title: [Is the response to anti-TNFalpha treatment influenced by the presence of IgM rheumatoid factor, in Rheumatoid Arthritis patients?].
abstract: OBJECTIVE
  To verify if the response to TNFalpha inhibitors is influenced by the presence of IgM rheumatoid factor (RF), in patients with RA.
  
  
  METHODS
  In this study, the patients with the diagnosis of RA treated with TNFa inhibitors followed in our hospital were recruited. A protocol was applied including demographic, clinical and laboratory data, in order to calculate DAS 28. The presence/absence of IgM RF and associated therapies were record.
  
  
  RESULTS
  Fifty-seven patients, 52 female, with a mean duration of anti-TNFa treatment of 30,9+/-15,9 months were studied. Twenty-four patients were being treated with infliximab, 17 with adalimumab and 16 with etanercept. Forty-one patients had IgM RF detectable in serum (RF positive group). In the RF positive group, the variation of DAS 28 was -1,75 +/- 1,53 vs -1,04 +/- 1,76 in the RF negative group (p=0,135). The mean duration of anti-TNFalpha treatment was similar in both groups (31,9+/-15,9 vs 29,5+/-16,16 months). Patients who were treated with methotrexate presented a higher variation of DAS 28 (-1,87 +/- 1,70 vs -0,80 +/- 1,09; p=0,041) and this variation was dose dependent (p=0,056).
  
  
  CONCLUSIONS
  Despite needing a replication in a larger cohort, our results suggest that the presence of IgM RF in the serum did not interfere with the response to treatment with TNFalpha inhibitors.
authors.affiliation: Serviço de Reumatologia do Centro Hospitalar de Lisboa Ocidental (CHLO), EPE, Hospital Egas Moniz, Lisboa, Portugal. filipamourao@yahoo.com
authors.forename: Ana Filipa
authors.initials: AF
authors.lastname: Mourão
authors.forename: Fm Pimentel
authors.initials: FP
authors.lastname: Santos
authors.forename: Sandra
authors.initials: S
authors.lastname: Falcão
authors.forename: Rita
authors.initials: R
authors.lastname: Barros
authors.forename: Teresa Laura
authors.initials: TL
authors.lastname: Pinto
authors.forename: Alexandra
authors.initials: A
authors.lastname: Mendes
authors.forename: Walter
authors.initials: W
authors.lastname: Castelão
authors.forename: Patrícia
authors.initials: P
authors.lastname: Nero
authors.forename: João Eurico
authors.initials: JE
authors.lastname: Fonseca
authors.forename: António Alves
authors.initials: AA
authors.lastname: Matos
authors.forename: Jaime C
authors.initials: JC
authors.lastname: Branco
mesh_terms: D000068879:Adalimumab; 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*; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood* / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012189:Retrospective Studies; D012217:Rheumatoid Factor / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D012217:Rheumatoid Factor; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept