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Submitted: 17 Jul 2025
Revision: 11 Dec 2025
Accepted: 24 Dec 2025
ePublished: 30 Aug 2026
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J Res Clin Med. 2026;14: 35472.
doi: 10.34172/jrcm.35472
  Abstract View: 11
  PDF Download: 12

Original Article

Molecular Analysis of SLC22A4 Gene Polymorphisms (Rs3792876, Rs1050152) in Palindromic Rheumatism and Rheumatoid Arthritis

Aynaz Asgharvand-Hejab 1 ORCID logo, Sima Shahmohammadi–Farid 2, Azam Safary 3, Alireza Khabbazi 3, Mehdi Jafarpour 3* ORCID logo

1 Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran
2 Department of Immunology, School of Medicine, Tabriz University of Medical Science, Tabriz, Iran
3 Connective Tissue Disease Research Center, Tabriz University of Medical Science, Tabriz, Iran
*Corresponding Author: Mehdi Jafarpour, Email: jafarpourmehdi1360@gmail.com

Abstract

Palindromic rheumatism (PR) is an inflammatory rheumatic disease distinguished by episodic, self-limiting flares of arthritis or periarthritis. It may progress over time to other rheumatic diseases, particularly rheumatoid arthritis (RA). SLC22A4, located on chromosome 5, encodes an organic cation transporter (OCTN1) that mediates the transport of small molecules across cell membranes. Immune cells express OCTN1, which regulates oxidative stress, cell survival, and inflammatory signaling by transporting specific small molecules. This study analyzes the SLC22A4 gene polymorphisms in PR and RA patients compared to healthy controls (HCs). We included 27 PR patients; 40 RA patients and 40 HCs matched for age and gender. All participants were Azeri. The SLC22A4 (rs3792876 and rs1050152) polymorphisms were genotyped. No notable differences were detected between the PR and control groups in the distribution of rs3792876 genotypes (CC, CT) and alleles (C, T). In addition, we examined the frequencies of rs1050152 genotypes (CC, CT, TT) and alleles (C, T) between the studied groups. No significant differences were detected. The similar distribution of genotypes and alleles across study groups indicates that these variants are unlikely to play a major role in susceptibility to PR or RA in the Azeri population. Future research should include larger sample sizes, additional candidate polymorphisms, and exploration of potential gene–gene and gene–environment interactions to more comprehensively define the genetic landscape underlying PR and RA.
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