Abstract: BACKGROUND: Accumulating evidence confirms the presence of pan-airway inflammation in allergic rhinitis patients. Smoking is known to affect the asthmatic airway inflammation. However, no study has evaluated the impact of smoking on airway inflammation of allergic rhinitis patients. OBJECTIVE: The aim of the present study was to evaluate the impact of smoking on inflammatory and oxidative stress biomarkers in patients with seasonal allergic rhinitis, using non-invasive methods for sample collection. METHODS: Forty patients with seasonal allergic rhinitis (20 smokers and 20 non-smokers) and 30 healthy subjects (15 smokers and 15 non-smokers) were recruited for the study during pollen season. All subjects were submitted to measurement of the fraction of exhaled NO (FeNO), exhaled breath condensate (EBC) collection, nasal lavage collection, pre- and post- bronchodilation spirometry and metacholine bronchial challenge testing. pH, leukotriene B(4) (LTB(4)) and 8-isoprostane were determined in EBC and nasal lavage samples. RESULTS: Patients with allergic rhinitis presented higher LTB(4) and 8-isoprostane levels in nasal lavage (P<0.0001 for both comparisons), with no significant differences between smokers and non-smokers. Patients with allergic rhinitis also presented higher LTB(4) levels and lower pH in EBC (P<0.001 and P=0.004, respectively), with prominent differences between smokers and non-smokers (P<0.0001 and P=0.003, for LTB(4) and pH, respectively). A significant correlation between nasal lavage and EBC LTB(4) values was observed (r(s)=0.313, P=0.048). CONCLUSIONS: Patients with allergic rhinitis present increased LTB(4) and 8-isoprostane in their nasal cavity, however, with no significant differences between smokers and non-smokers. In contrast, smokers with allergic rhinitis present higher LTB(4) levels and lower pH in EBC, suggesting that these patients may be more susceptible to the deleterious effects of smoking, compared with non-smokers.
Abstract: OBJECTIVE: To evaluate whether nasal continuous positive airway pressure (nCPAP) reduces oxidative stress in patients with severe obstructive sleep apnea (OSA) syndrome. MATERIALS AND METHODS: Forty-six patients with severe OSA (AHI30) requiring nasal CPAP treatment and 46 controls (subjects without OSA and with mild OSA as defined by an AHI<15) were enrolled. Oxidative stress was evaluated in blood samples with a commercially available automated spectrophotometric assay (D-ROMs test, Diacron, Grosseto, Italy). Blood samples were collected the evening before (10:00 p.m.) and the morning after (07:00 a.m.) a diagnostic polysomnography. Patients with severe OSA syndrome were subsequently submitted to a second polysomnography with nasal CPAP titration the following night. Using the same schedule we collected blood samples from the patients the morning after the nCPAP titration and after two months of nCPAP treatment. RESULTS: Patients with severe OSA presented higher levels of oxidative stress than patients with AHI<15 in the evening and in the morning (357.57+/-13.07UCarr vs. 319.28+/-12.66UCarr, p=0.038, and 371.83+/-12.83UCarr vs. 328.09+/-11.76UCarr, p=0.014, respectively). Patients with severe OSA presented a significant reduction the levels of oxidative stress the morning after the nCPAP titration study (371.83+/-12.83UCarr vs. 298.21+/-9.62UCarr, p=0.001) and this reduction was further preserved after a period of two months of nCPAP treatment (293.72+/-6.55UCarr, p=0.001 vs. baseline). Statistically significant correlations were observed between levels of oxidative stress and nocturnal polysomnography (NPSG) markers as oxygen desaturation index (ODI), arousal index (AI), lowest oxygen saturation of hemoglobin, and mean oxygen saturation of hemoglobin. CONCLUSIONS: Patients with severe OSA syndrome presented increased systemic oxidative stress. A single night of nCPAP treatment significantly reduced the levels of oxidative stress in patients with severe OSA syndrome, and this reduction was maintained at least after two months of nCPAP treatment.
Abstract: The pathways underlying chronic obstructive pulmonary disease exacerbations (ECOPD) remain unclear. This study describes the clinical, functional and biochemical changes during recovery from ECOPD. Thirty hospitalized patients with Anthonisen's type-I ECOPD were evaluated on days 0 (admission), 3, 10 and 40. A five-symptom score (TSS), performance status and quality of life were evaluated. Post-bronchodilator spirometry, blood gases, oxidative stress, C-reactive protein (CRP), serum amyloid-A (SAA), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and fibrinogen were also measured. Patients were classified as early- or late-recoverers, based on whether dyspnea had returned to pre-exacerbation level by day 10. Most clinical, functional and biochemical parameters improved during follow-up. CRP and IL-6 levels reduced on Day 3 (p<0.05), whereas SAA on Day 10 (p<0.01). TNF-alpha was reduced on Days 3 and 10, but on Day 40 its levels returned to baseline. Fibrinogen and WBC reduced only by day 40. TSS and dyspnea were correlated inversely with FEV(1) on days 3, 10 and 40. Although late-recoverers had lower FEV(1) on admission, none of the reported measurements on admission and day 3 predicted early recovery. During recovery from ECOPD, symptomatic improvement correlates only with post-bronchodilator FEV(1) whereas systemic inflammatory burden subsidence does not correlate with clinical and functional changes. Although late-recoverers have lower FEV(1) on admission, none of the measured parameters is able to predict early symptomatic recovery.
