Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Viewpoint
  • Published:

Why do some biologic agents induce psoriasis or psoriasiform lesions?

Nature Clinical Practice Rheumatology volume 4, pages 168–169 (2008)Cite this article

Evolving knowledge of the pathogenesis of autoimmune diseases has led to new treatment targets. Cytokine inhibitors, antibodies directed to B-cell antigens and cell-adhesion proteins, and inhibitors or modulators of T-cell activation are now on the market, and are increasingly used for the treatment of various immune inflammatory disorders.1

Tumor necrosis factor (TNF) blockers were the first biologic agents approved for the treatment of inflammatory bowel disease and rheumatoid arthritis (RA), and, subsequently, for the treatment of other immune-mediated disorders. Several types of skin lesions have been associated with the use of TNF blockers, including drug-related eruptions, vasculitis and skin infections.2 The first reported case of anti-TNF-induced psoriasis was in a patient with RA.3 More than 50 cases have now been described worldwide and, in most instances, the development of psoriasis was associated with the use of infliximab. Plaque and palmoplantar psoriasis are the most common forms of psoriasis induced by these biologic agents and, in more than half of the reported cases, the diagnosis of psoriasis was ascertained by histological confirmation and on clinical grounds.3 The onset of skin symptoms usually occurs well after the introduction of TNF antagonists: in the first reported case, psoriasis developed after the patient's seventh infusion of infliximab.3 Psoriasiform lesions tend to persist if treatment is continued or if one type of TNF inhibitor is exchanged for another; in most patients, lesions have resolved after discontinuation of anti-TNF therapy. It should be noted that psoriasis is not induced in all patients who are treated with anti-TNF therapy, and no reports of worsening of plain psoriatic skin lesions have been described in patients receiving this treatment.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

References

  1. Williams RO et al. (2007) Cytokine inhibitors in rheumatoid arthritis and other autoimmune diseases. Curr Opin Pharmacol 7: 412–417

    Article  CAS  Google Scholar 

  2. Flendrie M et al. (2005) Dermatological conditions during TNF-alpha-blocking therapy in patients with rheumatoid arthritis: a prospective study. Arthritis Res Ther 7: R666–676

    Article  CAS  Google Scholar 

  3. Grinblat B and Scheinberg M (2007) The enigmatic development of psoriasis and psoriasiform lesions during anti-TNF therapy: a review. Semin Arthritis Rheum [doi: 10.1016/j.semarthrit.2007.05.004]

  4. Carter JD (2006) Tumor necrosis factor inhibition causing psoriasis? A more plausible explanation exists. Ann Rheum Dis 65: 1680

    Article  CAS  Google Scholar 

  5. Hueber AJ and McInnes IB (2007) Immune regulation in psoriasis and psoriatic arthritis. Recent developments. Immunol Lett [doi: 10.1016/j.imlet.2007.08.009]

  6. de Gannes GC et al. (2007) Psoriasis and pustular dermatitis triggered by TNF-(alpha) inhibitors in patients with rheumatologic conditions. Arch Dermatol 143: 223–231

    CAS  PubMed  Google Scholar 

  7. Lowes MA et al. (2007) Pathogenesis and therapy of psoriasis. Nature 445: 866–873

    Article  CAS  Google Scholar 

  8. Torti DC and Feldman SR (2007) Interleukin-12, interleukin-23, and psoriasis: current prospects. J Am Acad Dermatol 57: 1059–1068

    Article  Google Scholar 

  9. Fife DJ et al. (2007) Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and the cytokine profiles. Dermatol Online J 13: 4

    PubMed  Google Scholar 

  10. Dass J et al. (2007) Development of psoriasis after B cell depletion with rituximab. Arthritis Rheum 56: 2715–2718

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. IMM Laurindo is Assistant Professor of Medicine in the Division of Rheumatology at the University of São Paulo, Brazil.,

    Ieda MM Laurindo

  2. M Scheinberg is a Physician and Research Associate at the Hospital Israelita Albert Einstein, and Scientific Director and Head of the Clinical Trials Unit at the Hospital Abreu Sodré-AACD (a bone and joint hospital), São Paulo, Brazil.,

    Morton Scheinberg

Authors
  1. Ieda MM Laurindo
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Morton Scheinberg
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Morton Scheinberg.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Laurindo, I., Scheinberg, M. Why do some biologic agents induce psoriasis or psoriasiform lesions?. Nat Rev Rheumatol 4, 168–169 (2008). https://doi.org/10.1038/ncprheum0738

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/ncprheum0738

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing