Evidence map›Paper›PMID 20577119›Full record

Trial reportJournal of hypertension2010

Pharmacogenetic association of hypertension candidate genes with fasting glucose in the GenHAT Study.

Marguerite R Irvin, Amy I Lynch, Edmond K Kabagambe, Hemant K Tiwari, Joshua I Barzilay, John H Eckfeldt, Eric Boerwinkle, Barry R Davis, Charles E Ford, Donna K Arnett

Open access · greenAbstract readMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in Journal of hypertension, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 36 citations in OpenAlex.

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  10. Association ofPharmacogenomics and personalized medicine · 2021
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  15. Association analysis of four candidate genetic variants with sporadic amyotrophic lateral sclerosis in a Chinese population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Marguerite R IrvinDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Amy I Lynch
Edmond K Kabagambe
Hemant K Tiwari
Joshua I Barzilay
John H Eckfeldt
Eric Boerwinkle
Barry R Davis
Charles E Ford
Donna K Arnett
University of Alabama at Birmingham · USThe University of Texas Health Science Center at Houston · USUniversity of Minnesota · USKaiser Permanente · US

Funding

GENHAT-GENETICS OF HYPERTENSION ASSOCIATED TREATMENTSR01HL063082 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 1999 to 2009
$5.1M
Genetics of Hypertension Associated Treatment "GenHAT"R01HL083498 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BOERWINKLE, ERIC A. · 2007 to 2009
$1.4M
NHLBI NIH HHS 5 R01 HL-63082NHLBI NIH HHS R01 HL063082NHLBI NIH HHS R01 HL083498
6 · The paper itself

Abstract

backgroundSeveral clinical studies report increased risk of diabetes mellitus with pharmacologic treatment for hypertension (HTN). HTN genes may modify glycemic response to antihypertensive treatment.

methodThe current study examined the association of 24 single nucleotide polymorphisms (SNPs) in 11 HTN candidate genes with fasting glucose measured at 2, 4, and 6 years after treatment initiation. The study sample included participants free of diabetes at baseline in the Genetics of Hypertension Associated Treatment (GenHAT) study (N = 9309). GenHAT participants were randomized to receive treatment with a diuretic (chlorthalidone), calcium channel blocker (amlodipine), or angiotensin-converting enzyme (ACE) inhibitor (lisinopril). Mixed models for repeated measures were employed to test for gene and pharmacogenetic associations with fasting glucose during follow-up.

resultsFasting glucose at year 2 increased on average 6.8, 4.8 and 3.0 mg/dl from baseline in the chlorthalidone, amlodipine and lisinopril groups, respectively. Carrying the I allele (rs1799752) of the ACE I/D polymorphism was associated with lower fasting glucose levels (P = 0.02). Additionally, an ACE promoter polymorphism (-262, rs4291) was associated with lower fasting glucose for the model AA/AT vs. TT, which remained significant after correction for multiple testing (P = 0.001). Finally, a SNP in the α-subunit of the amiloride-sensitive epithelial sodium channel (SCNN1A, rs2228576) modified the association of amlodipine vs. chlorthalidone treatment with fasting glucose (P < 0.001).

conclusionFurther examination of these genes and their relationships with cardiometabolic disease could foster development of pharmacogenetic guidelines aimed to prevent increases in fasting glucose during antihypertensive treatment.

Indexed as

PharmacogeneticsAgedAmlodipineAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsBlood GlucoseCalcium Channel BlockersChlorthalidoneDiabetes MellitusDiureticsDouble-Blind MethodEpithelial Sodium ChannelsFastingFemaleHumansHypertensionAmlodipineAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsBlood GlucoseCalcium Channel BlockersChlorthalidoneDiureticsEpithelial Sodium ChannelsLisinoprilSCNN1A protein, human

Identifiers

PMID20577119
PMCPMC2957368
OpenAlexW1992715760

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.