Abstract: COPD is a diverse disease entity with multiple dimensions that uniquely define the patient's performance, morbidity and mortality. FEV(1) is both the traditional metric used to define the progression of COPD as well as the strongest spirometric predictor of mortality in COPD patients. However, besides pulmonary functional abnormalities, COPD is also associated with significant systemic effects. Therefore, the global assessment of an affected patient should include different aspects of the consequences of this disorder, beyond the "gold-standard" assessment of airflow limitation. Quantification of the patient's dyspnea, body composition as expressed by BMI, simple measures of exercise capacity such as the 6MWD, assessment of comorbidities and identification of characteristics related to different phenotypes are features that may lead to more optimal management of such patients.
Abstract: Vascular endothelial growth factor (VEGF) is known to play crucial role in tumour angiogenesis. It is demonstrated that VEGF can be up-regulated by oxidative stress. The aim of this study was to determine the serum VEGF levels and oxidative stress in patients with primary lung cancer and to investigate their association with clinicopathologic factors. We measured serum VEGF levels and oxidative stress in 63 patients (age 63.02+/-1.12 S.E.M.) with primary lung cancer before any treatment (39 NSCLC and 24 SCLC; 6 patients stage I, 3 stage II, 25 stage III and 29 stage IV) and 25 normal subjects. The serum VEGF levels were measured with enzyme linked immunosorbent assay. Serum oxidative stress levels were detected by a commercially available assay (D-ROMs test, Diacron, Grossetto, Italy). The levels of oxidative stress in patients were higher than those in normal subjects (555.3+/-30.35 UCarr vs. 360.1+/-17.46 UCarr). Additionally, a significant difference was found in serum VEGF levels between lung cancer patients and healthy control subjects (428.1+/-38.42pg/ml vs. 298.8+/-19.89pg/ml, respectively, p=0.040). Interestingly, serum oxidative stress presented a significant correlation with serum VEGF levels in patients with lung cancer (r=0.542, p=0.002). Serum VEGF levels were significantly associated with the clinical staging (N-stage) of the patients (p=0.023), performance status (p=0.004) and age (p=0.004). In conclusion, oxidative stress and VEGF are significantly increased in patients with primary lung cancer. The correlation between them might implicate new aspects of the mechanisms controlling tumour angiogenesis and may present clinical interest in the future. Further studies are warranted to evaluate the role of oxidative stress and VEGF as possible biomarkers for the diagnosis and follow-up of patients with lung cancer.
Abstract: BACKGROUND: The fraction of exhaled NO (FeNO) is valuable for the follow-up of asthmatic patients. However, its usefulness as a screening tool for asthma is not established. METHODS: We screened a population of 961 university students with a modified European Community Respiratory Health Survey questionnaire that has been previously used for the screening of respiratory symptoms related to asthma. All subjects with a positive answer to at least one question (n = 149) were submitted to FeNO measurement with a portable nitric oxide analyzer. Subsequently, they were submitted to spirometry and evaluated by a physician blinded to FeNO measurements. Seventy students with no respiratory symptoms served as control subjects. RESULTS: Asthma was diagnosed in 63 subjects, and allergic rhinitis was diagnosed in 57 subjects. Asthmatics presented higher FeNO values than control subjects (median, 20 parts per billion [ppb]; interquartile range, 14 to 31 ppb; vs median, 11 ppb; interquartile range, 7 to 13 ppb, respectively; p < 0.0001), whereas they did not differ from patients with allergic rhinitis (median, 17 ppb; interquartile range, 12 to 23 ppb; p = 0.28). FeNO values > 19 ppb presented 85.2% specificity and 52.4% sensitivity for the diagnosis of asthma (area under the curve [AUC], 0.723). The diagnostic performance of FeNO was better in nonsmokers (AUC, 0.805), yet FeNO values > 25 ppb were characterized by specificity > 90% for the diagnosis of asthma both in smokers and in nonsmokers. However, FeNO was not a good marker for the differentiation between asthma and allergic rhinitis. CONCLUSIONS: FeNO measurement with a portable analyzer is useful for the screening for asthma in young adults. Significant confounding factors are allergic rhinitis and current smoking.
