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Communications to the Editor |

Effects of Pranlukast on Vascular Endothelial Growth Factor Levels in Asthma FREE TO VIEW

Hiroshi Kanazawa, MD
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Graduate School of Medicine, Osaka City University, Osaka, Japan

Correspondence to: Hiroshi Kanazawa, MD, Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, 1-4-3, Asahi-machi, Abenoku, Osaka, 545-8585, Japan; e-mail: kanazawa-h@med.osaka-cu.ac.jp



Chest. 2005;127(4):1461. doi:10.1378/chest.127.4.1461
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To the Editor:

We thank Dr. Medford for an interest regarding our study.1 There has been a clinical interest in the use of leukotriene receptor antagonists (LTRAs) in asthmatic patients who have already been treated with inhaled corticosteroids. However, a further benefit in symptoms and lung function from therapy combining LTRAs and inhaled corticosteroids is contrary to this finding. In this study, we found that pranlukast administration added little efficacy to inhaled corticosteroid therapy for reduction in vascular endothelial growth factor (VEGF) levels in induced sputum from asthmatic patients. However, it is possible that the trends toward reduction in airway VEGF levels after pranlukast administration in steroid-treated asthmatic patients might have reached statistical significance if more patients had been included in our study.

The mechanism of the reduction in airway VEGF levels in asthma induced by pranlukast administration is unclear. One report2has indicated that asthmatic patients exhibited a greater expression of VEGF receptors (flt-1 and flk-1) in the airway mucosa. Moreover, increased VEGF expression in asthmatic patients were identified by infiltrating inflammatory cells in the submucosa in order of abundance as CD34+ cells → eosinophils → macrophages → T cells → mast cells. Therefore, one possible explanation is that pranlukast administration decreased airway VEGF levels via the reduction of infiltrating inflammatory cells. We also think that analysis of cell-associated VEGF isoform (VEGF189 and VEGF206) expression is important to understand VEGF bioactivity in asthma. Though the results were not shown in our study, we examined cell-associated VEGF isoform expression by immunohistochemical analysis. On the basis of these results, we found a significant correlation between the expression of free VEGF and that of cell-associated VEGF. In our recent study,3 we determined that the interaction between airway microcirculation and VEGF may be a key element in the pathophysiology of asthma. Therefore, pranlukast administration might decrease airway microvascular permeability through, at least in part, a decrease in airway VEGF levels in asthmatic patients.

Kanazawa, H, Yoshikawa, T, Hirata, K, et al (2004) Effects of pranlukast administration on vascular endothelial growth factor levels in asthmatic patients.Chest125,1700-1705. [CrossRef] [PubMed]
 
Hoshino, M, Nakamura, Y, Hamid, QA Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma.J Allergy Clin Immunol2001;107,1034-1038. [CrossRef] [PubMed]
 
Kanazawa, H, Nomura, S, Yoshikawa, J Role of microvascular permeability on physiologic differences in asthma and eosinophilic bronchitis.Am J Respir Crit Care Med2004;169,1125-1130. [CrossRef] [PubMed]
 

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References

Kanazawa, H, Yoshikawa, T, Hirata, K, et al (2004) Effects of pranlukast administration on vascular endothelial growth factor levels in asthmatic patients.Chest125,1700-1705. [CrossRef] [PubMed]
 
Hoshino, M, Nakamura, Y, Hamid, QA Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma.J Allergy Clin Immunol2001;107,1034-1038. [CrossRef] [PubMed]
 
Kanazawa, H, Nomura, S, Yoshikawa, J Role of microvascular permeability on physiologic differences in asthma and eosinophilic bronchitis.Am J Respir Crit Care Med2004;169,1125-1130. [CrossRef] [PubMed]
 
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