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Kwiek B, Narbutt J, Sysa-Jędrzejowska A, et al. Long-term treatment of chronic plaque psoriasis with biological drugs can control platelet activation: targeting the bridge between inflammation and atherothrombosis. Postepy Dermatol Alergol. 2017;34(2):131-137doi: 10.5114/ada.2017.67077.
Kwiek, B., Narbutt, J., Sysa-Jędrzejowska, A., Langner, A., & Lesiak, A. (2017). Long-term treatment of chronic plaque psoriasis with biological drugs can control platelet activation: targeting the bridge between inflammation and atherothrombosis. Postepy dermatologii i alergologii, 34(2), 131-137. https://doi.org/10.5114/ada.2017.67077
Kwiek, Bartłomiej, et al. "Long-term treatment of chronic plaque psoriasis with biological drugs can control platelet activation: targeting the bridge between inflammation and atherothrombosis." Postepy dermatologii i alergologii vol. 34,2 (2017): 131-137. doi: https://doi.org/10.5114/ada.2017.67077
Kwiek B, Narbutt J, Sysa-Jędrzejowska A, Langner A, Lesiak A. Long-term treatment of chronic plaque psoriasis with biological drugs can control platelet activation: targeting the bridge between inflammation and atherothrombosis. Postepy Dermatol Alergol. 2017 Apr;34(2):131-137. doi: 10.5114/ada.2017.67077. Epub 2017 Apr 13. PMID: 28507492; PMCID: PMC5420605.
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Postepy Dermatol Alergol. 2017 Apr;34(2):131-137. doi: 10.5114/ada.2017.67077. Epub 2017 Apr 13.

Long-term treatment of chronic plaque psoriasis with biological drugs can control platelet activation: targeting the bridge between inflammation and atherothrombosis.

Postepy dermatologii i alergologii

Bartłomiej Kwiek, Joanna Narbutt, Anna Sysa-Jędrzejowska, Andrzej Langner, Aleksandra Lesiak

Affiliations

  1. Department of Dermatology and Immunodermatology, Medical University of Warsaw, Warsaw, Poland.
  2. Department of Dermatology, Medical University of Lodz, Lodz, Poland.
  3. Department of Social Sciences, University of Social Sciences, Lodz, Poland.

PMID: 28507492 PMCID: PMC5420605 DOI: 10.5114/ada.2017.67077

Abstract

INTRODUCTION: Platelet activation is elevated in moderate to severe psoriasis, and the reduction in platelet activation during short-term treatment has already been demonstrated. Soluble P-selectin is a well-established marker of platelet activation.

AIM: To show whether the long-term treatment of psoriasis with biological drugs can reduce elevated platelet activation.

MATERIAL AND METHODS: An observational study of 27 patients with chronic plaque psoriasis, treated with infliximab, adalimumab, etanercept, or ustekinumab for up to 12 months was conducted. Psoriasis area and severity index (PASI), serum P-selectin and interleukin (IL)-6 were monitored throughout the treatment.

RESULTS: There was no significant correlation between PASI and platelet activation in our patients. After 3 months of treatment, a significant reduction in PASI and IL-6 was found, while P-selectin was not significantly reduced. When a cohort of patients who had shown elevated P-selectin prior to the treatment was evaluated, a significant reduction in P-selectin was observed in all 8 patients following 3 months; a reduction that was sustained after 6 and 12 months of therapy.

CONCLUSIONS: We conclude that PASI is not a good predictor of platelet activity in patients with PASI near to 10. Biological drugs reduce platelet activation in patients who have increased platelet activation prior to treatment, and this effect is stable during chronic therapy.

Keywords: P-selectin; atherothrombosis; biological; comorbidities; platelets; psoriasis

Conflict of interest statement

The authors declare no conflict of interest.

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