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Concentrations of BAFF Correlate with Autoantibody Levels, Clinical Disease Activity, and Response to Treatment in Early Rheumatoid Arthritis

SILVIA BOSELLO, PIERRE YOUINOU, CAPUCINE DARIDON, BARBARA TOLUSSO, BOUTAHAR BENDAOUD, DONATELLO PIETRAPERTOSA, ALESSIA MORELLI, and GIANFRANCO FERRACCIOLI

ABSTRACT.

Objective.
To determine whether levels of B cell activating factor (BAFF), a member of the tumor necrosis factor family, relate to autoantibody levels, disease activity, and response to treatment in patients with early rheumatoid arthritis (ERA).

Methods. BAFF was measured by ELISA in 48 early RA patients; 21 were examined serially. These data were compared with 49 controls with longstanding RA (LSRA), 48 disease controls (DC), and 50 healthy controls (HC).

Results. BAFF levels were higher in ERA, compared with DC and HC [median 4.3 ng/ml (5th-95th: 0.8–38.8) vs 0.9 ng/ml (5th-95th: 0.7–4.5) and 2.0 ng/ml (5th-95th: 0.7–5.68), respectively; p < 10-4 both comparisons], but not with LSRA controls [median 8.7 ng/ml (5th-95th: 0.8–46.1); p = nonsignificant]. BAFF correlated with the titers of IgM rheumatoid factor and anti-cyclic citrullinated peptide autoantibody (r = 0.76 and r = 0.49; p < 0.00001, p = 0.0001 for the 2 correlations), and with the number of swollen joints (r = 0.37; p = 0.01). The followup study of 21 methotrexate-treated ERA patients revealed reduced levels of BAFF, with parallel improvement in clinical activity and decrease in autoantibody titers.

Conclusion. Elevated BAFF in a subset of ERA patients is related to autoantibody levels and synovitis. BAFF level diminished with treatment, along with autoantibody titers, suggesting a rationale to treat ERA patients with BAFF-targeted agents. (First Release June 1 2008; J Rheumatol 2008; 35:1256-64)

Key Indexing Terms:

B CELL ACTIVATING FACTOR
EARLY RHEUMATOID ARTHRITIS
DISEASE ACTIVITY
RHEUMATOID FACTOR
ANTI-CYCLIC CITRULLINATED PEPTIDE


From the Division of Rheumatology, Catholic University of the Sacred Heart, Rome, Italy; and Laboratory of Immunology, University Medical School, Brest, France.

Dr. Bosello is supported by a Leonardo da Vinci European scholarship.

S. Bosello, MD, Division of Rheumatology, Catholic University of the Sacred Heart; P. Youinou, MD, DSc; C. Daridon, PhD, Laboratory of Immunology, University Medical School Brest; B. Tolusso, MB, Division of Rheumatology, Catholic University of the Sacred Heart; B. Bendaoud, Pharm D, Laboratory of Immunology, University Medical School Brest; D. Pietrapertosa, MD; A. Morelli, MD; GF. Ferraccioli, MD, Professor, Director, Division of Rheumatology, Catholic University of the Sacred Heart.

Address reprint requests to Prof. GF. Ferraccioli, Division of Rheumatology, UCSC — Catholic University of Rome, Via G. Moscati 31, 00168 Rome, Italy. E-mail: gf.ferraccioli@rm.unicatt.it

Accepted for publication January 23, 2008.




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