Abstract: The data on long-term application of non-invasive ventilation (NIV) in patients with chronic respiratory failure due to COPD are contradictory. We evaluated the effect of the addition of NIV to optimal treatment for 1 year on the quality of life of stable hypercapnic COPD patients. NIV was offered to 49 of 58 initially enrolled consecutive patients, of whom 22 refused NIV and comprised the standard treatment group whereas 27 received NIV. Quality of life was assessed with the SF-36 questionnaire. Additional measurements included blood gases, pulmonary function tests, dyspnea, daytime sleepiness, exacerbations and hospitalizations. The NIV group showed a significant improvement in quality of life in the third month, both in the Physical (31+/-4 to 38+/-8, p<0.0001) and the Mental Component Summary Score (28+/-7 to 40+/-10, p=0.009), that was maintained until the twelfth month. PaCO2 decreased by the first month in the NIV group (54+/-4.5 to 44.6+/-5.6 mmHg, p<0.0001), and PaO2 rose during the sixth month (58.9+/-5.7 to 64.4+/-6.5 mmHg, p=0.004). Dyspnea and diurnal sleepiness improved significantly. No significant improvements were observed in the control group. Patients on NIV spent less days in the hospital compared to controls. NIV when added to optimal medical treatment has beneficial effects on quality of life in stable hypercapnic COPD patients, with additional improvements in arterial blood gases, dyspnea and daytime sleepiness.
Abstract: BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a fatal illness characterized by progressive fibrosis resulting in severe dyspnea and impairment of lung function. Although the mechanisms by which lung fibrosis develops are not fully ascertained, recent findings suggest that oxidative stress may play an important role in the pathogenesis of tissue fibrosis. AIM: To evaluate the oxidative stress in the serum of patients with IPF and to explore the relationship between oxidative stress levels, dyspnea and impairment of lung function. MATERIAL AND METHODS: Blood samples from 21 untreated patients with IPF, sequentially recruited over a period of 2 years, and 12 controls were analyzed. The level of oxidative stress in the blood was determined through a spectrophotometric procedure (D-ROMs test). FVC and DLCO were measured in all patients. The level of dyspnea was assessed by the Medical Research Council (MRC) chronic dyspnea scale. RESULTS: Serum levels of oxidative stress were significantly increased in patients with IPF compared to controls (mean+/-SEM: 356.8+/-14 and 201+/-10 Carratelli units respectively, p<0.001). Oxidative stress was negatively associated with FVC (p<0.01, r=-0.79) and with DLCO (p<0.01, r=-0.75). Furthermore, oxidative stress was significantly correlated with MRC dyspnea score (p<0.01, r=0.87). Oxidative stress measurements were highly reproducible on two consecutive measurements in the same patients. CONCLUSION: The levels of systemic oxidative stress are enhanced in patients with IPF and could provide useful information about the classification of IPF severity. Strategies to reduce the oxidant burden in IPF may be beneficial in reducing the progressive deterioration of these patients.
Abstract: Exhaled breath condensate (EBC) analysis, a rather appealing and promising method, can be used to evaluate conveniently and non-invasively a wide range of molecules from the respiratory tract, and to understand better the pathways propagating airway inflammation. A large number of mediators of inflammation, including adenosine, ammonia, hydrogen peroxide, isoprostanes, leukotrienes, prostanoids, nitrogen oxides, peptides and cytokines, have been studied in EBC. Concentrations of such mediators have been shown to be related to the underlying asthma and its severity and to be modulated by therapeutic interventions. Despite the encouraging positive results to date, the introduction of EBC in everyday clinical practice requires the resolution of some methodological pitfalls, the standardization of EBC collection and finally the identification of a reliable biomarker that is reproducible has normal values and provides information regarding the underlying inflammatory process and the response to treatment. So far, none of the parameters studied in EBC fulfils the aforementioned requirements with one possible exception: pH. EBC pH is reproducible, has normal values, reflects a significant part of asthma pathophysiology and is measurable on-site with standardized methodology although some methodological aspects of measurement of pH in EBC (e.g. the effect of ambient CO(2), sample de-aeration, time for pH measurement) require further research. However, EBC pH has not been evaluated prospectively as a guide for treatment, in a manner similar to exhaled NO and sputum eosinophils. EBC represents a simple and totally non-invasive procedure that may contribute towards our understanding of asthma pathophysiology. Besides the evaluation of new biomarkers, the standardization of the already existing procedures is warranted for the introduction of EBC in clinical practice.
