High House Dust Mite Serum-Specific Immunoglobulin E Indicates a High 5-Year Rhinitis-Asthma Conversion Rate: A Cross-Sectional Study
Allergic rhinitis (AR) and allergic asthma (AA) represent significant global health burdens, with AR serving as a well-established risk factor for the subsequent development of asthma. The progression from AR to AA, termed the rhinitis-asthma conversion rate (RACR), carries substantial implications for patient morbidity, healthcare costs, and mortality. House dust mites (HDMs) are recognized as a leading cause of allergic sensitization worldwide, particularly in China, where they dominate as allergens in patients with AR and AA. This study investigates the association between HDM-specific immunoglobulin E (sIgE) levels and the risk of asthma onset in AR patients, with a focus on quantifying the 5-year RACR and identifying predictive biomarkers for early intervention.
Study Design and Methodology
The cross-sectional study enrolled 393 participants aged 6–76 years from North China, all diagnosed with AR either with or without comorbid AA. Diagnoses were confirmed by senior allergists through clinical evaluations, including symptom assessment (nasal itching, sneezing, rhinorrhea, hyperemia), physical examinations, and confirmatory tests. Key inclusion criteria required a definitive living environment classification (basement, bungalow, or apartment), completion of HDM sIgE testing, and skin testing for inhaled allergens.
Diagnostic and Testing Protocols
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sIgE Measurement: Serum sIgE levels against HDMs were quantified using ImmunoCAP (Phadia 1000, Thermo Fisher Scientific). A threshold of ≥0.35 kU/L defined sensitization, with results stratified into six grades:
- Level 1: 0.35–0.7 kU/L
- Level 2: 0.7–3.5 kU/L
- Level 3: 3.5–17.5 kU/L
- Level 4: 17.5–50 kU/L
- Level 5: 50–100 kU/L
- Level 6: ≥100 kU/L
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Intradermal Skin Tests (IDT): Conducted using standardized allergen extracts (Xinhualian®) to assess sensitization to inhaled allergens.
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Statistical Analysis:
- Baseline characteristics between AR-with-asthma and AR-alone groups were compared using chi-squared or Student’s t-tests.
- Univariate and multivariate logistic regression models evaluated crude and adjusted odds ratios (ORs) for asthma risk factors. Four regression models were constructed:
- Model 1: sIgE levels alone.
- Model 2: sIgE, age, and gender.
- Model 3: Model 2 + food allergy and living environment.
- Model 4: Model 3 + drug allergy, AR duration, family allergy history, and pet ownership.
- Kaplan-Meier survival analysis estimated cumulative RACR over time, stratified by sIgE levels.
Key Findings
Participant Characteristics and Risk Factors
Of 321 eligible participants, 66.4% (213/321) had AR with AA, while 33.6% (108/321) had AR alone. Significant baseline differences included:
- sIgE Levels: High-grade sIgE (Levels 5–6) was more prevalent in the asthma group (21.6% [46/213] vs. 9.3% [10/108]; P < 0.01), yielding a crude OR of 3.163 (95% CI: 1.400–7.144).
- AR Duration: Prolonged AR (>15 years) correlated with asthma (14.6% [31/213] vs. 6.5% [7/108]; P < 0.01; OR = 3.452, 95% CI: 1.410–8.450).
- Living Environment: Residing in bungalows increased asthma risk (30.0% [63/210] vs. 14.2% [15/106]; P < 0.01; OR = 2.600, 95% CI: 1.398–4.837).
Multivariate Regression Analysis
All four models identified HDM sIgE as an independent predictor of AA onset:
- Model 1: Adjusted OR = 1.390 (95% CI: 1.108–1.744; P = 0.004).
- Model 2: Adjusted OR = 1.466 (95% CI: 1.160–1.852; P = 0.001).
- Model 3: Adjusted OR = 1.425 (95% CI: 1.119–1.815; P = 0.004).
- Model 4: Adjusted OR = 1.427 (95% CI: 1.109–1.838; P = 0.006).
Additional covariates in Model 4 revealed drug allergy (adjusted OR = 2.250, P = 0.004), AR duration (adjusted OR = 1.062 per year, P = 0.003), and living environment (adjusted OR = 1.950 for bungalows, P = 0.014) as significant risk factors.
Temporal Dynamics of Asthma Onset
Kaplan-Meier analysis demonstrated a strong dose-response relationship between sIgE levels and cumulative RACR (Figure 1):
- Within 5 years of AR diagnosis: Patients with sIgE Levels 5–6 exhibited a 70% RACR, compared to progressively lower rates in lower sIgE tiers.
- Beyond 10 years: Curve intersections occurred due to declining sample sizes and variable AR durations, but the early-phase trend remained clear.
Mechanistic and Clinical Implications
The study posits that elevated HDM sIgE reflects systemic allergic inflammation, propagating from nasal to bronchial mucosa. This “unified airway” hypothesis aligns with prior evidence linking upper and lower respiratory tract inflammation. IgE-mediated pathways exacerbate mucosal damage over time, increasing bronchial hyperreactivity and asthma susceptibility.
Clinical Relevance
- Biomarker Utility: HDM sIgE quantification offers a low-cost, non-redundant tool for stratifying AR patients by asthma risk. Early identification of high-sIgE individuals enables targeted monitoring and preventive measures.
- Intervention Opportunities: Anti-IgE therapies (e.g., omalizumab) or allergen-specific immunotherapy may mitigate progression in high-risk cohorts.
- Environmental Modifications: Reduced HDM exposure in bungalows—linked to higher asthma risk—could complement pharmacological strategies.
Strengths and Limitations
Strengths:
- Large, well-characterized cohort from a high-HDM-sensitization region.
- Rigorous adjustment for confounders across multiple regression models.
- Survival analysis providing temporal resolution of RACR.
Limitations:
- Cross-sectional design limits causal inference; longitudinal cohorts are needed.
- Potential underrepresentation of long-duration AR patients due to survival bias.
- Regional focus on North China may limit generalizability.
Conclusion
This study establishes high HDM sIgE levels as a robust predictor of 5-year asthma onset in AR patients, independent of other allergens or demographic factors. The 70% RACR observed in patients with sIgE Levels 5–6 underscores the urgency of early biomarker-guided interventions. Clinicians should prioritize sIgE testing in AR management to identify high-risk individuals, optimize therapeutic strategies, and reduce the global burden of asthma-related morbidity and mortality.
doi.org/10.1097/CM9.0000000000001790
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