Psoriasis is a chronic, systemic, immune-mediated disease with an incidence of approximately 2%. The pathogenesis of the disease is complex and not yet fully understood. Genetic factors play a significant role in the pathogenesis of the disease. In predisposed individuals, multiple trigger factors may contribute to disease onset and exacerbations of symptoms. Environmental factors (stress, infections, certain medications, nicotinism, alcohol, obesity) play a significant role in the pathogenesis of psoriasis. In addition, epigenetic mechanisms are considered result in modulation of individual gene expression and an increased likelihood of the disease. Studies highlight the significant role of epigenetic factors in the etiology and pathogenesis of psoriasis. Epigenetic mechanisms in psoriasis include DNA methylation, histone modifications and non-coding RNAs. Epigenetic mechanisms induce gene expression changes under the influence of chemical modifications of DNA and histones, which alter chromatin structure and activate transcription factors of selected genes, thus leading to translation of new mRNA without affecting the DNA sequence. Epigenetic factors can regulate gene expression at the transcriptional (via histone modification, DNA methylation) and posttranscriptional levels (via microRNAs and long non-coding RNAs). This study aims to present and discuss the different epigenetic mechanisms in psoriasis based on a review of the available literature.

Introduction and objective. Psoriasis isa quite common, chronic and immune-mediated skin disorder. The prevalence of psoriasis differs in various countries, but it is said to affect 2% of the world's population in general. Psoriasis has many different clinical features but all lesions have the same characteristic: erythema, thickening and scale, although other clinical features are also connected, such as psoriatic arthritis, obesity and metabolic syndrome. All of these may lead to conditions impairing the quality of life. This review is an attempt to summarize recent data regarding environmental factors, together with epigenetic markers and processes playing an important role in psoriasis. State of knowledge. Many different environmental factors play a role in genetically predisposed patients. This is causes epigenetic alternations which may be a linking part in the whole process. Many studies have indicated a connection between psoriasis and various genes and antigens. The presence of HLA-Cw6 is common as well a strong link between its presence and the onset of psoriasis being observed. The main alternations are DNA methylation, histone's modifications and the role of microRNA. Excessive reaction is usually not present without a triggering factor. Environmental factors are mostly rated, such as drugs, life style and habits (smoking, alcohol), diet, physical trauma (skin injury provoking Koebner phenomenon), stress, microorganism and infections. Conclusions. The correlation between pathogenesis of psoriasis and environmental risk factors, together with epigenetic alternations still require more investigation. Education about diet habits, nutrition, weight loss and healthy lifestyle seems to be important during the treatment of psoriasis.

Nail psoriasis is considered a significant psychological and social problem causing functional impairment in affected patients. Nail changes hamper their daily and occupational activities and contribute to a worse quality of life. Almost 50% of patients with psoriasis vulgaris and up to 80% of patients with psoriatic arthritis are afflicted with nail lesions. The important correlation between psoriatic arthritis and nail changes is well established – the presence of the latter is a strong predictor of the development of arthritis. There is a broad spectrum of nail dystrophies associated with psoriasis, ranging from the common pitting, subungual hyperkeratosis and loosening of the nail plate to less frequent discolouration and splinter haemorrhages. Some of these symptoms are also observed in other nail diseases, and further diagnostics should be performed. The assessment tools NAPSI (Nail Psoriasis Severity Index), mNAPSI (Modified Nail Psoriasis Severity Index), and PNSS (Psoriasis Nail Severity Score) are most commonly used to grade the severity of nail involvement in psoriasis and enable the evaluation of therapy effectiveness. The treatment of nail psoriasis is a major clinical challenge. It should be adjusted to the extent of dermal, articular and ungual lesions. Systemic therapies of psoriasis, especially biological agents, are most likely to be effective in treating nail psoriasis. However, as their use is limited in scope and safety, topical therapy remains a mainstay, and the combination of corticosteroids and vitamin D3 analogues is considered to be most helpful.

Psoriasis is a chronic inflammatory dermatosis affecting 1–3% of the general population. Patients with psoriasis represent a heterogeneous population with individual disease expression – different degrees and severity of skin involvement. Psoriatic lesions in particular localizations such as the face, scalp, intertriginous or palmoplantar areas significantly reduce quality of life. Patients often feel ashamed, embarrassed, or self-conscious about their symptoms. Furthermore, genital psoriasis significantly affects sexual health. Among patients with psoriasis, the prevalence of special localizations is estimated to be 23–27% on the nails, 49% on the face, 12–16% on the palms and soles, and up to 36% in intertriginous regions. Due to peculiar features of skin in these areas, adequate and specific management is required, which is discussed in this review.

Leptin is an adipokine, adipocyte-derived compound, which acts both as a hormone and cytokine. It is mainly synthesized by adipocytes of white adipose tissue. Leptin possesses pleiotropic functions including, among others, stimulation of angiogenesis and production of proinflammatory cytokines. The various types of leptin activity are related to the wide distribution of leptin receptors. This adipokine acts by activating intracellular signaling cascades such as JAKs (Janus kinases), STATs (signal transducers and activators of transcription), and others. In a course of obesity, an increased serum level of leptin coexists with tissue receptor resistance. It has been reported that enhanced leptin levels, leptin receptor impairment, and dysfunction of leptin signaling can influence skin and hair. The previous studies revealed the role of leptin in wound healing, hair cycle, and pathogenesis of skin diseases like psoriasis, lupus erythematosus, and skin cancers. However, the exact mechanism of leptin’s impact on the skin is still under investigation. Herein, we present the current knowledge concerning the role of leptin in psoriasis and selected skin diseases.