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Psoriasis and IgE-mediated allergy: correlation or mutual inhibition?

A prospective cohort study in patients with mild or moderate to severe psoriasis

  • 22.07.2020
  • original article
Erschienen in:

Summary

Background

Psoriasis is an autoimmune disease caused by overactivation of TH1 (Type 1 helper cells) and TH17 (T helper 17) cells. Overactivation of TH1 cells inhibits the activity of TH2 cells involved in type 1 allergies, therefore, psoriasis patients might be less affected by type 1 allergies. This study tested if allergies were less frequent in patients with moderate to severe than with mild psoriasis.

Methods

Psoriasis patients at the study site reported possible allergy symptoms and were tested for common allergens by skin prick test and IgE levels. Psoriasis was classified by PASI scores (Psoriasis Area and Severity Index) as mild (PASI <10) or moderate/severe (PASI ≥10). Patients without systemic therapy were assessed separately. Fisher’s exact test was used to test for differences.

Results

A total of 97 patients were included, 21 with mild and 76 with moderate to severe psoriasis. Allergies were found in 27.8%, most commonly against dust mites (23.4%) and grasses (18.1%). Allergies were found in 23.8% of the patients with mild vs. 29.0% allergic patients with moderate to severe psoriasis (P = 0.786). In patients without systemic medication, allergies were found in 21.1% vs. 35.3% (P = 0.463).

Conclusion

Allergy prevalence was not reduced in patients with moderate/severe psoriasis, and generally close to the prevalence in the general Austrian population (24%). The inhibiting effect of psoriasis on type 1 allergies was not confirmed.
Titel
Psoriasis and IgE-mediated allergy: correlation or mutual inhibition?
A prospective cohort study in patients with mild or moderate to severe psoriasis
Verfasst von
Anna Essl
Dagmara Loader
Robert Feldmann
Andreas Steiner
Dr. Paul Sator
Publikationsdatum
22.07.2020
Verlag
Springer Vienna
Erschienen in
Wiener klinische Wochenschrift / Ausgabe 19-20/2021
Print ISSN: 0043-5325
Elektronische ISSN: 1613-7671
DOI
https://doi.org/10.1007/s00508-020-01683-0
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