{"title":"慢性阻塞性肺病内皮功能障碍的遗传标记","authors":"A. K. Dausheva, E. G. Zarubina, Yu. V. Bogdanova","doi":"10.34215/1609-1175-2024-1-48-52","DOIUrl":null,"url":null,"abstract":"Objective. To analyze genetic markers of endothelial dysfunction in chronic obstructive pulmonary disease. Materials and methods. The study involved an examination of 285 patients with chronic obstructive pulmonary disease aged 67.12 ± 1.82, including males (73.68%) and females (26.32%). A control group consisted of 70 respondents, including 45 relatively healthy people, among whom males constituted 64.3% and females 35.7%. Polymorphisms of endothelial nitric oxide synthase NOS3 (C786T), endothelin-1 EDN1 Lys198Asn genes were examined by PCR method. Results. The cohort of COPD patients revealed a prevalence of pathological homozygous genotype 786SS NOS3 (χ2=12.84, df=1, p=0.0003). Carriage of heterozygous variant of LysAsn polymorphic marker Lys198Asn of EDN1 gene in COPD patients was detected in 32.5%. Conclusion. Manifestation of endothelial dysfunction in COPD patients is due to genotypic predisposition associated with carrying polymorphisms 786SS of NOS3 gene (OR 7.01, 95% CI 1.59-30.81) and Lys198Asn of EDN1 gene (OR 2.53, 95% CI 0.69-9.22)","PeriodicalId":19705,"journal":{"name":"Pacific Medical Journal","volume":"116 25","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Genetic markers of endothelial dysfunction in chronic obstructive pulmonary disease\",\"authors\":\"A. K. Dausheva, E. G. Zarubina, Yu. V. Bogdanova\",\"doi\":\"10.34215/1609-1175-2024-1-48-52\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective. To analyze genetic markers of endothelial dysfunction in chronic obstructive pulmonary disease. Materials and methods. The study involved an examination of 285 patients with chronic obstructive pulmonary disease aged 67.12 ± 1.82, including males (73.68%) and females (26.32%). A control group consisted of 70 respondents, including 45 relatively healthy people, among whom males constituted 64.3% and females 35.7%. Polymorphisms of endothelial nitric oxide synthase NOS3 (C786T), endothelin-1 EDN1 Lys198Asn genes were examined by PCR method. Results. The cohort of COPD patients revealed a prevalence of pathological homozygous genotype 786SS NOS3 (χ2=12.84, df=1, p=0.0003). Carriage of heterozygous variant of LysAsn polymorphic marker Lys198Asn of EDN1 gene in COPD patients was detected in 32.5%. Conclusion. Manifestation of endothelial dysfunction in COPD patients is due to genotypic predisposition associated with carrying polymorphisms 786SS of NOS3 gene (OR 7.01, 95% CI 1.59-30.81) and Lys198Asn of EDN1 gene (OR 2.53, 95% CI 0.69-9.22)\",\"PeriodicalId\":19705,\"journal\":{\"name\":\"Pacific Medical Journal\",\"volume\":\"116 25\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-05-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pacific Medical Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.34215/1609-1175-2024-1-48-52\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pacific Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.34215/1609-1175-2024-1-48-52","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Genetic markers of endothelial dysfunction in chronic obstructive pulmonary disease
Objective. To analyze genetic markers of endothelial dysfunction in chronic obstructive pulmonary disease. Materials and methods. The study involved an examination of 285 patients with chronic obstructive pulmonary disease aged 67.12 ± 1.82, including males (73.68%) and females (26.32%). A control group consisted of 70 respondents, including 45 relatively healthy people, among whom males constituted 64.3% and females 35.7%. Polymorphisms of endothelial nitric oxide synthase NOS3 (C786T), endothelin-1 EDN1 Lys198Asn genes were examined by PCR method. Results. The cohort of COPD patients revealed a prevalence of pathological homozygous genotype 786SS NOS3 (χ2=12.84, df=1, p=0.0003). Carriage of heterozygous variant of LysAsn polymorphic marker Lys198Asn of EDN1 gene in COPD patients was detected in 32.5%. Conclusion. Manifestation of endothelial dysfunction in COPD patients is due to genotypic predisposition associated with carrying polymorphisms 786SS of NOS3 gene (OR 7.01, 95% CI 1.59-30.81) and Lys198Asn of EDN1 gene (OR 2.53, 95% CI 0.69-9.22)