Abstract
Psoriasis is a chronic inflammatory immune-dependent genodermatosis, mainly affecting the skin, with a prevalence in the population from 1 to 5%. The pathogenesis of psoriasis is based on Th1-dependent autoimmune inflammation, which leads to a change in the aggregation properties of platelets, increased excretion of thromboxane-A2, which worsens microcirculation processes and causes the development of endothelial dysfunction. Psoriasis is associated with a number of concomitant nosologies, such as psoriatic arthritis, depression, inflammatory bowel disease and cardiometabolic syndrome. Platelets play an important role in the development of cardiovascular diseases, as mediators of hemostasis. However, the number of publications on their pathophysiological contribution to the development of cardiovascular risks in patients with psoriasis is insignificant. Understanding the role of platelet activation in psoriasis and the correct choice of laboratory methods for their assessment will allow the timely prevention of vascular platelet disorders and prognosis.
Published Version
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