The clinical utility of biomarkers in asthma and COPD
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摘要
Quantitative bacteriologic cultures, neutrophil elastase, myeloperoxidase (MPO), tumor necrosis factor alpha (TNF-α) and interleukin (IL)-8 were measured in bronchoalveoler lavage (BAL) in 39 patients with stable COPD [19 with frequent exacerbation (der=0 src="http://www.sciencedirect.com/scidirimg/entities/2a7e.gif" alt="greater-or-equal, slanted" title="greater-or-equal, slanted">3/year), and 20 with infrequent] and in 18 healthy controls (10 smokers and 8 non-smokers).

lass="h4">Results

BAL revealed the microorganisms with potential pathogenicity above the established threshold (der=0 src="http://www.sciencedirect.com/scidirimg/entities/2a7e.gif" alt="greater-or-equal, slanted" title="greater-or-equal, slanted">103 cfu/ml) in 68.4%of patients with frequent exacerbation, 55%of infrequent exacerbation, 40%of smokers and 12.5%of non-smokers controls (P=0.05). BAL MPO, IL-8 and TNF-α levels were found to be significantly higher in COPD as compared to controls (P=0.001). However, only IL-8 level was significantly higher in COPD patients with frequent exacerbation as compared to infrequent (P=0.001). Airway bacterial load correlated with levels of airway inflammation markers in COPD (P<0.05).

lass="h4">Conclusion

The bacterial load and airway inflammation contributes to each other in stable COPD. However, there is a link only between interleukine (IL)-8 and frequent exacerbations. Clearly, the relationship between bacterial colonization, airway inflammation and frequent exacerbations is of major importance in understanding of the COPD pathogenesis.


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ded3" onMouseOver="InfoBubble.show('infobubble_2','mlktLink_2')" onMouseOut="InfoBubble.timeout()">Prediction of treatment-response to inhaled corticoster...
Pulmonary Pharmacology & Therapeutics

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der=0 src="/scidirimg/jrn_nsub.gif" alt="You are not entitled to access the full text of this document" title="You are not entitled to access the full text of this document" width=12 height=14"> de0eb2a6c2bd1b7cfa86">Prediction of treatment-response to inhaled corticosteroids by mannitol-challenge test in COPD. A proof of concept
Pulmonary Pharmacology & TherapeuticsVolume 18, Issue 2April 2005, Pages 83-88
Jörg D. Leuppi, Ryan Tandjung, Sandra D. Anderson, Daiana Stolz, Martin H. Brutsche, Roland Bingisser, André P. Perruchoud, Christian Surber, Andreas Knoblauch, Morgan Andersson, Lennart Greiff, Hak-Kim Chan, Michael Tamm

Abstract
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lass="h4">Background

There are no predictors known that can identify COPD patients who will respond to treatment with ICS.

lass="h4">Method

We investigated 30 patients (median age 65 (range 44–83, 12 females) with mild to moderately severe COPD. All patients had post bronchodilator FEV1/forced vital capacity ratio of less than 70%and a reversibility of less than 12%and 200 ml from baseline. We wanted to determine if airway responsiveness (AHR) to histamine and mannitol could predict who would respond to a 3-month course of ICS.

lass="h4">Results

At baseline, all patients had AHR to histamine, but only 7 (23%) patients to mannitol. After 3 months of treatment with ICS, there was no significant change in spirometry or the quality of life when analysing all individuals together. However, FEV1%predicted improved from 67%(IQR12) to 79%(IQR16) in mannitol positive patients; whereas it was unchanged in the mannitol negative patients. The difference in the mean change of FEV1%predicted between the two groups was 12 (IQR13.5) and this was highly significant (p=0.001). The improvement in quality of life (SGRQ 30 (IQR10.5) to 21 (IQR12; p=0.01) was only significant in the patients positive to mannitol.

lass="h4">Conclusion

We propose that AHR to mannitol could predict ICS-responsiveness in mild to moderately severe COPD patients.


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Exercise Duration Rather than Peak Oxygen Uptake Better...
Archives of Medical Research

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der=0 src="/scidirimg/jrn_nsub.gif" alt="You are not entitled to access the full text of this document" title="You are not entitled to access the full text of this document" width=12 height=14"> Exercise Duration Rather than Peak Oxygen Uptake Better Correlates with Fev1 and Inspiratory Capacity in Chronic Obstructive Pulmonary Disease
Archives of Medical ResearchVolume 38, Issue 8November 2007, Pages 876-881
Gökhan Metin, Levent Öztürk, Esra Sönmez Duman, Tunçalp Demir

Abstract
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lass="h4">Background

Exercise duration of constant-load endurance tests has been recently demonstrated to be more sensitive in detecting the changes after bronchodilator administration than either walking distance or peak oxygen uptake in patients with COPD. In the present study, we questioned whether exercise duration of progressive load is better correlated with forced expiratory volume in 1 sec and inspiratory capacity than other indices of submaximal exercise test during stable period in patients with COPD.

lass="h4">Methods

Thirty-three stable COPD patients, and 26 age- and BMI-matched control subjects were recruited. Resting pulmonary function tests and incremental cycle exercise tests were performed. All indices of exercise and pulmonary function tests including exercise duration, peak oxygen uptake (VO2peak), and forced expiratory volume in 1 sec (FEV1) were recorded.

lass="h4">Results

Exercise capacity was lower in COPD than age- and BMI-matched controls as shown by exercise duration and ergometric work (535 ± 159 vs. 705 ± 115 sec, p <0.001 and 89.2 ± 26.6 vs. 117.8 ± 19.5 W, p <0.001). Statistical analysis revealed that exercise duration slightly better correlates with FEV1 and inspiration capacity (IC) (R = 0.600, p <0.001; R = 0.615, p <0.001) than peak oxygen uptake (R = 0.284, p >0.05; R = 0.127, p >0.05) in stable period COPD patients.

lass="h4">Conclusions

There is an impairment of aerobic capacity in stable period COPD patients compared to healthy controls. Exercise in COPD patients is ventilation-limited and exercise duration with respect to peak VO2 is better correlated with FEV1 and IC in stable COPD patients undergoing progressive-load cycling exercise.


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The clinical utility of biomarkers in asthma and COPD

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