scholarly journals AB0017 CONSTANT GENETIC MARKER IL1B T-31С IS ASSOCIATED WITH ANAMNESIS OF BIOLOGICAL DRUGS TREATMENT IN RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1312.2-1312
Author(s):  
V. Omelchenko ◽  
E. Letyagina ◽  
Y. Kurochkina ◽  
A. Akimova ◽  
A. Shevchenko ◽  
...  

Background:Rheumatoid arthritis (RA) is chronic progressive joint disease with erosions formation. Timely and effectiveness treatment is important due to quickly structural damage and progressive losing of active motion. Synthetic DMARDs didn’t have a sufficient effect. Using biological drugs seemed like a panacea, but according to investigations at least 30-40% RA-patients lost treatment efficiency. Biological drugs act through immune cascade, that’s why mutation in regulatory region of cytokine genes may partly determine treatment failure.Objectives:The objective of our study was to analyze the frequency ofIL1 T-31Csingle nucleotide polymorphism in patient with rheumatoid arthritis and its association with biological drugs prescribing.Methods:One hundred two Caucasian RA-patients (age – 56 yrs [45; 61]; DAS28 4.7 [3.8; 5.9]) were enrolled in our study. All of them had American College of Rheumatology (ACR)-defined RA (1987 classification criteria) and gave written inform consent. Single nucleotide polymorphismsIL1B T-31C(rs1143627),IL4 C-590T(rs2243250), IL10 C-592A (rs1800872),IL10 A-1082G(rs1800896) were determined by restriction fragment length polymorphism. Descriptive statistics, Chi-squared test were used for data analysis. Results are presented as median and 25th/75th percentiles (Me [25th percentile; 75th percentile]).Results:The most of SNPs analyzed had corresponded to the Hardy Weinberg equilibrium (HWE). The only exception was IL1B T-31C – the frequencies were differed statistically significant from HWE (p=0,03). Forty seven (46.1%) patients were treatment with biological drugs. Homozygotes IL1b -31CС were founded more frequently beside patients with biological treatment compare with other group (13 from 47 (27,7%) vs. 6 from 52 (11.5%), p=0,042). Other SNPs didn’t demonstrate any associations.Conclusion:Single nucleotide polymorphismIL1B T-31C(rs1143627) may be used for prognosis of basic anti-inflammatory therapy inefficiency and the needing for prescribing biological therapy.Disclosure of Interests:None declared

2012 ◽  
Vol 23 (2) ◽  
pp. 25-28
Author(s):  
Guadalupe Lima ◽  
Janette Furuzawa-Carballeda ◽  
Dolores Ramos-Bello ◽  
Juan Jakez-Ocampo ◽  
Virginia Pascual-Ramos ◽  
...  

2008 ◽  
Vol 58 (7) ◽  
pp. 2207-2208 ◽  
Author(s):  
Proton Rahman ◽  
Tara Snelgrove ◽  
Lynette Peddle ◽  
Fiotos Siannis ◽  
Vernon Farewell ◽  
...  

2019 ◽  
Vol 19 (4) ◽  
pp. 368-374 ◽  
Author(s):  
Cécile Luxembourger ◽  
Adeline Ruyssen-Witrand ◽  
Chayma Ladhari ◽  
Cécile Rittore ◽  
Yannick Degboe ◽  
...  

2019 ◽  
Vol 20 (12) ◽  
pp. 3093 ◽  
Author(s):  
Aisha M. Mergaert ◽  
Mandar Bawadekar ◽  
Thai Q. Nguyen ◽  
Laura Massarenti ◽  
Caitlyn L. Holmes ◽  
...  

