Plain language summary
Urticaria is an immune driven skin reaction, which manifests as hives and swelling and results in significantly decreased quality of life in those who suffer from it. The causes are currently unknown, however airborne substances such as house dust mites and plant pollen may play a role in its development. This systematic review and meta-analysis of 18 studies aimed to determine the role of airborne allergens in the development of chronic spontaneous urticaria (CSU). The results showed that individuals with CSU were more likely to have a sensitivity to airborne allergens and that house dust mites were a leading cause of sensitivity. It was concluded that airborne associated sensitivity is of importance to the development of CSU. This study could be used by healthcare professionals to understand that airborne allergens may be a cause of CSU and that house dust mites may be involved in its development. It is important to determine the cause and eliminate it, to increase the chances of successful treatment.
Abstract
BACKGROUND Current guidelines do not recommend performing aeroallergen skin prick testing (SPT) in chronic spontaneous urticaria (CSU). OBJECTIVE The objective of this review was to investigate the presence of aeroallergen sensitization and markers of T2 inflammation in subjects with CSU. METHODS Systematic literature reviews to identify all studies that evaluated the presence of T2 markers of allergic inflammation in CSU subjects were performed. RESULTS In 16 studies that assessed the prevalence of positive SPT to multiple aeroallergens in CSU, 38.5% of CSU subjects had positive SPT. In three controlled studies, 34.2% of CSU subjects had positive SPT to multiple aeroallergens, compared to 13.6% of controls (p = 0.047). In 18 studies that assessed the prevalence of house dust mite (HDM) positive SPT in CSU, 27.5% of CSU subjects had positive SPT. In three controlled studies, 27.5% of CSU subjects had positive SPT to HDM, compared to 2.1% of controls (p = 0.047). Overall, CSU subjects were 3.1 times more likely to be aeroallergen-sensitized (95% CI 1.7-5.8, p = 0.0002) and 6.1 times more likely to be HDM-sensitized (95% CI 3.7-9.9, p < 0.00001) than controls. Mean total serum IgE (tIgE) levels were 238 kU/L and median tIgE levels were 164 kU/L, which was greater than the upper 90th percentile of normal (< 137 kU/L). Compared to healthy controls, CSU subjects were 6.5 times more likely to have IgG autoantibody against FcεR1α (p = 0.001), 2.4 times more likely to have IgG anti-IgE antibody (p = 0.03) and 5 times more likely to have anti-thyroid peroxidase (anti-TPO) antibody (p = 0.02). When corticosteroids were withheld for ≥ 28 days, mean blood eosinophil percentage was elevated at 5.9% (normal < 4%), but other studies reporting absolute count found the mean was in the normal range, 239 × 10 6 / L (normal < 400 × 10 6 / L). CONCLUSION Increased aeroallergen sensitization, tIgE, autoantibodies and blood eosinophil percentage in the CSU subjects indicates the possible importance of T2 inflammation in the pathogenesis of CSU. Further studies may be warranted to determine if specific allergen avoidance, desensitization or improvement in the mucosal allergic inflammation present in asthma and/or rhinitis has any benefit in the management of CSU.
Methodological quality
Jadad score
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