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Abstract Number: 2151

Abatacept Related Infections: No Association with Gammaglobulin Reduction

Valquiria Dinis1, Vilma S. T. Viana1, Elaine P. Leon1, Clovis A Silva2, Carla G.S. Saad3, Julio C. B. Moraes3, Eloisa Bonfá3 and Ana C.M. Ribeiro4, 1Rheumatology, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil, 2Pediatric Rheumatology Unit, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil, 3Rheumatology Division, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil, 4Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Abatacept, co-stimulation, infection and rheumatoid arthritis (RA)

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Session Information

Title: Infections, Infection-related Biomarkers and Impact of Biologic Therapies

Session Type: Abstract Submissions (ACR)

Background/Purpose

A recent study reported that abatacept (ABA) reduces rheumatoid arthritis  (RA) related autoantibodies and gammaglobulins levels. However, the possible association of these findings with infections was not assessed. The aim of this study was, therefore, to evaluate immunoglobulins levels and infections in RA patients treated with ABA compared to anti-TNF agents, biological agents without any effect in immunoglobulin production.

Methods

Eighteen RA (ACR criteria) patients undergoing abatacept (ABA-RA) were selected and compared to 18 patients treated with anti-TNF (aTNF-RA) agents. Total and specific (IgG, IgM and IgA) gammaglobulin levels were assessed before and 6 months after biological treatment. Before entry, all patients were vaccinated for influenza/ pneumococcus and they were evaluated for tuberculosis. A systematic clinical screening protocol for infection was performed before each dose and at least monthly and when indicated virus, bacteria and fungus etiologies were investigated. Central nervous system, upper/lower respiratory tracts, cutaneous, gastrointestinal and genitourinary infections were classified in mild/moderate or severe (hospitalization). Demographic, clinical and laboratory data were also collected. Exclusion criteria were: low gammaglobulin level at baseline (<0.7) and previous abatacept or rituximab treatments. 

Results

At baseline, median current age (55 vs. vs. 53 years, p=0.96), frequencies of female gender (78 vs. 78%, p=1.0), DAS28 (5.73 vs. 5.67, p=0.34), ESR (21.5 vs. 22mm/1sth, p=0.84.), CRP (15.5 vs. 12mg/dL, p=0.37) and lymphocyte counts (2,200 vs. 1,800/mm3, p=0.42) were comparable in ABA-RA and aTNF-RA groups. Medians of gammaglobulin (1.4 vs. 1.35 g/dL, p=0.71), IgG (1167.5 vs. 1078.5 mg/dL, p=0.84), IgM (107.2 vs. 112.6 mg/dL, p=0.38) and IgA (333 vs. 322 mg/dL, p=0.74) were also alike in both groups. At 6 months, median percentage variations of gammaglobulin levels from baseline were distinct with a significant reduction for ABA-RA compared to aTNF-RA: total (-20 vs. +4%, p<0.001), IgG (-11 vs. +8 %, p<0.001), IgM (-15 vs+26%, p<0.001), IgA (-13 vs. +2%, p=0.002). Frequency of infections was similar in both groups (61 vs. 67%, p=0.73) with only one severe infection in ABA–RA and no death. Respiratory tract was the most frequent site in both groups (33 vs. 50%, p=0.34) followed by skin (29%) in aTNF-RA and urinary tract (28%) in ABA-RA. Of note, antibiotics or antifungal therapy were indicated less often for ABA than aTNF (44 vs. 85%, p= 0.028). ABA patients with and without infections had comparable levels at baseline and 6 months of IgG (p=0.28 and p=0.08) and IgM (p=0.78 and p=0.83). 

Conclusion

The present work provides novel data demonstrating that infection in ABA-RA patients is not associated with the observed reduction in gammaglobulins induced by this co-stimulatory agent. Infections seems, however, to be less severe with this agent than with aTNF agents.


Disclosure:

V. Dinis,
None;

V. S. T. Viana,
None;

E. P. Leon,
None;

C. A. Silva,

FAPESP 2009/51897-5, CNPq 302724/2011-7 and Federico Foundation ,

2;

C. G. S. Saad,
None;

J. C. B. Moraes,
None;

E. Bonfá,
None;

A. C. M. Ribeiro,
None.

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