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Related Experiment Videos

Triggered psoriasis.

R Wolf1, V Ruocco

  • 1Department of Dermatology, Tel-Aviv Sourasky Medical Center, Ichilov Hospital, Israel. wolf_r@netvision.net.il

Advances in Experimental Medicine and Biology
|December 22, 1999
PubMed
Summary
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Antimalarials can trigger existing psoriasis by inhibiting transglutaminase (TGase) activity, altering epidermal barrier function. This study confirms hydroxychloroquine sulfate (HCQS) inhibits TGase, suggesting it provokes psoriasis in predisposed individuals.

Area of Science:

  • Dermatology
  • Pharmacology
  • Biochemistry

Background:

  • Conflicting reports exist on antimalarial use in psoriatic patients.
  • Antimalarials are known to trigger psoriasis, unlike lithium or beta-blockers which can induce it de novo.
  • A hypothesis suggests antimalarials trigger psoriasis by modulating transglutaminase (TGase) activity due to structural similarities with TGase inhibitors.

Purpose of the Study:

  • To investigate the effect of hydroxychloroquine sulfate (HCQS) on cultured human skin and TGase activity.
  • To verify the hypothesis that antimalarials trigger psoriasis via TGase modulation.

Main Methods:

  • Review of 18 English-language publications on antimalarials and psoriasis.
  • In vitro experiments using cultured human skin explants.

Related Experiment Videos

  • Assay of TGase activity in the presence of varying concentrations of HCQS.

    • Main Results:

    • Significant changes in epidermal morphology were observed in skin explants treated with HCQS.
    • HCQS demonstrated a concentration-dependent inhibition of TGase activity.
    • Antimalarials were found to trigger, rather than induce de novo, psoriasis in most cases.

    Conclusions:

    • HCQS inhibits TGase activity, potentially disrupting the epidermal barrier function.
    • This disruption triggers a physiological response leading to epidermal proliferation, which may manifest as psoriasis in susceptible individuals.
    • Antimalarials primarily act as triggers for latent psoriasis, not as primary inducers.