Psoriasis is a chronic, systematic, inflammatory disease in which multiple metabolic and immunologic disturbances lead to lipid abnormalities, impaired glucose tolerance, metabolic syndrome, diabetes mellitus, atherosclerosis, hypertension, ischemic heart disease, and numerous metabolic disorders. In clinical practice, the most commonly used drugs in the treatment of lipid abnormalities are statins and fibrates. Statins are characterized by pleiotropic effects such as antioxidant, anti-inflammatory, anticoagulant, and antiproliferative. They work by reducing the concentrations of low-density lipoprotein (LDL), total cholesterol, and triglycerides and stabilizing atherosclerotic plaque. Fibrates are medications, which help to lower triglycerides, LDL, very low-density lipoprotein (VLDL) levels and increase lower high-density lipoprotein (HDL). In recent years, many new drugs were found to normalize the lipid profile in patients with psoriasis: glitazones (pioglitazone, troglitazone), and glucagon-like peptide-1 (GLP-1) receptor agonists. Pioglitazone improves the lipid profile, including the decrease of triglycerides, fatty acids, and LDL, as well as the increase of HDL. Glucagon-like peptide 1 (GLP-1) analogs decrease modestly low-density lipoprotein cholesterol (LDL-C), total cholesterol, and triglycerides. The purpose of this study is to assess the current state of knowledge on the effect of different hypolipidemic treatments on the course of psoriasis. The study includes literature from medical databases PubMed and Google Scholar. We were browsing PubMed and Google Scholar until the beginning of December. The systematic review includes 41 eligible original articles.

Psoriasis is a complex, chronic, immunologically mediated disease which involves skin and joints. Psoriasis is commonly connected with numerous other diseases such as liver diseases, metabolic syndrome, impaired glucose tolerance, diabetes mellitus, atherosclerosis, hypertension, and ischemic heart disease. Interestingly, comorbidities of psoriasis are an attention-grabbing issue. Additionally, it can cause impairment of quality of life and may be associated with depressive disorders. Altered levels of ceramides in psoriatic skin may lead to anti-apoptotic and pro-proliferative states, consequently leading to an over-proliferation of keratinocytes and the development of skin lesions. The pathophysiology of psoriasis and its comorbidities is not fully understood yet. Sphingolipids (including ceramides) and their disturbed metabolism may be the link between psoriasis and its comorbidities. Overall, the goal of this review was to discuss the role of sphingolipid disturbances in psoriasis and its comorbidities. We searched the PubMed database for relevant articles published before the beginning of May 2022. The systematic review included 65 eligible original articles.

Psoriasis is a complex chronic immunologically mediated disease that may involve skin, nails, and joints. It is characterized by hyperproliferation, deregulated differentiation, and impaired apoptosis of keratinocytes. Sphingolipids, namely ceramide, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate, are signal molecules that may regulate cell growth, immune reactions, and apoptosis. Fifteen patients with psoriasis and seventeen healthy persons were enrolled in the study. Skin samples were taken from psoriatic lesions and non-lesional areas. Tissue concentration of ceramides, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate was measured by liquid chromatography. We assessed that all levels of ceramides, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate were higher in lesioned psoriatic skin than in non-affected skin. The profile of bioactive lipids in the lesional skin of patients with psoriasis differed significantly from non-involved psoriatic skin and skin in healthy subjects.

Atopic dermatitis (AD) is a chronic, complex, and immunologically mediated skin disease. Its exact cause remains complex, multifaceted and yet to be discovered but is likely related to a combination of immunological, genetic and environmental factors. A medical literature search of PubMed (1992–present), Google Schoolar and Embase was performed using appropriate terms without date limitations in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. Nevertheless, chronic inflammation is believed to be a major player in the development of AD and a causative element in the development of metabolic syndrome (MetS). Metabolic syndrome is a cluster of common metabolic abnormalities including hypertension, insulin resistance, abdominal obesity, reduced high-density lipoprotein (HDL)–cholesterol levels and elevated triglyceride levels. High waist circumference is positively correlated with the risk of atopic dermatitis, but there is no significant correlation between adult-onset atopic dermatitis and hypertension. Some evidence suggests an association between AD and hypertension but only in patients with severe AD. On the other hand, the relationship between AD and hyperglycemia or AD and cholesterol levels seems inconclusive. The aim of this review is to present current knowledge on the association between atopic dermatitis and metabolic syndrome, including each of the components of metabolic syndrome.

Psoriasis is a chronic, complex, and immunologically mediated systemic disease that not only affects the skin, but also the joints and nails. It may coexist with various other disorders, such as depression, psoriatic arthritis, cardiovascular diseases, diabetes mellitus, and metabolic syndrome. In particular, the potential link between psoriasis and metabolic syndrome is an issue worthy of attention. The dysregulation of growth factors could potentially contribute to the disturbances of keratinocyte proliferation, inflammation, and itch severity. However, the pathophysiology of psoriasis and its comorbidities, such as metabolic syndrome, remains incompletely elucidated. Growth factors and their abnormal metabolism may be a potential link connecting these conditions. Overall, the objective of this review is to analyze the role of growth factor disturbances in both psoriasis and metabolic syndrome.

This review presents the current knowledge on the potential of mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) in the treatment of various skin diseases such as psoriasis, atopic dermatitis, contact dermatitis, systemic sclerosis, graft-versus-host disease, alopecia areata, and systemic lupus erythematosus. MSCs can modulate the immune response and release growth factors and cytokines that promote tissue regeneration and healing and reduce inflammation. In turn, EVs’ ability to transport various biological molecules, including microRNAs (miRNAs), makes them potential therapeutic agents. Moreover, EVs have been shown to reduce scaling, thickness, and erythema in psoriasis. In atopic dermatitis, EVs can alleviate clinical symptoms, lower serum IgE levels, and reduce immune cell infiltration. Mesenchymal stem cells like bone marrow-derived mesenchymal stem cells (BM-MSCs) exert their immunomodulatory effects by directly targeting various immune cell populations, including T cells, B cells, dendritic cells, and natural killer (NK) cells. To fully realize the potential of EVs in clinical practice, further research is needed to conduct well-designed clinical trials to evaluate the safety and efficacy of EV-based therapies in different skin diseases. Overall, EVs have the potential to revolutionize the treatment of skin diseases by offering a targeted and effective approach to address various underlying mechanisms, although further large-scale studies are needed.