Possible effects of vascular endothelial growth factor in the pathogenesis of chronic obstructive pulmonary disease.
PURPOSE: Expression of vascular endothelial growth factor (VEGF) is reduced in the lungs of patients with emphysema. We examined whether VEGF levels in sputum differed in patients with emphysema, bronchitis, or asthma, as compared with controls. METHODS: Fifty-nine patients with chronic obstructive pulmonary disease (COPD) (25 with emphysema, 19 with chronic bronchitis, and 15 with a mixed type), 20 patients with bronchial asthma, and 11 normal controls were included in the study. The concentration of VEGF in induced sputum and the correlations between VEGF levels and pulmonary function were examined. RESULTS: The mean (+/- SD) concentration of VEGF in induced sputum was significantly higher in patients with asthma (6440 +/- 1820 pg/mL, P <0.0001) or bronchitis (4120 +/- 1100 pg/mL, P <0.0001) than in normal controls (1860 +/- 1220 pg/mL), but significantly lower in patients with emphysema (500 +/- 300 pg/mL, P =0.03). The concentration of VEGF in sputum from patients with bronchitis correlated inversely with forced expiratory volume in 1 second (r = -0.87; P =0.0002); in contrast, there was a positive correlation between these two measurements in patients with emphysema (r = 0.82; P <0.0001). In addition, sputum VEGF concentrations correlated with the diffusing capacity of carbon monoxide in patients with emphysema (r = 0.87; P <0.0001), but not in those with bronchitis (r = -0.22; P =0.36). CONCLUSION: In patients with bronchitis, increased levels of VEGF in induced sputum were associated with airflow limitation. In contrast, decreased levels of VEGF were associated with airflow limitation and alveolar destruction in patients with emphysema. Thus, our findings suggest that VEGF may affect the pathogenesis of these two common types of COPD.[1]References
- Possible effects of vascular endothelial growth factor in the pathogenesis of chronic obstructive pulmonary disease. Kanazawa, H., Asai, K., Hirata, K., Yoshikawa, J. Am. J. Med. (2003) [Pubmed]
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