title: Biomarkers of good EULAR response to the B cell depletion therapy in all seropositive rheumatoid arthritis patients: clues for the pathogenesis.
abstract: OBJECTIVE
  To find out whether a high number of auto-antibodies can increase the probability of a "good-EULAR response" and to identify the possible biomarkers of response in seropositive rheumatoid arthritis (RA) patients undergoing the B cell depletion therapy (BCDT).
  
  
  METHODS
  One hundred and thirty-eight patients with long standing RA (LSRA), 75% non or poorly responsive to one or more TNFα blockers, all seropositive for at least one autoantibody (AAB) (RF-IgM, RF-IgA, RF-IgG, anti-MCV, ACPA-IgG, ACPA-IgA, ACPA-IgM) received one full course of BCDT. The major outcomes (moderate or good-EULAR response) were assessed after 6 months of therapy. The IL6 and BAFF levels were also determined.
  
  
  RESULTS
  At a 6-month follow-up, 33 (23.9%) of the RA patients achieved a good EULAR response. Having up to 5-AABs positivity increased the chances for treatment response. After a logistic regression analysis, however, only 4 baseline factors arose as associated with a good-EULAR response: no steroid therapy (OR = 6.25), a lymphocyte count <1875/uL (OR = 10.74), a RF-IgG level >52.1 IU/ml (OR = 8.37) and BAFF levels <1011 pg/ml (OR = 7.38). When all the AABs, except for RF-IgM and ACPA-IgG, were left in the analysis, the two final predictors were no-steroid therapy and low lymphocyte count.
  
  
  CONCLUSIONS
  The number of AABs increased the chances of being a "good-EULAR" responder. The only predictors, however, at the baseline of a good response in this seropositive cohort of RA patients were 2 simple variables--no steroids and lymphocyte count--and two laboratory assays--IgG-RF and BAFF.
authors.affiliation: Division of Rheumatology, Catholic University of the Sacred Heart, Rome, Italy. gf.ferraccioli@rm.unicatt.it
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Ferraccioli
authors.forename: Barbara
authors.initials: B
authors.lastname: Tolusso
authors.forename: Francesca
authors.initials: F
authors.lastname: Bobbio-Pallavicini
authors.forename: Elisa
authors.initials: E
authors.lastname: Gremese
authors.forename: Viviana
authors.initials: V
authors.lastname: Ravagnani
authors.forename: Maurizio
authors.initials: M
authors.lastname: Benucci
authors.forename: Edoardo
authors.initials: E
authors.lastname: Podestà
authors.forename: Fabiola
authors.initials: F
authors.lastname: Atzeni
authors.forename: Alice
authors.initials: A
authors.lastname: Mannocci
authors.forename: Domenico
authors.initials: D
authors.lastname: Biasi
authors.forename: Mariangela
authors.initials: M
authors.lastname: Manfredi
authors.forename: Piercarlo
authors.initials: P
authors.lastname: Sarzi-Puttini
authors.forename: Bruno
authors.initials: B
authors.lastname: Laganà
authors.forename: Carlomaurizio
authors.initials: C
authors.lastname: Montecucco
mesh_terms: D000368:Aged; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use; D019540:Area Under Curve; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000276:immunology / Q000628:therapy*; D001323:Autoantibodies / Q000097:blood; D053264:B-Cell Activating Factor / Q000097:blood*; D001402:B-Lymphocytes; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood*; D016015:Logistic Models; D008212:Lymphocyte Depletion; D008297:Male; D008875:Middle Aged; D012372:ROC Curve; D012189:Retrospective Studies; D000069283:Rituximab; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents; D001323:Autoantibodies; D053264:B-Cell Activating Factor; D015415:Biomarkers; C508600:IL6 protein, human; D015850:Interleukin-6; C505719:TNFSF13B protein, human; D000069283:Rituximab