Abstract: The aim of the present study was to evaluate the levels of VEGF, 8-isoprostane and TNF-alpha in EBC and serum of patients with primary lung cancer prior to the initiation of any treatment, in order to evaluate their possible diagnostic role. Furthermore, associations between VEGF, 8-isoprostane and TNF-alpha levels in EBC and serum with clinicopathologic factors were investigated. We enrolled 30 patients with lung cancer (mean age 65.2+/-10.5 years) and 15 age and gender-matched healthy smokers as controls. Serum and EBC were collected before any treatment. TNF-alpha, VEGF and 8-isoprostane levels in EBC and serum were analyzed by an immunoenzymatic method (ELISA). A statistically significant difference was observed between lung cancer patients and the control group regarding the values of TNF-alpha, both in EBC (52.9+/-5.0pg/ml vs. 19.4+/-3.9pg/ml, p<0.0001) and serum (44.5+/-6.3pg/ml vs. 22.2+/-4.3pg/ml, p=0.035). Moreover, EBC VEGF levels were higher in patients with T3-T4 tumor stage compared to T1-T2 (9.3+/-2.8pg/ml vs. 2.3+/-0.7pg/ml, p=0.047). A statistically significant correlation was also observed between serum and EBC values of VEGF (r=0.52, p=0.019). In addition, serum levels of VEGF were higher in lung cancer patients than in controls (369.3+/-55.1pg/ml vs. 180.5+/-14.7pg/ml, p=0.046). VEGF serum levels were also found higher in patients with advanced stage of disease (IIIB-IV) and distant nodal metastasis (N2-N3). No differences were observed in 8-isoprostane in EBC between lung cancer patients and controls. In contrast, serum 8-isoprostane levels were higher in lung cancer patients compared to controls (24.9+/-3.6pg/ml vs. 12.9+/-1.6pg/ml, p=0.027) and were higher in patients with advanced disease. All three biomarkers presented acceptable reproducibility in the EBC on two consecutive days. In conclusion, we have shown that TNF-alpha, VEGF and 8-isoprostane are elevated in the serum of lung cancer patients and increased serum VEGF and 8-isoprostane levels are related to advanced disease. In EBC, increased TNF-alpha levels were observed in lung cancer patients, whereas increased VEGF levels were observed in advanced T-stage. Further longitudinal studies are warranted for the evaluation of the prognostic role of these biomarkers in lung cancer.
Abstract: Cold air hyperventilation is an indirect challenge (cold air challenge, CACh) with high specificity and low sensitivity in defining asthmatic subjects. A small proportion of chronic obstructive pulmonary disease (COPD) patients present with positive CACh. The aim of this prospective study was to investigate the presence of factors related to cold air challenge (CACh) in COPD patients. Factors examined were FEV(1), FEV(1)/FVC, reversibility after bronchodilation, eosinophils in induced sputum, bronchial hyperresponsiveness to methacholine and the spirometric response to tiotropium compared to placebo. We studied 92 consecutive COPD patients in order to retrieve 15 CACh positive + patients. Fifteen COPD patients with negative CACh [CACh(-)], randomly selected from the initial group, were added in order to retrieve a group of 30 patients. Spearman's correlation coefficient was used in order to evaluate possible significant correlations between CACh values and study parameters. Sixteen percent of our subjects presented CACh+. CACh values were repeatable with an intraclass correlation coefficient between the two measurements 0.980 (95% CI 0.940-0.993). The only significant correlation observed was between Delta FEV(1) after CACh [Delta(C)FEV(1)] and trough FEV(1) values post tiotropium inhalation (r(2) = 0.62, p < 0.0001). When we analyzed the response to tiotropium in the 2 separate groups we found that patients with CACh+ presented significantly lower values of trough FEV(1) compared to those with CACh(-). In conclusion, a small proportion of COPD patients present with bronchial hyperresponsiveness to CACh. The only parameter related to CACh + in our study was a smaller bronchodilating effect of tiotropium.
Abstract: SETTING: A 750-bed tertiary referral hospital in Central Greece. OBJECTIVE: To determine the incidence of non-tuberculous mycobacteria (NTM) respiratory infection based on the isolation of NTM in respiratory specimens, to study their clinical significance and to evaluate the differences in clinical, radiological and demographic characteristics between patients with lung disease caused by NTM and that caused by Mycobacterium tuberculosis complex (MTC). DESIGN: A 3-year period prospective study to identify patients with positive NTM and MTC respiratory specimens. RESULTS: Between January 2004 and December 2006, 564 positive NTM cultures from 214 patients and 118 MTC cultures from the same number of patients were collected. The incidence rate of clinically significant NTM lung infection was 0.67, 0.54 and 0.94 cases per 100,000 population, and that of MTC infection of the lung was respectively 5.70, 5.28 and 5.10 cases/100,000 in the three study years. Smoking habits and chronic obstructive pulmonary disease were significant risk factors for NTM disease (P < 0.05 and P < 0.001, respectively). CONCLUSIONS: NTM incidence rates were lower than those reported in the rest of Europe and the USA. Further studies are needed to determine the prevalence and the significant geographic variability of NTM and their clinical significance at the national level.
Abstract: The need for non-invasive assessment of airway inflammation is imperative, since inflammatory airway diseases, such as asthma and COPD, are characterized by variation in their clinical presentation throughout their course. Exhaled breath condensate (EBC) collection represents a rather appealing method that can be used to conveniently and noninvasively collect a wide range of volatile and non-volatile molecules from the respiratory tract, without affecting airway function or inflammation. Although promising, EBC is currently used only as a research tool, due to the lack of appropriate standardization and the absence of reference values. The large number of measurable biomarkers and the diversity of the used methodologies are some of the points that hamper its wide clinical application. This review focuses mainly on the presentation of normal values of the most widely studied EBC markers as reported by investigators that have used healthy subjects as controls or as a basic study population. These biomarkers include hydrogen peroxide, NO-related products, arachidonic acid metabolites and pH. From those biomarkers, the only one with established reference values in healthy subjects is EBC pH, whereas the majority of the rest need further refinement and standardization of the methodologies used. Different subpopulations and the effect of various factors on healthy subjects are also reported, in an effort to delineate future directions that may lead to the establishment of reference values.
