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Purpose of review The goal of this review is to examine the relationship between psychological stress and chronic urticaria (CU), focusing on the underlying mechanisms and potential therapeutic interventions. The paper seeks to answer how stress exacerbates CU and the neuro-immunological pathways involved, providing insight into improving therapeutic strategies by considering the psychological dimensions of the disease. Recent findings Recent studies highlight the significant role of stress in aggravating CU through the dysregulation of the hypothalamic-pituitary-adrenal axis and neurogenic inflammation. Increased levels of neuropeptides like substance P and calcitonin gene-related peptide, as well as upregulated expression of the MRGPRX2 receptor, are implicated in the neuro-immune interactions that worsen CU symptoms. Additionally, psychological distress has been linked to poorer disease outcomes, with stress management strategies and psychopharmacological interventions showing promise in reducing disease severity. Summary This review concludes that stress significantly contributes to the exacerbation of CU through neuro-immune pathways, suggesting the need for holistic treatment approaches. Addressing both the physical and psychological aspects of CU may improve disease management and patient outcomes. Future research should focus on further elucidating the connection between stress and CU and developing targeted therapies that integrate stress reduction techniques into standard care.
Purpose of review The goal of this review is to examine the relationship between psychological stress and chronic urticaria (CU), focusing on the underlying mechanisms and potential therapeutic interventions. The paper seeks to answer how stress exacerbates CU and the neuro-immunological pathways involved, providing insight into improving therapeutic strategies by considering the psychological dimensions of the disease. Recent findings Recent studies highlight the significant role of stress in aggravating CU through the dysregulation of the hypothalamic-pituitary-adrenal axis and neurogenic inflammation. Increased levels of neuropeptides like substance P and calcitonin gene-related peptide, as well as upregulated expression of the MRGPRX2 receptor, are implicated in the neuro-immune interactions that worsen CU symptoms. Additionally, psychological distress has been linked to poorer disease outcomes, with stress management strategies and psychopharmacological interventions showing promise in reducing disease severity. Summary This review concludes that stress significantly contributes to the exacerbation of CU through neuro-immune pathways, suggesting the need for holistic treatment approaches. Addressing both the physical and psychological aspects of CU may improve disease management and patient outcomes. Future research should focus on further elucidating the connection between stress and CU and developing targeted therapies that integrate stress reduction techniques into standard care.
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