[Monitoring of clinical course in TNF inhibitor treatment for rheumatoid arthritis--efficacy evaluation, adverse effect detection, and prediction of clinical response]

Nihon Rinsho. 2007 Jul;65(7):1269-75.
[Article in Japanese]

Abstract

Tumor necrosis factor (TNF) inhibitors, such as infliximab (INF) and etanercept (ETA), are highly effective in patients with active rheumatoid arthritis (RA), but have the potential of serious toxicity. For evaluation of treatment with TNF inhibitors, RA patients should be determined for the ACR core set of measures, including tender joint count, swollen joint count, pain score, patient global assessment, physician global assessment, patient-reported functional disability, and acute phase reactants (ESR and CRP), and more practically for the 28-joint Disease Activity Score (DAS28) within the first 3-6 months, and the efficacy could be assessed using the ACR preliminary criteria and the EULAR criteria. Post-marketing surveillance of INF and ETA in Japan indicated that the most serious adverse effects were bacterial pneumonia, pneumocytosis, and interstitial pneumonia, as well as tuberculosis. Infections must be carefully monitored in the patients, particularly those with > or =65 years of age, diabetes, and pulmonary disease. So far no clinical predictors of response to TNF inhibitors have been identified, but genetic variation in the HLA-DRB1 and the LTA-TNF regions was shown to influence the response.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Antibodies, Monoclonal / adverse effects
  • Antibodies, Monoclonal / therapeutic use*
  • Antirheumatic Agents / adverse effects
  • Antirheumatic Agents / therapeutic use*
  • Arthritis, Rheumatoid / diagnosis
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / etiology
  • Arthritis, Rheumatoid / physiopathology
  • Drug Monitoring
  • Etanercept
  • Forecasting
  • HLA-DR Antigens / genetics
  • HLA-DRB1 Chains
  • Humans
  • Immunoglobulin G / adverse effects
  • Immunoglobulin G / therapeutic use*
  • Infliximab
  • Pharmacogenetics
  • Pneumonia / etiology
  • Receptors, Tumor Necrosis Factor / therapeutic use*
  • Treatment Outcome
  • Tuberculosis / etiology
  • Tumor Necrosis Factor-alpha

Substances

  • Antibodies, Monoclonal
  • Antirheumatic Agents
  • HLA-DR Antigens
  • HLA-DRB1 Chains
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Infliximab
  • Etanercept