Abstract: BACKGROUND: The aim of our study was to identify predictive factors for the development of residual pleural thickening (RPT) in patients with tuberculous pleurisy (TP). METHODS: A retrospective study of patients with pleural tuberculosis. The clinical and radiological characteristics, and measurements of microbiological and biochemical parameters or markers such as adenosine deaminase (ADA), interferon-gamma (IFN-gamma) and vascular endothelial growth factor (VEGF) in pleural fluid were studied. RESULTS: Thirty one patients (24 male and 7 female) with a mean age of 55.9 years were studied. There were 25 (80.6%) patients with RPT > 2 mm and 6 (19.4%) patients without RPT. Ten patients (32.2%) had RPT > or = 10 mm. The rate of pleural thickening was less in small effusions (p<0.05). IFN-gamma was higher in patients with RPT > or = 10 mm (p < 0.05) in comparison with those with RPT < 10 mm. CONCLUSIONS: Pleural fluid IFN-gamma may deserve further investigation in order to build up preventive and therapeutic strategies against RPT and its clinical complications.
Abstract: Acute-phase markers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), have been studied in inflammatory and malignant disorders. We examined the diagnostic value of these markers for the differentiation among parapneumonic, tuberculous and malignant effusions. We studied 124 patients with pleural effusions, classified as exudates [total (n=97), parapneumonic (n=15), tuberculous (n=25), malignant (n=57)] and transudates due to congestive heart failure (n=27). CRP, IL-6 and TNF-alpha were measured in pleural fluid and serum. Pleural fluid CRP was higher in parapneumonic compared to tuberculous and malignant effusions, providing 100% sensitivity for a cut-off point of 5.3mg/dL. IL-6 was higher in both parapneumonic and tuberculous compared to malignant effusions. TNF-alpha was higher in tuberculous compared to malignant effusions, providing 96.0% sensitivity, and 93.0% specificity for a cut-off point of 88.1 pg/mL. Pleural fluid CRP levels were lower than serum in all groups, probably reflecting systemic inflammation, whereas IL-6 and TNF-alpha were higher in pleural fluid indicating local production. Our data suggest that these markers may provide useful information for the differentiation of infectious and malignant effusions in clinical practice. However, further studies are needed for the validation of these findings in usual clinical circumstances.
Abstract: Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (SaO2 : 92 +/- 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (VO2max : 67.0 +/- 2.6 ml kg(-1) min(-1); mean +/- S.E.M.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 (64 +/- 2, 83 +/- 1, 91 +/- 1 and 96 +/- 1%) via variations in inspired O2 fraction (FiO2 : 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 +/- 3, 80 +/- 3, 85 +/- 3 and 90 +/- 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each FiO2. The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 +/- 28 and 382 +/- 22 cmH2O s min(-1). Ten minutes into recovery, twitch transdiaphragmatic pressure (P(di,tw)) determined by bilateral phrenic nerve stimulation, was significantly (P = 0.0001) reduced after all tests. After both hypoxic tests (FiO2 : 0.13, 0.17) the degree of fall in P(di,tw) (by 26.9 +/- 2.7 and 27.4 +/- 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 +/- 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability.
Abstract: BACKGROUND: Current guidelines suggest the use of non-invasive ventilation (NIV) in hypercapnic chronic obstructive pulmonary disease (COPD) exacerbations in patients presenting with a pH of 7.25-7.35. The aim of this study was to investigate the role of NIV in COPD patients with chronic hypercapnic respiratory failure admitted to the hospital with acute exacerbations and an arterial pH of 7.35 or higher. METHODS: Forty-seven COPD patients with chronic hypercapnic respiratory failure admitted for exacerbations and with a pH of 7.35 or higher were randomized to receive standard medical therapy (control group) or medical therapy plus NIV (NIV group). Arterial blood gases were measured at baseline, after 1 h, 6 h, 12 h, 24 h, 48 h, and at discharge. Need for admission to intensive care unit (ICU), death, and duration of hospitalization were recorded. The final analysis included 42 patients (21 controls and 21 NIV patients). RESULTS: NIV resulted in a shorter hospital stay (5.5+/-2.6 vs 10.1+/-4.4 days for controls, p=0.0004). Two patients from the control group were admitted to the ICU and one eventually died, whereas all NIV patients were successfully discharged. The NIV group showed a faster improvement in PaCO(2) and pH. At discharge, the NIV group had a lower PaCO(2) (6.5+/-0.6 kPa vs 7.5+/-1.1 kPa, p=0.01) but a comparable pH (7.43+/-0.03 vs 7.43+/-0.04, p=0.93). PaO(2) and PaO(2)/FiO(2) levels showed similar improvement in both groups at discharge. CONCLUSION: Early administration of NIV in COPD patients with chronic hypercapnic respiratory failure admitted for acute exacerbations with a pH of 7.35 or higher results in a reduced hospital stay and faster improvement of arterial blood gases.
