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Abstract
Psoriasis is one of the most common chronic recurrent systemic autoimmune multifactorial diseases, in which the skin, joints, internal organs and systems of the body are involved in the pathological process. Despite the significant prevalence of psoriasis and a large number of studies on this problem, there is still no single view on the pathogenesis of this dermatosis. To objectively understand the pathogenesis of psoriasis, it is necessary to take into account the insufficiently studied comorbidity of this pathology. Recently, an indisputable link between psoriasis and obesity has been proven. The scientific literature widely covers the issue of identical pathogenetic mechanisms of inflammatory processes in psoriasis and obesity. Given the current data on the role of systemic inflammation underlying the development of both psoriasis and obesity, the study of molecular mechanisms of its development and taking into account the role of proinflammatory nuclear transcription factors, thiazolidinediones are the pathogenetically justified drugs of choice for treatment of these diseases. In this study, we determined the effectiveness of using 15 mg of pioglitazone once a day for 6 months in the treatment of patients with extensive psoriasis vulgaris of moderate severity and concomitant grade І-ІІ alimentary obesity by clinical and immunological examination of systemic inflammation. Analyzing the results of the study, it was found that long-term use of pioglitazone, even in small doses, led to a decrease in systemic inflammation and contributed to a milder course of psoriasis in recurrence of the disease.
Highlights
Psoriasis is the most common chronic, genetically determined autoimmune, polyetiological inflammatory disease with impaired epidermal proliferation, provoked by exogenous and endogenous factors, manifested on the skin by erythematous and scaly papules and plaques with the involvement of the internal organs in the patho-Том 24, N 5-6 2020 р.logical process
Given the current role of systemic inflammation underlying the development of both psoriasis and obesity, the study of the molecular mechanisms of its development and taking into account the role of proinflammatory nuclear transcription factors (NTF), especially NFkB, activator protein-1, and the anti-inflammatory activity of other NTF receptors that are activated by PPAR [5, 6]
The aim of the study is to examine the effectiveness of pioglitazone at a dose of 15 mg per day for 6 months in the comprehensive treatment of patients with extensive psoriasis vulgaris of moderate severity, progressive stage, and concomitant grade I-II alimentary obesity by clinical and immunological examination of systemic inflammation
Summary
Psoriasis is the most common chronic, genetically determined autoimmune, polyetiological inflammatory disease with impaired epidermal proliferation, provoked by exogenous and endogenous factors, manifested on the skin by erythematous and scaly papules and plaques with the involvement of the internal organs in the patho-Том 24, N 5-6 2020 р.logical process. Obesity develops due to disorders of metabolism and eating behavior It is characterized by the accumulation of adipose tissue in the body. According to the results of the study, alimentary obesity in patients with psoriasis leads to metabolic disorders complicating the course of dermatosis, leading to worsening of patients’ DLQI, ineffectiveness of standard therapies and frequent exacerbations of psoriasis [3, 4]. Given the current role of systemic inflammation underlying the development of both psoriasis and obesity, the study of the molecular mechanisms of its development and taking into account the role of proinflammatory nuclear transcription factors (NTF), especially NFkB, activator protein-1, and the anti-inflammatory activity of other NTF receptors that are activated by PPAR [5, 6]. Pioglitazone binds to the PPARγ1, PPARγ2 and PPARδ receptors (double agonist PPARγ – PPARδ) with high affinity, being its potent activator, which promotes the suppression of proinflammatory cytokine production in macrophages – by inhibiting the nuclear transcription factor NFkB [7]
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