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Poster Presentations: Wednesday, October 26, 2011 |

Correlation of Impulse Oscillometry Pulmonary Function and Expression of PPAR? in Monocytes From COPD Patients FREE TO VIEW

Hui Zhao, MD
Chest. 2011;140(4_MeetingAbstracts):537A. doi:10.1378/chest.1119851
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Abstract

INTRODUCTION: Peroxisome Proliferator-Activated Receptor-γ (PPARγ) is a transcription factor that is being explored for its role in the process of lung inflammation and repair and PPARγ agonist has shown promise in the management of COPD. Thus, it would be interesting to know whether the expression of PPARγ can reflect the severity of COPD. Impulse oscillometric system (IOS) has recently been re-applied to pulmonary function test (PFT) and shown to be as sensitive as conventional spirometry but less effort-dependent. The aim of this study is to investigate the possible correlation between level of PPARγ and severity of COPD using IOS-PFT.

CASE PRESENTATION: METHODS All patients with COPD cared for in our Division during the 2 year-period of study (n=84) were recruited as a cohort. The study was approved by institutional IRB and informed consents were signed. The patients were divided into mild (n=11, 6 stable, 5 exacerbation), moderate (n=23, 13 stable and 10 exacerbation), severe (n=30, 14 stable and 16 exacerbation) and very severe (n=20, 19 stable and 1 exacerbation) according to GOLD classification. There were total 52 stable cases and 32 cases during exacerbation studied. Control group consisted 40 cases with no respiratory diseases. After measurement of PFT with conventional spirometry and IOS, 4ml venous blood were collected and monocytes were isolated and processed for RT-PCR analysis for expression of PPARγ. RESULTS The total respiratory resistance (R5), central and peripheral airway resistance (R20, R5-R20), total respiratory impedance (Z5), resonant frequency (Fres) correlated with PFT from spirometry and were significantly higher in COPD patients than in the controls (P<0.05 for all), while the surrounding elastic resistance(X5) was significantly lower in COPD patients than in the controls (P<0.05). The expression of PPARγ was significantly lower in COPD patients than in the control group (P<0.05 for all) and was even lower during acute exacerbation than during stable phase among COPD patients (P<0.05 for all). The level of PPARγ expression during acute phase negatively correlated with R5-R20 (r=-0.582, p<0.05).

DISCUSSION: The expression of PPARγ is down-regulated in patients with COPD. COPD exacerbation is characterized with a further reduction in the expression of PPARγ which negatively correlate with R5-R20.

CONCLUSIONS: Our results indicate that PPARγ expression reflects severity of COPD and plays an important role during COPD exacerbation.

Reference #1 Clin Experim Allergy 36:1494-1504, 2006

DISCLOSURE: The following authors have nothing to disclose: Hui Zhao

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