Evidence map›Paper›PMID 37948104›Full record

ArticleExperimental physiology2024

GST polymorphism as a predictive biomarker for modulating the susceptibility to chronic obstructive pulmonary disease: A North Indian study.

Harsh Yadav, Depanshi Pandit, Sidhartha Singh, Parul Sharma, Kranti Garg, Nidhi Girdhar, Karan Sharma, Vishal Chopra, Siddharth Chopra, Siddharth Sharma

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Article in Experimental physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Harsh YadavDepartment of Pulmonary Medicine Government Medical College, TB & Chest Diseases Hospital, Patiala, Punjab, India.
Depanshi PanditDepartment of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, India.
Sidhartha SinghDepartment of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, India.
Parul SharmaDepartment of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, India.
Kranti GargDepartment of Pulmonary Medicine Government Medical College, TB & Chest Diseases Hospital, Patiala, Punjab, India.
Nidhi GirdharDepartment of Pulmonary Medicine Government Medical College, TB & Chest Diseases Hospital, Patiala, Punjab, India.
Karan SharmaDepartment of Pulmonary Medicine Government Medical College, TB & Chest Diseases Hospital, Patiala, Punjab, India.
Vishal ChopraDepartment of Pulmonary Medicine Government Medical College, TB & Chest Diseases Hospital, Patiala, Punjab, India.
Siddharth ChopraDepartment of Internal Medicine, St. Joseph Mercy Oakland Hospital, Pontiac, Michigan, USA.
Siddharth SharmaDepartment of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, India.ORCID 0000-0001-9414-3771
Government Medical College · INThapar Institute of Engineering & Technology · INTrinity Health Oakland Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is commonly characterized by shortness of breath, coughing or expectoration. Smoking is the leading cause of COPD development, but only a small percentage of smokers develop symptoms, implying a genetic component. Glutathione S-transferase enzymes are responsible for detoxifying cigarette smoke components. The role of glutathione S-transferase T1 (GSTT1) and glutathione S-transferase M1 (GSTM1) gene polymorphism was assessed with COPD susceptibility and associated clinical parameters in the North Indian population. This was a cross-sectional study involving 200 COPD patients and 200 healthy individuals, with peripheral blood sampling and adequate questionnaires. Multiplex PCR was used for genotyping GSTT1 and GSTM1 gene polymorphism. Logistic regression was used to calculate the odds ratio and 95% confidence intervals to assess the COPD risk and GST polymorphisms. The GSTT1 gene deletion rate was higher in COPD cases (34.5%) than in healthy individuals (20.5%). A statistical relationship between the GSTT1(-) null genotype and COPD risk was observed (odds ratio = 2.04, 95% CI = 1.30-3.20, P = 0.0019). After adjusting for covariates like age, sex and smoking status, a significant association was found for GSTT1(-) null genotype and COPD risk (adjusted odds ratio = 2.90, 95% CI = 1.43-5.87, P = 0.003). The GSTT1(-) genotype was also significantly correlated with clinical parameters for COPD risk. Another primary observation was that females with the GSTT1(-) null genotype were more vulnerable to COPD than males with the same gene deletion. The GSTT1(-) null genotype strongly correlates with COPD development, while no association was observed in the GSTM1(-) null genotype in the North Indian population.

Indexed as

Genetic Predisposition to DiseasePulmonary Disease, Chronic ObstructiveBiomarkersCase-Control StudiesCross-Sectional StudiesFemaleGenotypeGlutathione TransferaseHumansMalePolymorphism, GeneticRisk FactorsBiomarkersGlutathione TransferaseCOPDGSTM1GSTT1multiplex PCRpolymorphism

Identifiers

PMID37948104
PMCPMC10988663
OpenAlexW4388564864

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LicenceCC BY
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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.