# Understanding the Intricate Pathophysiology of Psoriasis and Related Skin Disorders
## 4 Sporiasis and Associated Dermatologic Disorders
Elevated IL-31 levels were specifically observed in psoriasis patients with pruritus, though no clear link was found between IL-31 levels and the severity of the disease or the intensity of the itch. CSU patients with higher antinuclear antibody titers exhibited significantly higher IL-31 levels, suggesting a potential link between IL-31 and autoimmune aspects of CSU. The exact role of IL-31 in these diseases remains unclear, indicating a need for further research [18]. In the systematic review by [PERSON] et al. from 2021, several key associations and common mechanisms between psoriasis and urticaria are discussed. Both conditions are marked by chronic inflammation; psoriasis features persistent inflammation with well-defined plaques, while urticaria involves transient wheels and angioedema. The immune system plays a crucial role in both disorders. Psoriasis is driven by T-helper 17 (Th17) cells, whereas urticaria is associated with mast cell activation and immunoglobulin E (IgE) -mediated hypersensitivity reactions. Emerging evidence suggests that disruptions in the gut microbiome can influence systemic inflammation and immune responses, impacting both conditions. Alterations in gut microbiota have been linked to changes in immune function and inflammation in these skin disorders [19]. Mast cells (MCs) play a significant role in the pathogenesis of both psoriasis and CSU. In psoriasis, the role of MCs remains an area of ongoing research. Genetic predispositions and immune responses, involving Th1 and Th17 cells, dendritic cells, NK T cells, macrophages, and keratinocytes, contribute to the disease. In CSU, particularly when complicated by Kounis syndrome, MCs can significantly impact disease progression. Kounis syndrome, characterized by severe allergic reactions or anaphylaxis leading to coronary artery spasms or myocardial infarction due to MCs degranulation, involves various triggers such as certain drugs and foods. Management includes revascularization, corticosteroids, antihistamines, and careful use of vasodilators. Understanding MCs' roles could offer new therapeutic avenues for managing these complex skin diseases [20]. Both conditions are characterized by neurogenic inflammation, where sensory nerves in the skin release neuropeptides that exacerbate inflammation. MCs play a central role in the pathology of both diseases. In psoriasis, they contribute to chronic inflammation by secreting mediators that promote disease progression. In CSU, MCs are crucial for developing lives through the release of histamine and other inflammatory substances. The interplay between mast cells and sensory nerves is a key mechanism in the chronic inflammation and itch associated with these skin disorders [21]. The analysis of the link between psoriasis and CSU in patients treated with the IL-17A blocker izekizumab indicates that while this treatment is effective for psoriasis, it can cause urticaria in about 8.8% of patients. In cases of izekizumab-induced urticaria, IL-17A+ mast cells were found in the skin, which correlated with early relapses of psoriasis after discontinuing the drug. Standard treatments for urticaria, such as antihistamines, did not prevent the relapse of psoriasis, highlighting the need for mast cell stabilizers like cromolyn disodium salt, which have shown promise in reducing inflammation and delaying recurrence in experimental models. Further research is needed to clarify the role of MCs in both conditions and to improve strategies for managing drug-induced urticaria and psoriasis relapse [22]. A paper by [PERSON] et al. from 2022 examines the role of cyclosporine A in treating psoriasis and CSU, highlighting their shared immunological mechanisms. Both conditionsinvolve immune dysregulation: psoriasis is driven by an overactive Th1/Th17 response leading to chronic inflammation and skin cell proliferation, while CSU is marked by MCs activation and histamine release. cyclospor A, an immunosuppressive agent, modulates the immune system by inhibiting T-cell activation and cytokine production.