Abstract: AIMS: The aim of this study was to clarify the association between obstructive sleep apnoea/hypopnoea syndrome (OSAHS)-related symptoms and physician-diagnosed asthma and COPD. METHODS: 1501 subjects aged 19-90 years completed a structured questionnaire and underwent spirometry and respiratory physician assessment in 10 primary care centres. RESULTS: Frequent snoring was reported in 45.6%, breathing pauses during sleep in 11.0%, and excessive daytime sleepiness in 6.7% of the sample. COPD patients were more likely to report frequent snoring (OR=1.34; 95% CI:1.04-1.71), breathing pauses (OR=1.46; 95% CI:1.01-2.10), and excessive daytime sleepiness (OR=2.04; 95% CI:1.33-3.14). In contrast, there was no significant association between asthma patients and OSAHS-related symptoms. Gender differences were recognised as well. CONCLUSIONS: The increased likelihood for OSAHS-related symptoms in COPD patients, in contrast to patients with asthma, designates them as a target group for the screening of OSAHS in primary care.
Abstract: STUDY OBJECTIVE: Hypercapnic cerebral vascular reactivity (HCVR) is reduced in patients with congestive heart failure (CHF) and sleep-disordered breathing (SDB); this may be associated with an increased risk of stroke. We tested the hypothesis that reversal of SDB in CHF patients using adaptive servo ventilation (ASV) would increase morning HCVR. DESIGN: Interventional, cross-over clinical study. SETTING: Research sleep laboratory. PATIENTS: Ten CHF patients with SDB, predominantly obstructive sleep apnea. INTERVENTIONS: The HCVR was measured from the change in middle cerebral artery velocity, using pulsed Doppler ultrasound. HCVR was determined during the evening (before) and morning (after) 1 night of sleep on ASV and 1 night of spontaneous sleep (control). MEASUREMENTS AND RESULTS: Compared with the control situation, ASV decreased the apnea-hypopnea index (group mean +/- SEM, control: 48 +/- 12, ASV: 4 +/- 1 events per hour). HCVR was 23% lower in the morning, compared with the evening, on the control night (evening: 1.3 +/- 0.2, morning: 1.0 +/- 0.2 cm/sec per mm Hg, P < 0.05) and 27% lower following the ASV night (evening: 1.5 +/- 0.2, morning: 1.1 +/- 0.2 cm/sec per mm Hg, P < 0.05). The effect of ASV on the evening-to-morning reduction in HCVR was not significant, compared with the control night (0.02 cm/sec per mm Hg, 95% confidence interval: -0.28, 0.32 P = 0.89). CONCLUSIONS: In CHF patients with SDB, HCVR was reduced in the morning compared with the evening. However, removal of SDB for 1 night did not reverse the reduced HCVR. The relatively low morning HCVR could be linked with an increased risk of stroke.
Abstract: We have examined the role of age on the continuous positive airway pressure (CPAP) levels required to treat two groups of elderly (n=70) and young (n=70) sleep apneic patients, matched for disease severity (apnea/hypopnea index), body mass index and neck circumference. Elderly patients required lower CPAP levels compared to young [mean (sd): 6.9(1.9)cm H(2)O and 9.4(3.5)cm H(2)O, respectively; P<0.0001]. To investigate this finding, we studied the effects of CPAP and its components (inspiratory and expiratory positive airway pressure) on lung volume and upper airway resistance in two groups of elderly [n=9, age 71.7(3.3) years] and young [n=9, age 36.7(4.4)] patients with sleep apnea during wakefulness. CPAP produced a greater decrease in airway resistance (P=0.009) and a greater increase in lung volume (P=0.008) in the elderly compared to young patients. We conclude that both the greater lung inflation and the greater direct splinting of the upper airway contributed to the lower CPAP level required by the elderly. Ageing may be an important determinant of therapeutic CPAP levels in clinical practice, especially in older sleep apneic patients.
Abstract: PURPOSE: To prospectively study the perioperative changes in serum magnesium (sMg) after major lung resections and their effect to the generation of cardiac dysrhythmias, and to present a brief review of the literature surrounding this phenomenon. PATIENTS AND METHODS: We studied 33 patients with non small cell lung cancer (NSCLC), scheduled for major pulmonary resection. Three patients were excluded from the study due to preoperative medication with beta-blocker and calcium (Ca) antagonists. Pneumonectomy was performed in 10 patients and lobectomy in 20. Heparinized arterial blood samples for the assessment of sMg, potassium (K) and Ca concentration were obtained before surgery, on arrival to the High Dependency Unit (HDU), and on the morning of the first and the second postoperative day. No patient had evidence of cardiac disease. RESULTS: Atrial fibrillation occurred in 3 (10%) patients. There was no statistically significant association between sMg and dysrhythmias. A statistically significant difference after adjusting for age was found between sMg concentration, just after the operation and the first post-operative day and the baseline measurement (before the operation). The type of surgical procedure was not found to be associated with the sMg concentration or the appearance of dysrhythmia. The serum K and Ca concentration for all samples was within normal range. CONCLUSION: Serum concentration of Mg decreases significantly within the first 24 hours of major lung resection. Although our study didn't demonstrate a relationship between decreases in sMg and the generation of arrhythmias, this link is well established in other fields and thus we support the prophylactic MgSO(4) administration in their prevention in such cases whilst we await further larger studies.
