title: [Correlation between different clinical activity and anti CC-P (anti-cyclic citrullinated peptide antibodies) titres in rheumatoid arthritis treated with three different tumor necrosis factors TNF-alpha blockers].
abstract: TNF-alpha role in RA is confirmed by the improvement on joint inflammation and physical function and by the slowing of radiographic damage induced by TNF-alpha blockers, that also reduce Rheumatoid Factor (RF) and anti-CC-P titres. (1) To evaluate the effects of 3 TNF-alpha blockers on (a) disability (HAQ), disease activity (DAS28), acute phase reactants (ERS, CRP); (b) autoantibodies: IgM RF, anti-CCP abs. (2) To evaluate if anti-CCP abs could be useful for testing the efficacy of anti-TNF-alpha agents in the follow-up of RA patients. 34 patients with RA (25 F, 9 M; mean age: 59.1 +/- 12.1 years, mean disease duration: 9.6 +/- 2.3 years; 23/34 positive for anti-CCP abs, 19/34 for IgM RF) were enrolled: 18 received Etanercept (25 mg twice weekly subcutaneously), 8 received Infliximab (3 mg/kg intravenously every 8 weeks) and 8 Adalimumab (40 mg every 14 days). All the patients were evaluated for the above mentioned parameters at baseline (t0) and after 6 months of therapy (t6). Anti-TNF-alpha agents differently reduced HAQ and DAS28, ERS and CRP, RF and anti-CCP ab titres RA patients whose RF (14) and/or anti-CCP abs (17) titres were significantly lowered at the end of the study, at t6 presented a significant reduction in respect to t0 of VES, PCR, DAS28 and HAQ values (p < 0.05 for all comparison). This effect was not shown in patients in whose RF (5) and/or anti-CCP abs (6) titres were not reduced in respect to baseline. In RA, anti-TNF-alpha agents, especially Etanercept, reduce disability, disease activity and acute phase reactants expecially in patients showing reduction of RF and anti CC-P titres.
authors.affiliation: Unità Operativa Semplice di Reumatologia, Dipartimento Medicina Interna, Nuovo Ospedale S. Giovanni di Dio, Firenze. maubenucci@tiscali.it
authors.forename: Maurizio
authors.initials: M
authors.lastname: Benucci
authors.forename: Stefano
authors.initials: S
authors.lastname: Turchini
authors.forename: Paola
authors.initials: P
authors.lastname: Parrochi
authors.forename: Piero
authors.initials: P
authors.lastname: Boccaccini
authors.forename: Roberto
authors.initials: R
authors.lastname: Manetti
authors.forename: Emanuela
authors.initials: E
authors.lastname: Cammelli
authors.forename: Mariangela
authors.initials: M
authors.lastname: Manfredi
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000276:immunology*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D001323:Autoantibodies; D007074:Immunoglobulin G; D010456:Peptides, Cyclic; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; C487763:cyclic citrullinated peptide; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept