TOPLINE

Anti-carbamylated fibrinogen (ACa-Fib) antibodies of immunoglobulin (Ig) G and IgA isotypes were present in some patients with very early rheumatoid arthritis (RA), including those negative for anti-cyclic citrullinated peptide (anti-CCP). IgG levels declined over 2 years, whereas IgA levels stayed stable.

METHODOLOGY

• Researchers used data from the multicentre French ESPOIR cohort to determine whether ACa-Fib antibodies (IgG and IgA) added diagnostic or prognostic value in patients with very early RA.
• They included 575 adults aged 18-70 years with untreated arthritis of under 6 months' duration who were followed up for at least 10 years. The mean age of patients was 49 years, and 76.7% were women.
• Clinical and biological data were collected at baseline and 6, 12, and 24 months. Rapid radiographic progression was defined as an increase in the total Sharp score of at least 5 points between baseline and 12 months.
• ACa-Fib IgG and IgA levels were measured using an in‑house technique, and the results were compared to antibody status, clinical data, C-reactive protein levels, patient history, and treatment outcomes.

TAKEAWAY

• At baseline, 27.8% of patients had ACa-Fib IgG and 8.4% had IgA. Among those negative for anti‑CCP, 16.6% were positive for IgG and 6.3% were positive for IgA.
• The levels and positivity for ACa Fib IgG declined over 24 months, whereas the levels and positivity for ACa Fib IgA remained largely stable.
• Higher ACa-Fib IgA levels at baseline were associated with a longer duration of smoking (P = .003) and greater cumulative smoking exposure in pack-years (P = .016).
• Baseline levels of ACa-Fib IgG were associated with an increased risk for rapid radiographic progression (global P = .004). Patients in the highest quartile of ACa‑Fib IgA also had an increased risk (P = .031).

IN PRACTICE

"[The] results support the value of ACa-Fib IgG and IgA as complementary biomarkers for improving prognostic stratification beyond established markers such as anti-CCP and RF [rheumatoid factors]," the authors of the study wrote.

SOURCE

The study was led by Pauline Brevet, MD, PhD, University of Rouen Normandy, Rouen, France. It was published online on July 27, 2026, as a brief report in Arthritis & Rheumatology.

LIMITATIONS

Some subgroup analyses had limited statistical power. The analysis focused on a single carbamylated antigen (fibrinogen).

DISCLOSURES

The study received funding from Novartis, Roche Chugai, and Lilly France. The ESPOIR cohort received support from Merck Sharp & Dohme and INSERM, with additional support from commercial and non-commercial entities. The authors did not declare any conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.