title: Anti-TNF-alpha treatment in rheumatoid arthritis with anti-Ro/SSA antibodies. Analysis of 17 cases among a cohort of 322 treated patients.
abstract: OBJECTIVE
  To compare the efficacy and safety of anti-TNF-alpha treatment in RA patients with and without anti-Ro antibodies, in order to detect any change in their immunological or clinical profile.
  
  
  METHODS
  Autoantibodies in 322 patients being treated with anti-TNF-alpha drugs were studied; 17 were found to be anti-Ro positive, while 305 were anti-Ro negative.
  
  
  RESULTS
  Two groups, comparable in terms of sex distribution, RA duration and anti-TNF-alpha drug employed, showed symmetrical, erosive polyarticular RA with high disease activity. Anti-TNF-alpha led to significant improvement in both groups. At baseline rheumatoid factor and ANA, globally positive in 68.6% and 40%, were more frequent in anti-Ro positive sera. ANA showed a rising trend beginning in the 6th month of treatment in both groups, which was always statistically significant compared to baseline. Anti-dsDNA antibodies, measured using either CLIFT and ELISA or the Farr assay, remained stable in the first 6 months, then increased at 12th and 18th month, and subsequently declined. No difference was detected between the two groups regarding the number or cause of dropouts, but lupus-like disease was more frequent in anti-Ro positive subjects (p = 0.012). In addition, two cases of NHL were detected.
  
  
  CONCLUSIONS
  Anti-TNF-alpha treatment was shown to be effective in patients with anti-Ro antibodies. Although anti-dsDNA and lupus-like disease were more frequent in anti-Ro positive patients, severe manifestations of systemic involvement were not observed. A longer follow-up is warranted to evaluate the risk of NHL in these patients.
authors: Rheumatology and Clinical Immunology Unit and Chair, Spedali Civili, University of Brescia, Italy. ilaricava@virgilio.it
authors: I
authors: I
authors: Cavazzana
authors: F
authors: F
authors: Bobbio-Pallavicini
authors: F
authors: F
authors: Franceschini
authors: C
authors: C
authors: Bazzani
authors: A
authors: A
authors: Ceribelli
authors: E
authors: E
authors: Bravi
authors: S
authors: S
authors: Zingarelli
authors: R
authors: R
authors: Caporali
authors: R
authors: R
authors: Cattaneo
authors: C M
authors: CM
authors: Montecucco
mesh_terms: D000368:Aged; D000974:Antibodies, Antinuclear / Q000276:immunology*; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood; D015331:Cohort Studies; D004247:DNA / Q000276:immunology; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use*; D000069285:Infliximab; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis / Q000209:etiology; D008228:Lymphoma, Non-Hodgkin / Q000175:diagnosis / Q000209:etiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000974:Antibodies, Antinuclear; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D001323:Autoantibodies; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; C035356:SS-A antibodies; D014409:Tumor Necrosis Factor-alpha; D004247:DNA; D000069285:Infliximab; D000068800:Etanercept