Efficacy in current practice of switching between anti-tumour necrosis factor- α agents in spondyloarthropathies.
OBJECTIVE
Anti-TNF-α agents are remarkably effective in the treatment of SpAs. However, 30% of patients withdraw from anti-TNF-α agents yearly because of inadequate efficacy or side effects. The objective of this study was to assess in current practice the response to a second and a third anti-TNF-α.


METHODS
Retrospectively, all records of patients who had received at least two anti-TNF-α agents have been studied. For axial forms, treatment was considered effective if 3 months after switching the patient had a favourable expert opinion or showed an improvement in BASDAI of at least 2 on a scale of 0-10 or an improvement of 50% (BASDAI 50). For peripheral forms, the treatment was considered effective if the patient had a favourable expert opinion or if a clinical improvement of >30% of the swollen and tender joint counts was established. The reasons for switching were: (i) primary non-responder; (ii) loss of efficacy; and (iii) occurrence of side effects. To identify response predictor factors bivariate analysis was performed.


RESULTS
Three hundred and seventy-seven patients under anti-TNF-α agents were treated and 99 patients had received at least two anti-TNF-α agents. Twenty-eight of these 99 patients had been treated with three anti-TNF-α agents. Following the failure of a first anti-TNF-α, the response to a second agent was satisfactory in 80.8%. Patients who had received a third anti-TNF-α following failure of the first two also showed a satisfactory response in 82.1%. The reason for switching from the first or second agent was not predictive of the response.


CONCLUSIONS
In the event of failure or intolerance to anti-TNF-α in the treatment of SpAs, performing a first or second switch produces a satisfactory therapeutic response.
Department of Rheumatology, University Hospital of Lille, Lille Cedex, France. julienpaccouj@yahoo.fr
Julien
J
Paccou
Elisabeth
E
Solau-Gervais
Eric
E
Houvenagel
Julia
J
Salleron
Hélène
H
Luraschi
Peggy
P
Philippe
Bernard
B
Duquesnoy
René-Marc
RM
Flipo
D000068879:Adalimumab; D000328:Adult; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use*; D000069285:Infliximab; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017410:Practice Guidelines as Topic; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012189:Retrospective Studies; D025242:Spondylarthropathies / Q000188:drug therapy*; D017211:Treatment Failure; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept