Anti-TNFα discontinuation in rheumatoid and psoriatic arthritis: is it possible after disease remission?

Autoimmun Rev. 2011 Aug;10(10):636-40. doi: 10.1016/j.autrev.2011.04.015. Epub 2011 Apr 21.

Abstract

Anti-TNFα blockers have rapidly become a standard treatment for rheumatoid (RA) and psoriatic arthritis (PsA) because of their acceptable safety profile and efficacy. Clinical and radiological remission may now be a realistic outcome and constitutes the best achievable state. However, clinical practice guidelines and consensus statements on the criteria of introduction, duration and cessation of treatment are under constant revision. Evidence supports that the early use of biologic DMARDs would produce rapid and sustained suppression of inflammatory disease and preserve function and joint erosions. Proof of this concept, anti-TNFα agents would be effective in maintaining response after cessation of treatment. Conversely, when therapy with anti-TNFα is withdrawn, the disease rapidly returns. Remission may be defined as minimal or no clinically detectable disease activity in the presence of continuing drug treatment and a rapid control of disease activity may prevent irreversible damage and disability. The use of US-PD and MRI in the early detection of disease recurrence could become necessary to prevent the relapse and direct the clinician's choice concerning a re-treatment regimen. The use of biological treatment can be for a limited period, at a time when it has the greatest opportunity to make the difference.

Publication types

  • Review

MeSH terms

  • Animals
  • Antirheumatic Agents / pharmacology
  • Antirheumatic Agents / therapeutic use*
  • Arthritis, Psoriatic / drug therapy*
  • Arthritis, Psoriatic / physiopathology
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / physiopathology
  • Humans
  • Practice Guidelines as Topic
  • Remission Induction
  • Secondary Prevention
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Withholding Treatment

Substances

  • Antirheumatic Agents
  • Tumor Necrosis Factor-alpha