Evidence map›Paper›PMID 32270333›Full record

ArticleClinical rheumatology2020

TGF-β1 +869C/T polymorphism increases susceptibility to rheumatoid arthritis in North Indian population.

Sipahee Lal Patel, Jaya Prakash, Varsha Gupta

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Article in Clinical rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 41% of its field
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sipahee Lal PatelRheumatology Laboratory, Department of Biotechnology, Chhatrapati Shahu Ji Maharaj University, Kanpur, India.
Jaya PrakashCommunity Health Center, Shivrajpur, Kanpur, India.
Varsha GuptaRheumatology Laboratory, Department of Biotechnology, Chhatrapati Shahu Ji Maharaj University, Kanpur, India. guptavarsha0210@gmail.com.
Chhatrapati Shahu Ji Maharaj University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRheumatoid arthritis (RA) is a heterogeneous autoimmune disease, characterized by chronic inflammation, hyperplasia (swelling), tenderness, erosion of cartilage and bones in synovial joints. Transforming growth factor-β1 (TGF-β1) is an important regulator of inflammation, and its polymorphism is implicated in several diseases. Therefore, the study was done to determine whether TGF-β1 C/T gene polymorphism was associated with RA in North Indian population.

methodsEighty-seven (male/female: 29/58) healthy controls and 76 (male/female: 17/59) RA patients were recruited for association study between TGF-β1 +869C/T polymorphism. TGF-β1 +869C/T polymorphism was genotyped by allele specific amplification refractory mutation system polymerase chain reaction (ARMS-PCR) to test susceptibility to clinical presentation of RA patients in North Indian population by comparing RA genotypes with control groups.

resultsThe genotypic association studies and dominant, recessive, and allelic models revealed that TGF-β1 +869C/T gene polymorphism is involved in the onset of RA. TGF-β1 +869 T (either TT or CT) allele and TT v/s CC (OR = 36.18, 95% CI = 11.98-109.31, P = 0.001); TT + CT v/s CC (OR = 0.16, 95% CI = 0.08-0.33, P = 0.001); TT v/s CC + CT (OR = 0.04, 95% CI = 0.1-0.09, P = 0.001); and T v/s C (OR = 0.12, 95% CI = 0.07-0.2, P = 0.001) show significant association with RA as compared with CC genotype or C alleles (P = 0.001). The patient carrying T alleles showed significant associations with increased ESR, uric acid, CRP, DAS28-ESR, and number of tender joints as compared to other genotypes. In the presence of RF, DAS-28-ESR was high in CT genotype. ESR, CRP, and swollen joint count were highest in TT genotype of RF negative patients.

conclusionsTGF-β1 polymorphism is associated with disease activity of RA. Disease activity is strongly modulated in the presence of serum RF and TGF-β1 polymorphism. Key Points •TGF-β1 +869C/T polymorphism was found to be associated with RA in the patients. •The polymorphism showed significant association with all inflammatory parameters as ESR, CRP, and DAS-28 in RA subjects. •RF negative patients showed high ESR, CRP, and swollen joint count with TT genotype. •TGF-β1 polymorphism and serum RF are modulating disease activity in RA.

Indexed as

Arthritis, RheumatoidTransforming Growth Factor beta1Asian PeopleCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMalePolymorphism, Single NucleotideTGFB1 protein, humanTransforming Growth Factor beta1ARMS-PCRGenetic polymorphismRheumatoid arthritisSusceptibilityTGF-β1 869C/T

Identifiers

PMID32270333
OpenAlexW3016042148

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