Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia

La Preeclampsia (PE), es una enfermedad frecuente que ocurre entre el 5a 7% de todos los embarazos en el mundo, sin embargo, las marcada variaciones geográficas, sociales, económicas y étnicas determinan poblaciones que alcanzan incidencias hasta tres veces mayores. En Colombia es la principal causa...

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Autores:
Serrano Díaz, Norma Cecilia
Páez Leal, María Carolina
Mesa Cornejo, Viviana Matilde
Tipo de recurso:
Investigation report
Fecha de publicación:
2002
Institución:
Universidad Autónoma de Bucaramanga - UNAB
Repositorio:
Repositorio UNAB
Idioma:
spa
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oai:repository.unab.edu.co:20.500.12749/22851
Acceso en línea:
http://hdl.handle.net/20.500.12749/22851
Palabra clave:
Maternal morbidity and mortality
Genetic disease
Racial pigmentation
Polymorphism
Hypertension in pregnancy
Genetics
Polimorfismo
Preeclampsia
Hipertensión en el embarazo
Genética
Morbimortalidad materna
Enfermedad genética
Pigmentación racial
Rights
License
http://creativecommons.org/licenses/by-nc-nd/2.5/co/
id UNAB2_e0190e46c71c66e3bf77af37b8bee77b
oai_identifier_str oai:repository.unab.edu.co:20.500.12749/22851
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network_name_str Repositorio UNAB
repository_id_str
dc.title.spa.fl_str_mv Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
dc.title.translated.spa.fl_str_mv Glu298Asp polymorphism of NOSe in a black Colombian population with preeclampsia
title Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
spellingShingle Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
Maternal morbidity and mortality
Genetic disease
Racial pigmentation
Polymorphism
Hypertension in pregnancy
Genetics
Polimorfismo
Preeclampsia
Hipertensión en el embarazo
Genética
Morbimortalidad materna
Enfermedad genética
Pigmentación racial
title_short Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
title_full Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
title_fullStr Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
title_full_unstemmed Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
title_sort Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsia
dc.creator.fl_str_mv Serrano Díaz, Norma Cecilia
Páez Leal, María Carolina
Mesa Cornejo, Viviana Matilde
dc.contributor.author.none.fl_str_mv Serrano Díaz, Norma Cecilia
Páez Leal, María Carolina
Mesa Cornejo, Viviana Matilde
dc.contributor.cvlac.spa.fl_str_mv Páez Leal, María Carolina [0000066656]
Serrano Díaz, Norma Cecilia [0000066613]
dc.contributor.googlescholar.spa.fl_str_mv Páez Leal, María Carolina [BAPR3-cAAAAJ]
Serrano Díaz, Norma Cecilia [iDn0AAAAAJ&hl=es&oi=ao]
dc.contributor.orcid.spa.fl_str_mv Páez Leal, María Carolina [0000-0002-0310-0125]
Serrano Díaz, Norma Cecilia [0000-0003-3532-2002]
dc.contributor.scopus.spa.fl_str_mv Páez Leal, María Carolina [12243485600]
Serrano Díaz, Norma Cecilia [7003706613]
dc.contributor.researchgate.spa.fl_str_mv Páez Leal, María Carolina [Maria_Paez-Leal]
dc.contributor.researchgroup.spa.fl_str_mv Grupo de Estudio Genético de Enfermedades Complejas
Grupo de Investigaciones Clínicas
dc.subject.keywords.spa.fl_str_mv Maternal morbidity and mortality
Genetic disease
Racial pigmentation
Polymorphism
Hypertension in pregnancy
Genetics
topic Maternal morbidity and mortality
Genetic disease
Racial pigmentation
Polymorphism
Hypertension in pregnancy
Genetics
Polimorfismo
Preeclampsia
Hipertensión en el embarazo
Genética
Morbimortalidad materna
Enfermedad genética
Pigmentación racial
dc.subject.lemb.spa.fl_str_mv Polimorfismo
