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Observational analysis reveals a link between hepatitis infections and chronic spontaneous urticaria, suggesting immune dysregulation as a contributing factor.
Chronic urticaria (CU) is a common dermatological condition characterized by persistent wheals lasting more than six weeks. Chronic spontaneous urticaria (CSU), the most prevalent CU subtype, significantly impairs patients' quality of life. Although its precise pathogenesis remains unclear, current evidence implicates multiple factors including immune dysregulation, stress, certain medications, and viral infections in its development and exacerbation. Among infectious triggers, hepatitis B (HBV) and C (HCV) viruses have emerged as potential CSU inducers. These viruses may trigger urticarial symptoms through various mechanisms, particularly immune system activation and cutaneous inflammatory responses. While the exact pathogenic pathways require further elucidation, clinical evidence suggests antiviral therapy may occasionally improve urticarial symptoms. Standard management of virus-associated CSU involves second-generation antihistamines as first-line treatment. For refractory cases, targeted therapies like omalizumab may be considered. Notably, successful HCV eradication has in some cases led to significant CSU improvement, an effect less frequently observed with HBV treatment. This study investigates the association between hepatitis infections and CSU, focusing particularly on elucidating how HBV and HCV could contribute to CSU pathogenesis.
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Jafari-Sales et al. (2025) studied this question.
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