Effect of biologics targeting interleukin‐23/‐17 axis on subclinical atherosclerosis: results of a pilot study

Summary Background Psoriasis is associated with an increased risk of developing atherosclerotic vascular disease. The hypothesis that treatment of the skin inflammation may decrease the risk of developing atherosclerosis and consequently, cardiovascular disease, is currently a focus of significant a...

Full description

Saved in:
Bibliographic Details
Published inClinical and experimental dermatology Vol. 45; no. 5; pp. 560 - 564
Main Authors Marovt, M., Marko, P. B., Pirnat, M., Ekart, R.
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.07.2020
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Summary Background Psoriasis is associated with an increased risk of developing atherosclerotic vascular disease. The hypothesis that treatment of the skin inflammation may decrease the risk of developing atherosclerosis and consequently, cardiovascular disease, is currently a focus of significant attention. Aim To assess the effect of biologic drugs targeting the interleukin (IL)‐23/IL‐17 axis on selected subclinical atherosclerosis parameters in patients with psoriatic disease. Methods In a series of patients with moderate to severe psoriasis who were eligible for biologic therapy, pulse wave velocity (PWV) and intima–media thickness (IMT) were determined before therapy and after 6 months of treatment with biologics (ustekinumab, secukinumab, ixekizumab). Results After 6 months of treatment, a marked clinical improvement of skin lesions was observed in all patients. No significant changes in PWV or IMT values were observed before (8.59 ± 1.96 mm and 0.54 ± 0.9 mm, respectively) and after 6 months (8.89 ± 2.02 mm and 0.53 ± 0.9 mm) of therapy (P = 0.16 and P = 0.74). Conclusions Systemic treatment of patients with a psoriatic disease with biologics targeting the IL‐23/IL‐17 axis has a possibly neutral effect on atherosclerosis. Additional studies are needed to assess the impact of newer biologic treatments on atherosclerosis.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0307-6938
1365-2230
DOI:10.1111/ced.14180