The inflammatory and remodelling processes that underlie asthma result from a highly complex interaction between various cell types. Through the release of mediators, cytokines, chemokines and growth factors, epithelial and mesenchymal cells cause persistence of the inflammatory infiltrate and induce structural changes in the airway wall, such as increased thickness of the basement membrane, leading to a reduced baseline airway calibre and exaggerated airway narrowing. Aim of the study was to compare the BMT and the BAL eosinophil count in mild and moderate atopic asthma; in mild and moderate non-atopic GER-related asthma, never previously investigated to our knowledge.
After their informed consent, 8 mild atopic asthmatics (MIAA, 32–63y, 4 m., FEV1 = 94.8% pred. ± 9.9sd), 8 moderate atopic asthmatics (MOAA, 30–64 y, 4 m., FEV1 = 68.6% pred. ± 8.8 sd), 8 non-atopic GER-related mild asthmatics (MIAGER, 24-64 y, 2 m, FEV1 = 96.2 % pred. ± 7.7sd), 7 non-atopic GER –related moderate asthmatics (MOAGER, 36–64y, 3 m., FEV1 = 66.6 % pred. ± 4.7 sd), non-smoker, underwent endobronchial biopsy and BAL for eosinophil count (EOS). BMT was expressed in mm, and EOS in % total cell count. Statistics: Wilcoxon test, p < 0.05 accepte.
Results (mean ± sd) in tab. 1.
1) when GER-related, mild asthma seems characterized by a much smaller BMT than atopic asthma; 2) also eosinophilic inflammation proves lower in these circumstances; 3) in moderate-asthma, when eosonophilic inflammation is predominant, atopic and ger-related asthma the basement membrane thickness is similar.
Present data lead to suggests GER-related asthma as a peculiar nosologic entity in the earlier phase of the disease.
Claudio Micheletto, None.