts up-regulate soluble fms-like tyrosine kinase-1 expression under reduced oxygen: an implication for the placental vascular development and the pathophysiology of preeclampsia. Endocrinology, 145(11), 4838–4845. https://doi.org/10.1210/en.2004-0533.
Kwiatkowski, S., Dołegowska, B., Kwiatkowska, E., Rzepka, R., Marczuk, N., Loj, B., & Torbè, A. (2017). Maternal endothelial damage as a disorder shared by early preeclampsia, late preeclampsia and intrauterine growth restriction. Journal of perinatal medicine, 45(7), 793–802. https://doi.org/10.1515/jpm-2016-0178.
Alahakoon, T. I., Zhang, W., Trudinger, B. J., & Lee, V. W. (2014). Discordant clinical presentations of preeclampsia and intrauterine fetal growth restriction with similar pro- and anti-angiogenic profiles. The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 27(18), 1854–1859. https://doi.org/10.3109/14767058.2014.880882.
Levine, R. J., Maynard, S. E., Qian, C., Lim, K. H., England, L. J., Yu, K. F., Schisterman, E. F., Thadhani, R., Sachs, B. P., Epstein, F. H., Sibai, B. M., Sukhatme, V. P., & Karumanchi, S. A. (2004). Circulating angiogenic factors and the risk of preeclampsia. The New England journal of medicine, 350(7), 672–683. https://doi.org/10.1056/NEJMoa031884.
George, E. M., Palei, A. C., & Granger, J. P. (2012). Endothelin as a final common pathway in the pathophysiology of preeclampsia: therapeutic implications. Current opinion in nephrology and hypertension, 21(2), 157–162. https://doi.org/10.1097/MNH.0b013e328350094b.
Maynard, S. E., Min, J. Y., Merchan, J., Lim, K. H., Li, J., Mondal, S., Libermann, T. A., Morgan, J. P., Sellke, F. W., Stillman, I. E., Epstein, F. H., Sukhatme, V. P., & Karumanchi, S. A. (2003). Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. The Journal of clinical investigation, 111(5), 649–658. https://doi.org/10.1172/JCI17189.
Conrad, K. P., Miles, T. M., & Benyo, D. F. (1998). Circulating levels of immunoreactive cytokines in women with preeclampsia. American journal of reproductive immunology (New York, N.Y. : 1989), 40(2), 102–111. https://doi.org/10.1111/j.1600-0897.1998.tb00398.x.
Stark J. M. (1993). Pre-eclampsia and cytokine induced oxidative stress. British journal of obstetrics and gynaecology, 100(2), 105–109. https://doi.org/10.1111/j.1471-0528.1993.tb15203.x.
Sunderland, N. S., Thomson, S. E., Heffernan, S. J., Lim, S., Thompson, J., Ogle, R., McKenzie, P., Kirwan, P. J., Makris, A., & Hennessy, A. (2011). Tumor necrosis factor α induces a model of preeclampsia in pregnant baboons (Papio hamadryas). Cytokine, 56(2), 192–199. https://doi.org/10.1016/j.cyto.2011.06.003.
Shibuya M. (2001). Structure and function of VEGF/VEGF-receptor system involved in angiogenesis. Cell structure and function, 26(1), 25–35. https://doi.org/10.1247/csf.26.25.
Vuorela, P., Helske, S., Hornig, C., Alitalo, K., Weich, H., & Halmesmäki, E. (2000). Amniotic fluid--soluble vascular endothelial growth factor receptor-1 in preeclampsia. Obstetrics and gynecology, 95(3), 353–357. https://doi.org/10.1016/s0029-7844(99)00565-7.
Robinson, E. S., Khankin, E. V., Karumanchi, S. A., & Humphreys, B. D. (2010). Hypertension induced by vascular endothelial growth factor signaling pathway inhibition: mechanisms and potential use as a biomarker. Seminars in nephrology, 30(6), 591–601. https://doi.org/10.1016/j.semnephrol.2010.09.007
Baksu, B., Davas, I., Baksu, A., Akyol, A., & Gulbaba, G. (2005). Plasma nitric oxide, endothelin-1 and urinary nitric oxide and cyclic guanosine monophosphate levels in hypertensive pregnant women. International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics, 90(2), 112–117. https://doi.org/10.1016/j.ijgo.2005.04.018
Nishikawa, S., Miyamoto, A., Yamamoto, H., Ohshika, H., & Kudo, R. (2000). The relationship between serum nitrate and endothelin-1 concentrations in preeclampsia. Life sciences, 67(12), 1447–1454. https://doi.org/10.1016/s0024-3205(00)00736-0
Verdonk, K., Saleh, L., Lankhorst, S., Smilde, J. E., van Ingen, M. M., Garrelds, I. M., Friesema, E. C., Russcher, H., van den Meiracker, A. H., Visser, W., & Danser, A. H. (2015). Association studies suggest a key role for endothelin-1 in the pathogenesis of preeclampsia and the accompanying renin-angiotensin-aldosterone system suppression. Hypertension (Dallas, Tex. : 1979), 65(6), 1316–1323. https://doi.org/10.1161/HYPERTENSIONAHA.115.05267
Rath, G., Aggarwal, R., Jawanjal, P., Tripathi, R., & Batra, A. (2016). HIF-1 Alpha and Placental Growth Factor in Pregnancies Complicated With Preeclampsia: A Qualitative and Quantitative Analysis. Journal of clinical laboratory analysis, 30(1), 75–83. https://doi.org/10.1002/jcla.21819
Caniggia, I., Mostachfi, H., Winter, J., Gassmann, M., Lye, S. J., Kuliszewski, M., & Post, M. (2000). Hypoxia-inducible factor-1 mediates the biological effects of oxygen on human trophoblast differentiation through TGFbeta(3). The Journal of clinical investigation, 105(5), 577–587. https://doi.org/10.1172/JCI8316
Chappell, L. C., Seed, P. T., Briley, A. L., Kelly, F. J., Lee, R., Hunt, B. J., Parmar, K., Bewley, S. J., Shennan, A. H., Steer, P. J., & Poston, L. (1999). Effect of antioxidants on the occurrence of pre-eclampsia in women at increased risk: a randomised trial. Lancet (London, England), 354(9181), 810–816. https://doi.org/10.1016/S0140-6736(99)80010-5