Preeclampsia
Hipertensión en el embarazo
Genética
dc.subject.proposal.spa.fl_str_mv Morbimortalidad materna
Enfermedad genética
Pigmentación racial
description La Preeclampsia (PE), es una enfermedad frecuente que ocurre entre el 5a 7% de todos los embarazos en el mundo, sin embargo, las marcada variaciones geográficas, sociales, económicas y étnicas determinan poblaciones que alcanzan incidencias hasta tres veces mayores. En Colombia es la principal causa de morbimortalidad materna, con más del 42% de fallecimientos atribuibles a este desorden, además se asocia con un incremento de cinco veces en la mortalidad perinatal. A pesar del gran impacto social y económico, la etiología y fisiopatología de la PE no están totalmente determinadas. Se considera una enfermedad compleja con una susceptibilidad genética de base y múltiples factores medioambientales y concomitantes a la gestación que determinan la aparición y el curso de la enfermedad. Nuestro grupo ha venido trabajando con pacientes Preeclámpticas de cuatro regiones colombianas, estableciendo la frecuencia del polimorfismo Glu298Asp de la Óxido Nítrico Sintasa Endotelial (NOSe), el cual se ha asociado con varias enfermedades que tienen en común a la PE, disfunción endotelial. Hemos encontrado una frecuencia mayor del polimorfismo en las pacientes con PE comparado con las gestantes normotensas; pero la muestra estudiada corresponde a mujeres en su mayoría mestizas con predominio blanco o indígena. Dado que los polimorfismos genéticos pueden variar su frecuencia dependiendo de la etnia estudiada, y que es bien conocido que en la etnia negra la PE en más frecuente y de mayor severidad, pretendemos analizar la frecuencia del polimorfismo Glu298Asp en población negra y comparar los resultados con los obtenidos en nuestro estudio preliminar (PREGENO), tratando de establecer si existen diferencias significativas que pudieran explicar la mayor frecuencia y severidad de la Preeclampsia en la población negra a estudio.
publishDate 2002
dc.date.issued.none.fl_str_mv 2002
dc.date.accessioned.none.fl_str_mv 2023-11-20T16:14:14Z
dc.date.available.none.fl_str_mv 2023-11-20T16:14:14Z
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dc.type.local.spa.fl_str_mv Informe de investigación
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dc.relation.references.spa.fl_str_mv López-Jaramillo P, Casas JP, Serrano N. Preeclampsia: from epidemiological observations to molecular mechanism. Braz J Med Biol Res: 2001;10: 1227-35.
Gómez P. Ruiz N, Pulido J. Mortalidad materna e el Instituto Materno Infantil de Santafé de Bogotá D.C. 1985-1989. Rev Col Obst Ginecol 1993;44:39-47.
Higgins JR, de Suite M. Blood-pressure measurement and classification in pregnancy. Lancet 2001;357:131-35.
Dekker GA, Sibai BM. Etiology and patogenesis of preeclampsia: current concepts. Am J Obstet Gynecol 1998; 179:1359-75.
Atallah AN, Hofmeyr Gl], Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Library number: CDO01059.
Dekker G, Sibai B. Primary, secondary and tertiary prevention of pre- eclampsia. Lancet 2001;357:209-15.
Roberts JM, Cooper DW. Pathogenesis and genetics of pre-eclampsia. Lancet 2001;357:53-6.
Arngrímsson R, Bjórnsson H, Reynir T. Analysis of different inheritance patterns in preeclampsia/eclampsia syndrome. Hypertens Pregnancy 1995;14:27-38.
Graves JV. Genomic imprinting, development and disease: is pre-eclampsia caused by a maternally imprinted gene? Reprod Fertil Dev 1998;10:23-9.
Ros HS; Lichtenstein P, Lipworth L, et al. Genetic effects on the liability of developing pre-eclampsia and gestacional hypertension. Am J Med Genet 2000;91:256-60.
