Journal Article10.1046/J.1365-2222.2001.01071.X
Inhaled corticosteroids decrease vascularity of the bronchial mucosa in patients with asthma
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TL;DR: The effect of inhaled corticosteroids on increased airway mucosal vascularity in asthmatics has been little studied.
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Abstract: Background Increased vascularity in airway mucosa is a distinctive feature of airway remodelling in asthma. While corticosteroids have proved most effective in modifying airway inflammation, the effect of inhaled corticosteroids on increased airway mucosal vascularity in asthmatics has been little studied. Objective We examined the effect of inhaled corticosteroid on airway vascularity in bronchial biopsy specimens taken from asthmatic patients. Subjects and methods We studied bronchial biopsies from 28 asthmatic patients before and after treatment with inhaled beclomethasone dipropionate (BDP) 800 μg/daily, or placebo, for 6 months in a double-blind manner. Biopsy specimens were evaluated for number of vessels and percentage of area occupied by vessels, using computerized image analysis after staining for type IV collagen in vessel walls. Specimens were also examined for extent of collagen III in the subepithelial basement membrane. In addition, we compared asthmatic specimens with biopsy specimens taken from non-asthmatic control subjects. Results There was a significant increase in number of vessels (P < 0.01) and percent vascularity (P < 0.001) in the submucosa of asthmatic patients compared with control subjects. After 6 months of treatment, we observed significant improvements in forced expiratory volume in 1 s (FEV 1 ), FEV 1 % and airway responsiveness (P < 0.05, each) in the BDP treatment group compared with the placebo group. This was accompanied by significant decreases in both vessel number and percent vascularity in the airways of BDP-treated patients (P < 0.05, each). We also observed a significant correlation between change in percent vascularity and change in collagen III thickness in the BDP-treated patients (r s = 0.90, P < 0.001). Furthermore, the change in percent vascularity was inversely correlated with both FEV 1 (r s = -0.49, P < 0.05) and airway responsiveness (r s = -0.36, P < 0.05). Conclusion These findings suggest that inhaled corticosteroid treatment of asthma reduced airway wall vascularity during airway remodelling.
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Airway remodeling in asthma: what really matters.
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TL;DR: The number of vessels in the medium and small airways in asthma patients shows a greater increase than those in COPD patients, and the vascular area in the small airway is increased in COPd patients but not in asthma Patients.
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Vascular component of airway remodeling in asthma is reduced by high dose of fluticasone.
Alfredo Chetta,Andrea Zanini,Antonio Foresi,Mario Del Donno,Antonio Castagnaro,Raffaele D’Ippolito,Simonetta Baraldo,Renato Testi,Marina Saetta,Dario Olivieri +9 more
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TL;DR: A review will evaluate the development of remodeling in asthmatic subjects and the effects of treatment on these processes, and the need to identify novel asthma indices and phenotypes that correlate with remodeling and might specifically respond to new therapies.
References
Vascular endothelial growth factor is a secreted angiogenic mitogen
TL;DR: DNA sequencing suggests the existence of several molecular species of VEGF, a heparin-binding growth factor specific for vascular endothelial cells that is able to induce angiogenesis in vivo.
5.4K
•Journal Article
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TL;DR: T tumors have "borrowed" fundamental mechanisms that developed in multicellular organisms for purposes of tissue defense, renewal, and repair and taught us something new about angiogenesis, namely, that vascular hyperpermeability and consequent plasma protein extravasation are important, perhaps essential, elements in its generation.
3.3K
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