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Войти в исследования Arthritis & rheumatology (Hoboken, N.J.) · 2026
Anti-Carbamylated Fibrinogen Autoantibodies of IgG and IgA Isotypes Contribute to a Better Prognostic Stratification in Very Early Rheumatoid Arthritis: Data From the French National ESPOIR Cohort.
СтатьяНазвание и аннотация: Перевод в очереди
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Brevet Pauline, Guérin Olivia, Le Goaréguer Léna, Halbourg Élisa, Golinski Marie-Laure, Candon Sophie, Boyer Olivier, Lequerré Thierry, Schaeverbeke Thierry, Devauchelle-Pensec Valérie, Vittecoq Olivier, Fréret Manuel
Аннотация
OBJECTIVE: The aim of this study was to investigate the prevalence and longitudinal evolution of anti-carbamylated fibrinogen antibodies (ACa-Fib) of IgG and IgA isotypes in early rheumatoid arthritis (RA) and determine whether these antibodies provide additional diagnostic and prognostic information beyond anti-cyclic citrullinated peptide (anti-CCP) antibodies and rheumatoid factors.
METHODS: ACa-Fib IgG and IgA were quantified by in-house enzyme-linked immunosorbent assay at baseline and 6 and 24 months in 619 patients with available 2010 American College of Rheumatology/EULAR classification criteria, including 575 patients with RA, from the French ESPOIR cohort. Clinical, biologic, and radiographic data were collected. Multivariable models and appropriate statistical analyses were used to assess associations between ACa-Fib levels and disease activity, therapeutic response, smoking exposure, C-reactive protein concentrations, and structural progression.
RESULTS: At baseline, ACa-Fib IgG and IgA were detected in 16.6% and 6.3% of patients with anti-CCP-negative RA, respectively. Baseline ACa-Fib levels were not associated with therapeutic response or remission. Over 24 months, ACa-Fib IgG levels decreased, whereas IgA levels remained stable. Higher ACa-Fib IgA levels were associated with longer smoking duration (P = 0.003) and cumulative smoking exposure (P = 0.016). Patients in the highest quartile of ACa-Fib IgG (≥20.29 arbitrary units [AU]) had an increased risk of rapid radiographic progression (global P = 0.004). Despite its markedly lower prevalence, ACa-Fib IgA (≥3.07 AU) was also associated with structural progression (odds ratio 1.9, 95% confidence interval 1.1-3.4, P = 0.031).
CONCLUSION: The distinct longitudinal behavior and prognostic associations of ACa-Fib IgG and IgA highlight a previously underappreciated component of the anti-carbamylated protein response and support their utility as complementary biomarkers for improved risk stratification in early RA.
METHODS: ACa-Fib IgG and IgA were quantified by in-house enzyme-linked immunosorbent assay at baseline and 6 and 24 months in 619 patients with available 2010 American College of Rheumatology/EULAR classification criteria, including 575 patients with RA, from the French ESPOIR cohort. Clinical, biologic, and radiographic data were collected. Multivariable models and appropriate statistical analyses were used to assess associations between ACa-Fib levels and disease activity, therapeutic response, smoking exposure, C-reactive protein concentrations, and structural progression.
RESULTS: At baseline, ACa-Fib IgG and IgA were detected in 16.6% and 6.3% of patients with anti-CCP-negative RA, respectively. Baseline ACa-Fib levels were not associated with therapeutic response or remission. Over 24 months, ACa-Fib IgG levels decreased, whereas IgA levels remained stable. Higher ACa-Fib IgA levels were associated with longer smoking duration (P = 0.003) and cumulative smoking exposure (P = 0.016). Patients in the highest quartile of ACa-Fib IgG (≥20.29 arbitrary units [AU]) had an increased risk of rapid radiographic progression (global P = 0.004). Despite its markedly lower prevalence, ACa-Fib IgA (≥3.07 AU) was also associated with structural progression (odds ratio 1.9, 95% confidence interval 1.1-3.4, P = 0.031).
CONCLUSION: The distinct longitudinal behavior and prognostic associations of ACa-Fib IgG and IgA highlight a previously underappreciated component of the anti-carbamylated protein response and support their utility as complementary biomarkers for improved risk stratification in early RA.