Abstract: Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 +/- 1.6 ml kg(-1) min(-1); mean +/-s.e.m.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O(2) saturation (S(a,O(2))): 92 +/- 1%) and one hyperoxic (F(I,O(2)): 0.5% O(2); S(a,O(2)) : 97 +/- 1%) 5 min exercise test at intensities equal to 80 +/- 3 and 90 +/- 3% of maximal work rate (WR(max)), respectively, producing the same tidal volume (V(T)) and breathing frequency (f) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P(di,tw)) during recovery. Hyperoxic exercise at 90% WR(max) induced significantly (P= 0.022) greater post-exercise reduction in P(di,tw) (15 +/- 2%) than did normoxic exercise at 80% WR(max) (9 +/- 2%), despite the similar mean ventilation (123 +/- 8 and 119 +/- 8 l min(-1), respectively), breathing pattern (V(T): 2.53 +/- 0.05 and 2.61 +/- 0.05 l, f: 49 +/- 2 and 46 +/- 2 breaths min(-1), respectively), mean changes in P(di) during exercise (37.1 +/- 2.4 and 38.2 +/- 2.8 cmH(2)O, respectively) and end-exercise arterial lactate (12.1 +/- 1.4 and 10.8 +/- 1.1 mmol l(-1), respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S(a,O(2)) tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.
Abstract: Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis which has multiple effects in lung development and physiology. VEGF is expressed in several parts of the lung and the pleura while it has been shown that changes in its expression play a significant role in the pathophysiology of some of the most common respiratory disorders, such as acute lung injury, asthma, chronic obstructive pulmonary disease, obstructive sleep apnea, idiopathic pulmonary fibrosis, pulmonary hypertension, pleural disease, and lung cancer. However, the exact role of VEGF in the lung is not clear yet, as there is contradictory evidence that suggests either a protective or a harmful role. VEGF seems to interfere in a different manner, depending on its amount, the location, and the underlying pathologic process in lung tissue. The lack of VEGF in some disease entities may provide implications for its substitution, whereas its overexpression in other lung disorders has led to interventions for the attenuation of its action. Many efforts have been made in order to regulate the expression of VEGF and anti-VEGF antibodies are already in use for the management of lung cancer. Further research is still needed for the complete understanding of the exact role of VEGF in health and disease, in order to take advantage of its benefits and avoid its adverse effects. The scope of the present review is to summarize from a clinical point of view the changes in VEGF expression in several disorders of the respiratory system and focus on its diagnostic and therapeutic implications.
Abstract: The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean +/- SE: age, 25 +/- 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P < 0.001) and a significant decrease in R-R interval at 3 s (P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 +/- 3 to 104 +/- 3 mmHg; O, 86 +/- 3 to 105 +/- 3 mmHg; P = 0.99. R-R interval: C, 1.12 +/- 0.03 to 0.89 +/- 0.04 s; O, 1.11 +/- 0.02 to 0.87 +/- 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P < 0.001); this increase was not different between the two conditions (C: 4.40 +/- 0.29 to 6.76 +/- 0.61 l/min, O: 4.35 +/- 0.34 to 7.65 +/- 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.
Abstract: STUDY OBJECTIVES: Some patients with COPD present with significant reversibility of airflow limitation after receiving bronchodilation therapy. Leukotriene B(4) (LTB(4)) has been implicated in the pathophysiology of both COPD and asthma. We tested the hypothesis that COPD patients with airflow reversibility and asthmatic patients who smoke might have similar levels of LTB(4) in exhaled breath condensate (EBC) and sputum supernatant. The repeatability and stability of LTB(4) measurements were additionally studied. DESIGN: Prospective, cross-sectional study. PATIENTS OR PARTICIPANTS: We studied 30 patients with COPD (15 smokers [FEV(1), 56% predicted; SD, 6% predicted]; 15 patients with significant reversibility in airway obstruction after bronchodilation [FEV(1), 14% predicted; SD, 2% predicted]). Fifteen asthmatic patients who smoked, with similar FEV(1) and reversibility were also studied. Ten healthy smokers served as control subjects. SETTING: A hospital research laboratory. INTERVENTIONS: Spirometry and reversibility testing were performed on the first visit. On the following day, EBC was collected for the measurement of LTB(4), and induced sputum was collected for differential cell counts and LTB(4) measurement in the sputum supernatant. MEASUREMENTS AND RESULTS: LTB(4) levels in EBC [mean (SD)] were increased in COPD patients (mean, 86.7 pg/mL; SD, 19 pg/mL) and asthmatic patients (mean, 97.5 pg/mL; SD, 15 pg/mL) compared to control subjects (mean, 32.3 pg/mL; SD, 10 pg/mL; p < 0.0001 for both groups). COPD patients with airflow reversibility (mean, 99.8 pg/mL; SD, 12 pg/mL) had values similar to those of asthmatic patients (mean, 97.5 pg/mL; SD, 15 pg/mL; p = 0.2) and higher than those of COPD patients without airflow reversibility (mean, 73.7 pg/mL; SD, 17 pg/mL; p = 0.002). Similar results were observed in the sputum supernatant. Measurements of LTB(4) in EBC and sputum were repeatable on two consecutive days, but measurements in the frozen samples of EBC and sputum were not stable after 3 weeks. CONCLUSIONS: Patients with asthma and reversible COPD presented with higher LTB(4) values compared to patients with nonreversible COPD and healthy smokers. This difference may be mainly attributed to the presence of reversibility in airway obstruction, probably as part of a common underlying inflammatory process.
