A predominant involvement of the triple seropositive patients and others with rheumatoid factor in the association of smoking with rheumatoid arthritis
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Cristina Regueiro; Luis Rodriguez-Rodriguez; López Mejías, Raquel; Laura Nuño; Ana Triguero-Martinez; Eva Perez-Pampin; Alfonso Corrales; Alejandro Villalba; Yolanda Lopez-Golan; Lydia Abasolo; Sara Remuzgo-Martínez; Ana M. Ortiz; Eva Herranz; Ana Martínez-Feito; Carmen Conde; Antonio Mera-Varela; Alejandro Balsa; Isidoro Gonzalez-Alvaro; González-Gay Mantecón, Miguel Ángel; [et al.]Fecha
2020Derechos
Attribution 4.0 International © The Author(s)
Publicado en
Scientific Reports (2020)10:3355
Editorial
Nature Publishing Group
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Resumen/Abstract
The major environmental risk factor for rheumatoid arthritis (RA) is smoking, which according to a widely accepted model induces protein citrullination in the lungs, triggering the production of anticitrullinated protein antibodies (ACPA) and RA development. Nevertheless, some research findings do not fit this model. Therefore, we obtained six independent cohorts with 2253 RA patients for a detailed analysis of the association between smoking and RA autoantibodies. Our results showed a predominant association of smoking with the concurrent presence of the three antibodies: rheumatoid factor (RF), ACPA and anti-carbamylated protein antibodies (ACarPA) (3 Ab vs. 0 Ab: OR = 1.99, p = 2.5 × 10?8). Meta-analysis with previous data (4491 patients) confirmed the predominant association with the concurrent presence of the three antibodies (3 Ab vs. 0 Ab: OR = 2.00, p = 4.4 ×10?16) and revealed that smoking was exclusively associated with the presence of RF in patients with one or two antibodies (RF+ 1+2 vs. RF? 0+1+2: OR = 1.32, p = 0.0002). In contrast, no specific association with ACPA or ACarPA was found. Therefore, these results showed the need to understand how smoking favors the concordance of RA specific antibodies and RF triggering, perhaps involving smoking-induced epitope spreading and other hypothesized mechanisms.
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