Guo G, Wilton AN, Fu Y, et al. Angiotensinogen gene variation in a population case-control study of preeclampsia/eclampsia in Australians and Chinese. Electrophoresis 1997; 18:1646-49.
Lachmeijer AM, Arngrímsson R, Batiaans EJ, et al. Mutations in the gene for methylenetetrahydrofolate reductase, homocysteine levels, and vitamin status in women with a history of preeclampsia. Am J Obstet Gynecol 2001;184:394-402.
Kaiser T, Brennecke S, Moses E. Methylenetetrahydorfolate resuctase polymorphisms are not a risk factor for pre-eclampsia/eclampsia in Australian women. Gynecol Obstet Invest 2000;50:100-02.
Zusterzeel P, Visser W, Blom HJ, et al. Methylenetetrahydorfolate resuctase polymorphisms in preeclampsia and the Hellp syndrome. Hypertens Pregnancy 2000;19:299-307.
Page NM, Woods RJ, Gardiner SM, et al. Excessive placental secretion of neurokinin B during the third trimester causes pre-eclampsia. Nature 2000;405:787-800,
Dizon-Townson DS, Major H, Ward K. A promoter mutation in the tumor necrosis factor alpha gene is nor associated with preeclampsia. J Reprod Immunol 1998;38:55-61.
Kahn Sr. Severe preeclampsia associated with coinheritance of factor V Leiden mutation and protein S deficiency. Obstet Gynecol 1998;91:812-14.
Hubel CA, Roberts JM, Ferrell RE. Association of pre-eclampsia with common coding sequence variations in the lipoprotein lipase gene. Cli Genet 1999;56:289-96.
Harrinson GA, Humphrey KE, Jones N et al. A genome wide linkage study of preeclampsia/eclampsia reveals evidence for a candidate region on 44. Am J Hum Genet 1997;60:1158-67.
Arngrímsson R, Siguroardottir S, Frigge M, et al. A genome-wide scan reveals a maternal susceptibility locus for pre-eclampsia on chromosome 2p13. Hum Molec Genet 1999;8:1799-1805.
Moses EK, Lade JA, Guo G, et al. A genome scan in families from Australia and New Zeland confirms the presence of a maternal susceptibility locus for pre-eclampsia, on chromosome 2. Am J Hum Genet 2000;67:1581-85.
rngrimsson R, Hayward C, Nadaud S, et al. Evidence for a familial pregnancy-induced hypertension locus in the eNOS-Gene region. Am J Hum Genet 1007;61:354-62.
Guo GL, Lade JA, Wilton AN et al. Genetic susceptibility to pre-eclamsia and ) chromosome 7q36. Hum Genet 1999;105:641-647.
Kilpatrick DC, Liston WA, Gibson F et al. Association between susceptibility to pre-eclampsia within families and HLA DR4. Lancet 1989 11:1063-65
ilton AN, Cooper DW, Brennecke SP et al. Absence of close linkage ] between maternal genes for susceptibility to pre-eclampsia/eclampsia and HALA DR-beta. Lancet 1990;336:653-57.
Hayward C, Livingstone J, Holloway S et al. An exclusion map for preeclampsia: assuming autosomal recessive inheritance. Am J Hum Genet 1992;50:749-57.
Palmer RM, Ferrige AG, Mocada S. Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature1987;327:524-26.
Sladek SM, Magness RR, Conrad KP. Nitric oxide and pregnancy. Am J Physiol 1997;272:441-463.
Davidge ST, Stranko CP, Roberts JM. Urine but not plasma nitric oxide metabolites are decreased in women with preeclampsia. Am J Obstet Gynecol 1996;174:1008-1013.
Nobunaga T, Tokugawa Y, Hashimoto K, et al. Plasma nitric oxide levels in pregnant patients with preeclampsia and essential hypertension. Gynecol Obstet Invest 1996;41:189-193.
