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Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study

Elevated serum uric acid (UA) level has been shown to be influenced by multiple genetic variants, but it remains uncertain how UA‐associated variants differ in their influence on hyperuricemia risk in people taking antihypertensive drugs. We examined a total of 43 UA‐related variants at 29 genes in...

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Autores principales: Chen, Yu, Yang, Yunyun, Zhong, Yixuan, Li, Jian, Kong, Tao, Zhang, Shuyuan, Yang, Shujun, Wu, Cunjin, Cui, Bing, Fu, Li, Hui, Rutai, Zhang, Weili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9306909/
https://www.ncbi.nlm.nih.gov/pubmed/35023146
http://dx.doi.org/10.1111/cge.14110
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author Chen, Yu
Yang, Yunyun
Zhong, Yixuan
Li, Jian
Kong, Tao
Zhang, Shuyuan
Yang, Shujun
Wu, Cunjin
Cui, Bing
Fu, Li
Hui, Rutai
Zhang, Weili
author_facet Chen, Yu
Yang, Yunyun
Zhong, Yixuan
Li, Jian
Kong, Tao
Zhang, Shuyuan
Yang, Shujun
Wu, Cunjin
Cui, Bing
Fu, Li
Hui, Rutai
Zhang, Weili
author_sort Chen, Yu
collection PubMed
description Elevated serum uric acid (UA) level has been shown to be influenced by multiple genetic variants, but it remains uncertain how UA‐associated variants differ in their influence on hyperuricemia risk in people taking antihypertensive drugs. We examined a total of 43 UA‐related variants at 29 genes in 1840 patients with hypertension from a community‐based longitudinal cohort during a median 2.25‐year follow‐up (including 1031 participants with normal UA, 440 prevalent hyperuricemia at baseline, and 369 new‐onset hyperuricemia). Compared with the wild‐type genotypes, patients carrying the SLC2A9 rs3775948G allele or the rs13129697G allele had decreased risk of hyperuricemia, while patients carrying the SLC2A9 rs11722228T allele had increased risk of hyperuricemia, after adjustment for cardiovascular risk factors and correction for multiple comparisons; moreover, these associations were modified by the use of diuretics, β‐blockers, or angiotensin converting enzyme inhibitors. The rs10821905A allele of A1CF gene was associated with increased risk of hyperuricemia, and this risk was enhanced by diuretics use. The studied variants were not observed to confer risk for incident cardiovascular events during the follow‐up. In conclusion, the genes SLC2A9 and A1CF may serve as potential genetic markers for hyperuricemia risk in relation to antihypertensive drugs therapy in Chinese hypertensive patients.
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spelling pubmed-93069092022-07-28 Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study Chen, Yu Yang, Yunyun Zhong, Yixuan Li, Jian Kong, Tao Zhang, Shuyuan Yang, Shujun Wu, Cunjin Cui, Bing Fu, Li Hui, Rutai Zhang, Weili Clin Genet Original Articles Elevated serum uric acid (UA) level has been shown to be influenced by multiple genetic variants, but it remains uncertain how UA‐associated variants differ in their influence on hyperuricemia risk in people taking antihypertensive drugs. We examined a total of 43 UA‐related variants at 29 genes in 1840 patients with hypertension from a community‐based longitudinal cohort during a median 2.25‐year follow‐up (including 1031 participants with normal UA, 440 prevalent hyperuricemia at baseline, and 369 new‐onset hyperuricemia). Compared with the wild‐type genotypes, patients carrying the SLC2A9 rs3775948G allele or the rs13129697G allele had decreased risk of hyperuricemia, while patients carrying the SLC2A9 rs11722228T allele had increased risk of hyperuricemia, after adjustment for cardiovascular risk factors and correction for multiple comparisons; moreover, these associations were modified by the use of diuretics, β‐blockers, or angiotensin converting enzyme inhibitors. The rs10821905A allele of A1CF gene was associated with increased risk of hyperuricemia, and this risk was enhanced by diuretics use. The studied variants were not observed to confer risk for incident cardiovascular events during the follow‐up. In conclusion, the genes SLC2A9 and A1CF may serve as potential genetic markers for hyperuricemia risk in relation to antihypertensive drugs therapy in Chinese hypertensive patients. Blackwell Publishing Ltd 2022-01-24 2022-04 /pmc/articles/PMC9306909/ /pubmed/35023146 http://dx.doi.org/10.1111/cge.14110 Text en © 2022 The Authors. Clinical Genetics published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Chen, Yu
Yang, Yunyun
Zhong, Yixuan
Li, Jian
Kong, Tao
Zhang, Shuyuan
Yang, Shujun
Wu, Cunjin
Cui, Bing
Fu, Li
Hui, Rutai
Zhang, Weili
Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title_full Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title_fullStr Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title_full_unstemmed Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title_short Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study
title_sort genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: a longitudinal study
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9306909/
https://www.ncbi.nlm.nih.gov/pubmed/35023146
http://dx.doi.org/10.1111/cge.14110
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