Evidence map›Paper›PMID 42535691›Full record

Observational studyPharmacogenomics2026

Association of ACE I/D polymorphism with blood pressure response to valsartan-hydrochlorothiazide combination therapy in hypertensive patients from Khyber Pakhtunkhwa, Pakistan.

Aftab Ullah, Abdur Rahim, Asif Jan, Muhammad Khan, Junaid Iqbal, Mequanente Dagnaw

Abstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Pharmacogenomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Aftab UllahDepartment of Pharmacy, Hazara University Mansehra, Mansehra, Pakistan.
Abdur RahimDepartment of Pharmacy, CECOS University of IT & Emerging Sciences, Peshawar.
Asif JanDistrict Headquarter Hospital Charsadda, Charsadda, Pakistan.ORCID 0000-0003-3880-5579
Muhammad KhanDepartment of Biotechnology and Genetic Engineering, Hazara University, Mansehra, Pakistan.
Junaid IqbalDepartment of Pharmacy, Qurtaba University, Peshawar, Pakistan.
Mequanente DagnawDepartment of Epidemiology and Biostatistics, Institute of Public Health, University of Gondar, Gondar, Ethiopia.ORCID 0009-0006-0290-9025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterindividual variability in antihypertensive response may be partly explained by genetic variation. The angiotensin-converting enzyme insertion/deletion polymorphism (ACE I/D; rs1799752) has been associated with variable response to renin-angiotensin-aldosterone system-targeting therapies, but evidence for valsartan-hydrochlorothiazide (Val-HCTZ) combination therapy remains limited, particularly in South Asian populations.

methodsIn this multicenter prospective cohort study, 645 hypertensive patients from Khyber Pakhtunkhwa, Pakistan, receiving fixed-dose Val-HCTZ were enrolled; 627 were included in the final analysis after excluding 18 patients with poor adherence (<80%) followed for 3 months. ACE I/D genotyping was performed by polymerase chain reaction with confirmatory testing. The primary analysis evaluated blood pressure reduction across ACE I/D genotypes using regression models adjusted for age, sex, and body mass index. Achievement of target blood pressure (<140/90 mmHg) was analyzed as a secondary outcome.

resultsGenotype distribution was in Hardy-Weinberg equilibrium (

conclusionACE I/D genotype was associated with variation in blood pressure response to fixed-dose Val-HCTZ therapy in this Pakistani cohort, with the most robust finding being poorer response among ID carriers. These findings support further investigation of ACE I/D as a candidate pharmacogenetic marker in genotype-stratified and interventional studies.

Indexed as

Antihypertensive AgentsBlood PressureHydrochlorothiazideHypertensionPeptidyl-Dipeptidase AValsartanDrug Therapy, CombinationFemaleGenotypeHumansMaleMiddle AgedPakistanPolymorphism, GeneticProspective StudiesACE protein, humanAntihypertensive AgentsHydrochlorothiazidePeptidyl-Dipeptidase AValsartanACE I/D polymorphismhypertensionpersonalized medicinePharmacogeneticsrs1799752valsartan-hydrochlorothiazide

Identifiers

PMID42535691
PMCPMC13556926

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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.