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Sinus and adenoid inflammation in children with chronic rhinosinusitis and asthma
Antony Anfuso1, Hassan Ramadan1, Andrew Terrell1
1Department of Otolaryngology, West Virginia University, Morgantown, West Virginia.
Insights
Children with chronic rhinosinusitis (CRS) and asthma exhibit more severe upper airway inflammation than those with CRS alone. This suggests treating sinus disease is key for managing pediatric asthma.
Area of Science:
- Pediatric Allergy and Immunology
- Otolaryngology
- Respiratory Medicine
Background:
- Chronic rhinosinusitis (CRS) frequently co-occurs with asthma in children, but the underlying mechanisms remain unclear.
- Direct measurements of upper airway mucosal inflammation are lacking in pediatric CRS and asthma studies.
Purpose of the Study:
- To investigate the pathophysiologic mechanisms of coexisting CRS and asthma in children.
- To analyze inflammatory cytokine and chemokine expression in sinus and adenoid tissues of pediatric patients with refractory CRS.
Main Methods:
- Prospective study of 28 children (2-12 years) with CRS (with or without asthma) and 10 controls.
- Surgical removal of sinus and adenoid tissues for analysis.
- Multiplex assay used to measure mucosal expression of 40 inflammatory cytokines, normalized to total protein.
Main Results:
- Children with CRS and asthma showed significantly higher sinus levels of tumor necrosis factor-alpha compared to those with CRS alone.
- Elevated adenoid levels of epidermal growth factor, eotaxin, fibroblast growth factor-2, growth-related oncogene, and platelet-derived growth factor-AA were observed in children with CRS and asthma.
Conclusions:
- The inflammatory response in pediatric CRS with asthma is more severe than in CRS without asthma.
- Findings support the hypothesis that severe upper airway inflammation contributes to or exacerbates asthma in children.
- Treating sinus disease is crucial for managing pediatric asthma, supported by direct airway inflammation measurements.
Background:
Chronic rhinosinusitis (CRS) and asthma frequently coexist in children and adults. However, the precise pathophysiologic mechanism of this interaction is still poorly understood, especially in children, owing to the lack of direct measurements of mucosal inflammation in the upper airways.
Objective:
To determine the pathophysiologic mechanism by analyzing the expression of a large array of inflammatory cytokines and chemokines in the sinus and adenoid tissues surgically removed from pediatric patients with CRS refractory to medical management.
Methods:
Twenty-eight children 2 to 12 years old diagnosed with CRS with or without asthma and 10 controls were included in this prospective, nonrandomized study. Mucosal expression of 40 inflammatory cytokines was measured with a multiplex assay and was normalized to total tissue protein.
Results:
Compared with children with CRS and without asthma, children with CRS and asthma had significantly higher sinus levels of tumor necrosis factor-α and adenoid levels of epidermal growth factor, eotaxin, fibroblast growth factor-2, growth-related oncogene, and platelet-derived growth factor-AA.
Conclusion:
The inflammatory response in the upper airway mucosa of children with asthma and CRS was similar, but more severe, compared with children with CRS without asthma. This observation is consistent with the hypothesis that asthma in these patients is caused or exacerbated by severe upper airway disease and supports the concept that treating sinus disease is paramount in the management of chronic asthma in children using, for the first time, direct measurements of airway inflammation in children.
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