Bartha JL, Comino Delgado R, Bedoya FJ, et al. Maternal serum nitric oxide levels associated with biochemical and clinical parameters in hypertension in pregnancy. Eur J Obstet Gynecol Reprod Biol 1999;82:201-207.
Di loro R, Marinoni E, Emiliani S, et al. Nitric oxide in preeclampsia: lack of evidence for decreases production. Eur J Obstet Gynecol Reprod Biol 1998;76:65-70.
Morris NH, Eaton BM, Dekker G. Nitric oxide, the endothelium pregnancy and pre-eclampsia. Br J Obstet Gynecol 1996;103:4-15.
Hingorani AD, Liang CF, Fatibene J, et al. A common variant of the endothelial nitric oxide synthase (Glu298Asp) is a major risk factor for coronary artery disease in the UK. Circulation 1999;100:1515-20.
Yoshimura M. A missense Glu298Asp variant in the endothelial nitric oxide synthase gene is associated with coronary spasm in the Japanese. Hum Genet 1998;103:65-69.
Yoshimura M et al. Genetic risk factor for coronary artery spasm: significance of endothelial nitric oxide synthase gene T786C and missense Glu298Asp variants. J Invest Med 2000;48:367-74.
Miyamoto Y, Saito Y, Kajiyama N, et al. Endothelial nitric oxide synthase gene is positively associated with essential hypertension. Hypertension 1998;32:3-8.
Shoji M et al. Positive association of endothelial nitric oxide synthase gene polymorphism with hypertension in northern Japan. Life Sci 2000;66:2557- 62.
Shimasaki Y, et al. Association of the missense Glu298Asp variant of the nitric oxide synthase gene with myocardial infarction. 3 Am Coll Cardiol 1999;31:1506-10.
McNamara DM, et al. The Asp298 variant of endothelial nitric oxide synthase (eNOS) improves survival in patients with heart failure. Circulation 1999;100:1507.
Yoshimura T, Yoshimura M, Tabata A, et al. Association of the missense Glu298Asp variant of the endothelial nitric oxide synthase gene with severe preeclampsia. J Soc Gynecol Invest 2000;7:238-41.
ai H, et al. The Glu298Asp (G894T) mutation al exon 7 of the endothelial nitric oxide synthase gene and coronary artery disease. J Mol Med 1999:77:511-14.
Lacolle P, et al. Nitric oxide synthase gene polymorphisms, blood pressure and aortic stiffness in normotensive and hypertensive subjects. J Hypertens 1999;16:31-5.
ato N, et al. Lack of evidence for association between the endothelial nitric oxide gene and hypertension. Hypertension 1999:33:933-36.
oirier O, et al. Polymorphisms of the endothelial nitric oxide synthase gene ) no consistent association with myocardial infarction in the ECTIM study. Eur J Clin Invest 1999;29:284-90.
Hibi K, et al. Endothelial nitric oxide synthase gene polymorphism and acute myocardial infarction. Hypertension 1998;32:521-526.
