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Genetic polymorphisms of the renin-angiotensin system in preterm delivery and premature rupture of membranesUniversidad de Colima, Facultad de Ciencias Químicas. Kilometro 9 carretera Colima-Coquimatlán, Colima, México. 28400, lauravaldez @ucol.mx, Universidad de Guadalajara Centro Universitario de Ciencias de la Salud Estudios de Posgrado en Genética Humana Sierra Mojada No. 950 Col. Independencia (puerta 7). Guadalajara, Jalisco, México. 44340
Universidad de Guadalajara Centro Universitario de Ciencias de la Salud Estudios de Posgrado en Genética Humana Sierra Mojada No. 950 Col. Independencia (puerta 7). Guadalajara, Jalisco, México. 44340
Instituto Mexicano del Seguro Social Hospital General Regional No. 46 Lazaro Cardenas 2063 Col. Morelos Guadalajara, Jalisco, México. 44910
Instituto Mexicano del Seguro Social Centro de Investigación Biomédica de Occidente Sierra Mojada 800 Col. Independencia, Guadalajara, Jalisco, México. 44340
Instituto Mexicano del Seguro Social Centro de Investigación Biomédica de Occidente Sierra Mojada 800 Col. Independencia, Guadalajara, Jalisco, México. 44340
Instituto Mexicano del Seguro Social Centro de Investigación Biomédica de Occidente Sierra Mojada 800 Col. Independencia, Guadalajara, Jalisco, México. 44340
Secretaría de Salud Jalisco Hospital General de Occidente Av. Zoquipan 1050 Col. Seattle Zapopan, Jalisco, México. 45130
Universidad de Guadalajara Departamento de Salud publica Sierra Morena No. 950 Edificio N Col. Independencia Guadalajara, Jalisco, México. 44340
Universidad de Colima Facultad de Ciencias Químicas. Kilometro 9 carretera Colima-Coquimatlán, Colima, México. 28400
Instituto Mexicano del Seguro Social Centro de Investigación Biomédica de Occidente Sierra Mojada 800 Col. Independencia, Guadalajara, Jalisco, México. 44340 Introduction. Premature rupture of membranes (PRM) is a late pregnancy complication commonly associated with preterm delivery (PD).Although several markers related to the renin-angiotensin system (RAS) have been evaluated in certain pregnancy complications, only the angiotensin-converting enzyme (ACE) I/D variant has been studied in PD-PRM.The aim of this survey was to investigate the association of the polymorphisms (angiotensin II type 1 [AT1] receptor T174M and M235T, renin G2805A,ACE I/D and AT1-receptor A1166C) of the genes of RAS in women with PD-PRM. Design. Deoxyribonucleic acid samples from 89 Mexican Mestizo women with PD and PRM and 224—288 controls were studied. Polymorphisms were analysed by polymerase chain reaction-sequence specific primer assays. restricted fragment length polymorphism or sequence specific prim assays. Results. For all loci , genotype distribution was in agreement with Hardy—Weinberg expectations in the control group. Significant intergroup difference (case vs. control) was seen for angiotensinogen (AGT) M235T polymorphism, with an increased allele M235 in affected cases (50% vs. 40% in controls).Analysis of two-locus haplotype agrees with an independent segregation of physically unlinked genes. Haplotype AGT 174T-235M was also increased (50 % vs. 40% in controls). Conclusions. Physically unlinked genes involved in RAS segregate independently. The AGT 174—235 region is associated with PD-PRM in this population.
Key Words: angiotensin renin system polymorphism preterm delivery premature rupture of membranes haplotype analysis linkage disequilibrium
Journal of Renin-Angiotensin-Aldosterone System, Vol. 8, No. 4,
160-168 (2007) |
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