Impact of hepatitis B and C virus on chronic spontaneous urticaria; potential pathogenic triggers and aggravating factors
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.
Authors
- Abolfazl Jafari-Sales (ORCID: https://orcid.org/0000-0002-5710-4076)
- Mehrdad Pashazadeh (ORCID: https://orcid.org/0000-0001-9103-6276)
- Shabnam Khakpour-Ziaei (ORCID: https://orcid.org/0009-0002-1462-4079)
- Safa Meskini-Marandi
Institutions
- Islamic Azad University of Tabriz (IR)
- Islamic Azad University Kazeron (IR)
Publication Details
- Journal
- Journal of Current Biomedical Reports
- Published
- 2025-03-30
- DOI
- https://doi.org/10.61882/jcbior.6.1.302
- Primary Topic
- Urticaria and Related Conditions
- Type
- article
- Field-Weighted Citation Impact
- 0.00