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Active Helicobacter pylori Infection as a Marker of an Activity-Linked Phenotype in Chronic Spontaneous Urticaria
Nguyen Thi Lien1, Tran Vuong The Vinh2, Nguyen Thi Thanh Thanh Huyen1
1Department of Dermatology, Hai Phong University of Medicine and Pharmacy, Hai Phong, Vietnam.
Background:
Chronic spontaneous urticaria (CSU) exhibits heterogeneous disease activity patterns, suggesting underlying biological variability. Active Helicobacter (H.) pylori infection has been proposed as a potential contributor to inflammatory amplification in CSU. The aim of the study was to evaluate whether active H. pylori infection identifies a distinct activity-linked clinical phenotype in CSU and to examine its relationship with symptom intensity and quality-of-life impact.
Methods:
In the retrospective observational study, 245 adults with CSU underwent stool antigen testing for active H. pylori infection. Disease activity was assessed using the daily Urticaria Activity Score (UAS; range 0-6). Gradient analysis across UAS levels, phenotype feature enrichment, correlation with antigen burden, and multivariable modeling were performed. External quality-of-life impact was also evaluated.
Results:
Active H. pylori infection was detected in 64.9% of patients and was strongly associated with amplified disease activity. A graded increase in infection prevalence was observed across UAS categories, and antigen burden correlated positively with UAS (ρ = 0.540; P < 0.001). Infected patients demonstrated enrichment of severe pruritus, very high wheal counts, and angioedema. After adjustment for age, sex, and disease duration, infection remained independently associated with high disease activity (P < 0.001). Although overall quality-of-life impairment was modest, disease activity showed a weak positive correlation with external impact (P = 0.046).
Conclusions:
Active H. pylori infection may represent a marker of an activity-linked inflammatory phenotype in CSU characterized by severity gradient and phenotype clustering. While causality cannot be inferred, these findings support further prospective studies to determine whether infection-targeted strategies influence disease trajectory.
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