Southmead Hospital, Bristol, UK
Correspondence to: Andrew R. L. Medford, MBChB, BSc, Southmead Hospital, Bristol, UK; e-mail: email@example.com
Kanazawa et al1 have reported an interesting reduction in airway permeability with pranlukast that correlated with a reduction in airway vascular endothelial growth factor (VEGF) levels. However, no such reduction in VEGF levels was observed in steroid-treated asthmatics. In contrast, a clinical study2 has shown a further benefit in symptoms and lung function in the combination of leukotriene receptor antagonists and inhaled steroids. It is therefore perhaps surprising that no further reduction in airway VEGF occurred with pranlukast added to the steroid-treated patients.
Other questions remain. What is the mechanism of the reduction in measured airway VEGF level in asthma? Is there a VEGF receptor up-regulation in the airway or an increase in sflt binding free VEGF? Could this reduction be secondary to cellular changes in the airway epithelium, a known source of VEGF. Are there other significant sources of VEGF in asthma?
One limitation of the VEGF enzyme-linked immunosorbent assay is its inability to measure the more cell-associated VEGF isoforms (VEGF189 and VEGF206) that still have bioactivity. Analysis of their expression would increase understanding of the changes in VEGF bioactivity in asthma.
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