Tanus-Santos JE, Desai M, Flockhart DA. Effects of ethnicity on the distribution of clinically relevant endothelial nitric oxide variants. Pharmacogenetics 2001;11:719-25,
Stein CM, Lang CC, Xie HG, et al. Hypertension in black people: study of specific genotypes and phenotypes will provide a grater understanding of | interindividual and interethnic variability in blood pressure
Teasuro M, Thompson WC, Rogliani P et al. Intracellular processing of | endothelial nitric oxide synthase isoforms associated with differences in severity of cardiopulmonary diseases: cleavage of proteins with aspartate vs. glutamate at position 298. Proc Natl Acad Sci USA 2000 97;2832-35
Greenland S. Modeling and variable selection in epidemiologic analysis. Am J Public Health 1989; 79:340-9,
.Hosmer DW, Taber S, Lemeshaw S. The importance of assessing the fit of logistic regression models: A case study. Am J Public Halth 1991; 81:1630- 5,
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spelling Serrano Díaz, Norma Cecilia6d35f45d-5845-4d5a-a85d-46c2dd24bbc3Páez Leal, María Carolina4c30d3de-095b-4497-b14c-f1501234ab69Mesa Cornejo, Viviana Matildea5c3bff9-a721-49e8-aa7c-3342091cf68cPáez Leal, María Carolina [0000066656]Serrano Díaz, Norma Cecilia [0000066613]Páez Leal, María Carolina [BAPR3-cAAAAJ]Serrano Díaz, Norma Cecilia [iDn0AAAAAJ&hl=es&oi=ao]Páez Leal, María Carolina [0000-0002-0310-0125]Serrano Díaz, Norma Cecilia [0000-0003-3532-2002]Páez Leal, María Carolina [12243485600]Serrano Díaz, Norma Cecilia [7003706613]Páez Leal, María Carolina [Maria_Paez-Leal]Grupo de Estudio Genético de Enfermedades ComplejasGrupo de Investigaciones ClínicasBucaramanga (Santander, Colombia)2002UNAB Campus Bucaramanga2023-11-20T16:14:14Z2023-11-20T16:14:14Z2002http://hdl.handle.net/20.500.12749/22851instname:Universidad Autónoma de Bucaramanga - UNABreponame:Repositorio Institucional UNABrepourl:https://repository.unab.edu.coLa Preeclampsia (PE), es una enfermedad frecuente que ocurre entre el 5a 7% de todos los embarazos en el mundo, sin embargo, las marcada variaciones geográficas, sociales, económicas y étnicas determinan poblaciones que alcanzan incidencias hasta tres veces mayores. En Colombia es la principal causa de morbimortalidad materna, con más del 42% de fallecimientos atribuibles a este desorden, además se asocia con un incremento de cinco veces en la mortalidad perinatal. A pesar del gran impacto social y económico, la etiología y fisiopatología de la PE no están totalmente determinadas. Se considera una enfermedad compleja con una susceptibilidad genética de base y múltiples factores medioambientales y concomitantes a la gestación que determinan la aparición y el curso de la enfermedad. Nuestro grupo ha venido trabajando con pacientes Preeclámpticas de cuatro regiones colombianas, estableciendo la frecuencia del polimorfismo Glu298Asp de la Óxido Nítrico Sintasa Endotelial (NOSe), el cual se ha asociado con varias enfermedades que tienen en común a la PE, disfunción endotelial. Hemos encontrado una frecuencia mayor del polimorfismo en las pacientes con PE comparado con las gestantes normotensas; pero la muestra estudiada corresponde a mujeres en su mayoría mestizas con predominio blanco o indígena. Dado que los polimorfismos genéticos pueden variar su frecuencia dependiendo de la etnia estudiada, y que es bien conocido que en la etnia negra la PE en más frecuente y de mayor severidad, pretendemos analizar la frecuencia del polimorfismo Glu298Asp en población negra y comparar los resultados con los obtenidos en nuestro estudio preliminar (PREGENO), tratando de establecer si existen diferencias significativas que pudieran explicar la mayor frecuencia y severidad de la Preeclampsia en la población negra a estudio.Preeclampsia (PE) is a common disease that occurs between 5 to 7% of all pregnancies in the world; however, marked geographic, social, economic and ethnic variations determine populations that reach incidences up to three times higher. In Colombia it is the main cause of maternal morbidity and mortality, with more than 42% of deaths attributable to this disorder, and it is also associated with a five-fold increase in perinatal