Autoantibodies against citrullinated proteins are a hallmark of rheumatoid arthritis, a destructive inflammatory arthritis. Peptidylarginine deiminase 4 (PAD4) has been hypothesized to contribute to rheumatoid arthritis by citrullinating histones to induce neutrophil extracellular traps (NETs), which display citrullinated proteins that are targeted by autoantibodies to drive inflammation and arthritis. Consistent with this theory, PAD4-deficient mice have reduced NETs, autoantibodies, and arthritis. However, PAD4′s role in human rheumatoid arthritis is less clear. Here, we determine if single nucleotide polymorphism rs2240335 in PADI4, whose G allele is associated with reduced PAD4 in neutrophils, correlates with NETs, anti-histone antibodies, and rheumatoid arthritis susceptibility in North Americans. Control and rheumatoid arthritis subjects, divided into anti-cyclic citrullinated peptide (CCP) antibody positive and negative groups, were genotyped at rs2240335. In homozygotes, in vitro NETosis was quantified in immunofluorescent images and circulating NET and anti-histone antibody levels by enzyme linked immunosorbent assay (ELISA). Results were compared by t-test and correlation of rheumatoid arthritis diagnosis with rs2240335 by Armitage trend test. NET levels did not significantly correlate with genotype. G allele homozygotes in the CCP− rheumatoid arthritis group had reduced anti-native and anti-citrullinated histone antibodies. However, the G allele conferred increased risk for rheumatoid arthritis diagnosis, suggesting a complex role for PAD4 in human rheumatoid arthritis.


2012 ◽  
Vol 276 (1-2) ◽  
pp. 168-175 ◽  
Author(s):  
Liliana Portales-Cervantes ◽  
Perla Niño-Moreno ◽  
Mariana Salgado-Bustamante ◽  
Mariana H. García-Hernández ◽  
Lourdes Baranda-Candido ◽  
...  

2010 ◽  
Vol 38 (2) ◽  
pp. 264-270 ◽  
Author(s):  
JI-YIH CHEN ◽  
CHIN-MAN WANG ◽  
YEONG-JIAN JAN WU ◽  
SHIN-NING KUO ◽  
CHIUNG-FANG SHIU ◽  
...  

Objective.To investigate the association of the functional FCRL3 single-nucleotide polymorphism (SNP) −169T/C with disease phenotypes and susceptibility to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in Taiwanese.Methods.FCRL3 SNP −169T/C was genotyped in 573 patients with SLE, 670 patients with RA, and 758 controls. Genotype distributions and allele frequencies were compared among the 3 groups as aggregates or as stratified by clinical characteristics, autoantibody profile, and sex within patient groups.Results.Overall, FCRL3 SNP −169T/C was not associated with susceptibility to either SLE or RA. However, −169CC genotype was significantly reduced in leukopenia-positive SLE patients as compared to the leukopenia-negative SLE patients (CC vs CT+TT, p = 6 × 10−4, OR 0.444, 95% CI 0.279–0.708) and controls (p = 6.1 × 10−3, OR 0.583, 95% CI 0.396–0.857). On the other hand, −169TT genotypes were significantly more numerous in RA patients with non-destructive disease as compared with patients with destructive disease (CC+CT vs TT: p = 0.007, OR 1.672, 95% CI 1.149–2.432). The −169T allele frequency was also significantly increased in non-destructive RA compared with patients with destructive disease (C vs T: p = 0.010, OR 1.423, 95% CI 1.089–1.859). FCRL3 SNP −169TT homozygous donors were significantly more numerous among female cyclic citrullinated peptide (CCP)-negative RA patients versus female CCP-positive RA patients (CC+CT vs TT: p = 0.019, OR 1.64, 95% CI 1.085–2.479).Conclusion.The functional FCRL3 SNP −169T/C appears to play important roles in the development of certain phenotypes such as SLE leukopenia and RA disease severity in Taiwanese patients with SLE and RA.


2004 ◽  
Vol 5 (5) ◽  
pp. 559-569 ◽  
Author(s):  
Prabha Ranganathan ◽  
Robert Culverhouse ◽  
Sharon Marsh ◽  
Ranjeet Ahluwalia ◽  
William D Shannon ◽  
...  

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