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Distinct Clinical and Laboratory Profiles in Chronic Spontaneous Urticaria Requiring High-Intensity Treatment
Ji-Su Shim1, Min-Ho Kim2, Kyung-Min Ahn1
1Department of Internal Medicine, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
Patients with chronic spontaneous urticaria (CSU) requiring extensive treatment often have longer disease duration and distinct laboratory findings. These high-treatment-requirement CSU (HTR-CSU) cases show elevated neutrophils, IgE, and D-dimer, suggesting unique immune responses.
Area of Science:
- Immunology
- Dermatology
- Clinical Medicine
Background:
- Second-generation H1-antihistamines are first-line for chronic spontaneous urticaria (CSU).
- A significant portion of CSU patients remain symptomatic despite standard treatment.
- Identifying characteristics of patients with high treatment requirements is crucial for optimizing care.
Purpose of the Study:
- To identify clinical and laboratory features associated with high treatment requirements in CSU patients.
- To differentiate characteristics between high-treatment-requirement CSU (HTR-CSU) and non-HTR-CSU.
Main Methods:
- Retrospective cohort study of 6,033 adult CSU patients in a Korean tertiary hospital (2002-2020).
- HTR-CSU defined by simultaneous use of ≥4 H1-antihistamines or omalizumab treatment.
- Comparison of clinical data, medication use, and laboratory findings between HTR-CSU and non-HTR-CSU groups.
Main Results:
- 34.5% of patients were classified as HTR-CSU.
- HTR-CSU patients had longer follow-up durations and higher rates of cholinergic urticaria.
- HTR-CSU was associated with elevated white blood cell counts, neutrophils, total IgE, complement C3/C4, and D-dimer, alongside reduced IgG levels.
Conclusions:
- High-treatment-requirement CSU is linked to longer disease duration and a greater medication burden.
- Distinct laboratory profiles in HTR-CSU, including elevated neutrophils, complement, D-dimer, and IgE, with decreased IgG, suggest unique immunological mechanisms.
- Further research into these mechanisms may lead to more targeted therapies for refractory CSU.
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