mortality. Despite the great social and economic impact, the etiology and pathophysiology of PE are not fully determined. It is considered a complex disease with an underlying genetic susceptibility and multiple environmental and pregnancy-related factors that determine the onset and course of the disease. Our group has been working with Preeclamptic patients from four Colombian regions, establishing the frequency of the Glu298Asp polymorphism of Endothelial Nitric Oxide Synthase (eNOS), which has been associated with several diseases that have endothelial dysfunction in common with PE. We have found a higher frequency of the polymorphism in patients with PE compared to normotensive pregnant women; but the sample studied corresponds to mostly mestizo women with white or indigenous predominance. Given that genetic polymorphisms can vary in frequency depending on the ethnic group studied, and that it is well known that in black ethnic groups PE is more frequent and of greater severity, we intend to analyze the frequency of the Glu298Asp polymorphism in the black population and compare the results with those obtained in our preliminary study (PREGENO), trying to establish if there are significant differences that could explain the greater frequency and severity of Preeclampsia in the black population under study.Modalidad Presencialapplication/pdfspahttp://creativecommons.org/licenses/by-nc-nd/2.5/co/Abierto (Texto Completo)Atribución-NoComercial-SinDerivadas 2.5 Colombiahttp://purl.org/coar/access_right/c_abf2Polimorfismo Glu298Asp de la NOSE en población negra colombiana con preeclampsiaGlu298Asp polymorphism of NOSe in a black Colombian population with preeclampsiaResearch reportinfo:eu-repo/semantics/workingPaperInforme de investigaciónhttp://purl.org/coar/resource_type/c_18wshttp://purl.org/coar/resource_type/c_8042info:eu-repo/semantics/acceptedVersionhttp://purl.org/redcol/resource_type/IFIUniversidad Autónoma de Bucaramanga UNABFacultad Ciencias de la SaludMaternal morbidity and mortalityGenetic diseaseRacial pigmentationPolymorphismHypertension in pregnancyGeneticsPolimorfismoPreeclampsiaHipertensión en el embarazoGenéticaMorbimortalidad maternaEnfermedad genéticaPigmentación racialLópez-Jaramillo P, Casas JP, Serrano N. Preeclampsia: from epidemiological observations to molecular mechanism. Braz J Med Biol Res: 2001;10: 1227-35.Gómez P. Ruiz N, Pulido J. Mortalidad materna e el Instituto Materno Infantil de Santafé de Bogotá D.C. 1985-1989. Rev Col Obst Ginecol 1993;44:39-47.Higgins JR, de Suite M. Blood-pressure measurement and classification in pregnancy. Lancet 2001;357:131-35.Dekker GA, Sibai BM. Etiology and patogenesis of preeclampsia: current concepts. Am J Obstet Gynecol 1998; 179:1359-75.Atallah AN, Hofmeyr Gl], Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Library number: CDO01059.Dekker G, Sibai B. Primary, secondary and tertiary prevention of pre- eclampsia. Lancet 2001;357:209-15.Roberts JM, Cooper DW. Pathogenesis and genetics of pre-eclampsia. Lancet 2001;357:53-6.Arngrímsson R, Bjórnsson H, Reynir T. Analysis of different inheritance patterns in preeclampsia/eclampsia syndrome. Hypertens Pregnancy 1995;14:27-38.Graves JV. Genomic imprinting, development and disease: is pre-eclampsia caused by a maternally imprinted gene? Reprod Fertil Dev 1998;10:23-9.Ros HS; Lichtenstein P, Lipworth L, et al. Genetic effects on the liability of developing pre-eclampsia and gestacional hypertension. Am J Med Genet 2000;91:256-60.Guo G, Wilton AN, Fu Y, et al. Angiotensinogen gene variation in a population case-control study of preeclampsia/eclampsia in Australians and Chinese. Electrophoresis 1997; 18:1646-49.Lachmeijer AM, Arngrímsson R, Batiaans EJ, et al. Mutations in the gene for methylenetetrahydrofolate reductase, homocysteine levels, and vitamin status in women with a history of preeclampsia. Am J Obstet Gynecol 2001;184:394-402.Kaiser T, Brennecke S, Moses E. Methylenetetrahydorfolate resuctase polymorphisms are not a risk factor for pre-eclampsia/eclampsia in Australian women. Gynecol Obstet Invest 2000;50:100-02.Zusterzeel P, Visser W, Blom HJ, et al. 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