Abstract

Psoriasis is an immune-mediated skin disease associated with an increased risk of comorbidities and a significant negative impact on the quality of life of patients. In moderate and severe forms of psoriasis it is necessary to assign systemic therapies. The newest paradigm of treatment has become possible as a result of constant deepening of knowledge of pathophysiology of the disease. A clear mechanism is finally known down to the molecular level as to which cytokines are involved in the pathogenesis of psoriatic disease. Interleukin (IL)-23 mediates the activation of the Th17 pathway, which is hypothesised to be a major contributor to he inflammation observed in psoriasis, as proven, among other things, by the high efficacy of IL-23 inhibitor biological agents. It is obvious that great progress has been made in the field of genetically engineered biological therapy for psoriasis, both in terms of safety and efficacy. However, the issue of selecting a biologic drug individually in each patient is pressing, including in the case of initiation of the first genetically engineered biological drug in bionaive patients. The article provides an overview of the key points in the process of biological drug selection depending on the present comorbidities, and also describes a clinical case of successful therapy of a bionaive patient with concomitant depressive disorder in the anamnesis against the backdrop of a severe course of psoriasis. Successful use of IL-23 inhibitor (Guselkumab) allowed to achieve persistent remission and improve the quality of life, which in turn had a positive effect on the patient’s comorbid profile. This observation allows us to conclude that the use of guselkumab as the first biological agent is a rather effective, safe and promising option in the treatment of severe psoriasis.

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