ArticlePharmacogenetics and genomics2013
Impact of TCF7L2 single nucleotide polymorphisms on hydrochlorothiazide-induced diabetes.
Article in Pharmacogenetics and genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Genome Wide Association Study Identifies theJournal of the American Heart Association · 2018Pooled it
- Genome-wide association study identifies pharmacogenomic loci linked with specific antihypertensive drug treatment and new-onset diabetes.The pharmacogenomics journal · 2018Trial
- Pharmacogenomics in Diabetes: Population-Specific Insights from Colombia.Journal of personalized medicine · 2025Article
- Article
- Pharmacogenomic studies of hypertension: paving the way for personalized antihypertensive treatment.Expert review of precision medicine and drug development · 2018Article
- Pharmacogenomics of hypertension and heart disease.Current hypertension reports · 2015Review
- Genetics, ancestry, and hypertension: implications for targeted antihypertensive therapies.Current hypertension reports · 2014Review
- Untangling the interplay of genetic and metabolic influences on beta-cell function: Examples of potential therapeutic implications involving TCF7L2 and FFAR1.Molecular metabolism · 2014Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThiazide diuretics have been associated with increased risk for new onset diabetes (NOD), but pharmacogenetic markers of thiazide-induced NOD are not well studied. Single nucleotide polymorphisms (SNPs) in the transcription factor 7-like 2 gene (TCF7L2) represent the strongest and most reproducible genetic associations with diabetes. We investigated the association of tag SNPs in TCF7L2 with thiazide-induced NOD.
methodsWe identified cases that developed NOD and age, sex, and race/ethnicity-matched controls from the INternational VErapamil SR-Trandolapril STudy (INVEST). INVEST compared cardiovascular outcomes between two antihypertensive treatment strategies in ethnically diverse patients with hypertension and coronary artery disease. We genotyped 101 TCF7L2 tag SNPs and used logistic regression to test for pharmacogenetic (SNP×hydrochlorothiazide treatment) interactions. Permuted interaction P values were corrected with the PACT test and adjusted for diabetes-related variables.
resultsIn INVEST whites, we observed three TCF7L2 SNPs with significant SNP×treatment interactions for NOD. The strongest pharmacogenetic interaction was observed for rs7917983 [synergy index 3.37 (95% CI 1.72-6.59), P=5.0×10, PACT=0.03], which was associated with increased NOD risk in hydrochlorothiazide-treated patients [odds ratio 1.53 (1.04-2.25), P=0.03] and decreased NOD risk in non hydrochlorothiazide-treated patients [odds ratio 0.48 (0.27-0.86), P=0.02]. The TCF7L2 SNP rs4506565, previously associated with diabetes, showed a similar, significant pharmacogenetic association.
conclusionOur results suggest that hydrochlorothiazide treatment is an environmental risk factor that increases diabetes risk beyond that attributed to TCF7L2 variation in white, hypertensive patients. Further study and replication of our results is needed to confirm pharmacogenetic influences of TCF7L2 SNPs on thiazide-induced NOD.
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