Abstract: BACKGROUND AND PURPOSE: The reduction in hypercapnic cerebral vascular reactivity that occurs in the morning after sleep is associated with an increased risk of cerebral ischemia and stroke. It is not known if the cerebral vascular response to hypoxia is similarly reduced in the morning, but such a reduction could be considered a further risk factor for cerebral vascular disease. METHODS: To test if the cerebral vascular response to hypoxia is reduced in the morning, the overnight changes in the left middle cerebral artery velocity (MCAV) in response to isocapnic hypoxia (IH) and hypercapnia before and after a normal night sleep were determined in 18 individuals. RESULTS: From evening to morning, hypercapnic cerebral vascular reactivity decreased significantly (evening 2.0+/-0.4, morning 1.3+/-0.2 cm/sec/mm Hg; P<0.05); in contrast, the increase in MCAV in response to IH (-10% SaO2) was unchanged (evening 9.0+/-1.4, morning 8.7+/-2.2%; P>0.05). CONCLUSIONS: Our findings indicate that substantial differences exist in the regulation of the cerebral circulation in response to hypoxia and hypercapnia on waking from sleep. An intact cerebral vascular response to IH, during this time period, could be interpreted as a protective mechanism against cerebral ischemia and stroke; this is of particular relevance to patients with obstructive sleep apnea who arouse from sleep during hypoxia.
Abstract: STUDY OBJECTIVES: Oxidative stress has been associated with various respiratory disorders. We tested the hypothesis that exudates would present higher levels of oxidative stress compared to transudates, expressing the increased local oxidative burst in the former. DESIGN: Prospective, cross-sectional study. PATIENTS OR PARTICIPANTS: One hundred six consecutive patients who had undergone thoracentesis were studied. Ninety patients with a final diagnosis of pleural effusion were further analyzed. SETTING: The respiratory department and a clinical laboratory of a tertiary hospital. INTERVENTIONS: Subjects underwent diagnostic thoracentesis, and standard biochemical parameters (ie, total protein, lactate dehydrogenase, and albumin levels) were measured in pleural fluid and serum. Oxidative stress levels were assessed with a commercially available method (d-ROMs test; Diacron; Grosseto, Italy) that uses conventional Carratelli units (UCarr). In 14 patients, duplicate measurements of oxidative stress and a second thoracentesis were performed on the following day for the assessment of the repeatability of measurements. Receiver operating characteristic (ROC) analysis was performed in order to determine the optimal cutoff level for the differentiation between exudates and transudates. MEASUREMENTS AND RESULTS: Oxidative stress levels were higher in exudates compared to transudates (mean [+/- SD] stress level, 274 +/- 72 vs 126 +/- 34 UCarr, respectively; p < 0.0001). No significant differences were found among the levels of oxidative stress in exudative effusions of different etiologies. The area under the ROC curve was 0.992 (95% confidence interval, 0.945 to 0.997), and the method provided high sensitivity (96.8%), high specificity (96.3%), and high accuracy (96.7%) for the diagnosis of exudates at a cutoff level for oxidative stress of 186 UCarr. Consecutive measurements of oxidative stress in the same samples and on fluid from two different thoracenteses performed on 2 consecutive days presented excellent repeatability. CONCLUSIONS: Oxidative stress levels are higher in exudative pleural effusions compared to transudative effusions, probably due to reactive oxygen species produced in the former.
Abstract: OBJECTIVES: The purpose of the study is to investigate the contribution of lymphatic spread in operable non-small cell lung cancer (NSCLC) in relation to the cancer location. METHODS: We retrospectively studied 557 consecutive patients [514 males and 43 females, mean age 62.5 +/- 9.1 years (range, 20-84)] who underwent a major lung resection due to NSCLC in our department, from January 1995 to December 1999. Preoperative staging for metastatic disease was negative. Extended mediastinal lymph node dissection was performed in all lung resections. RESULTS: The pathology report revealed 220 adenocarcinomas, 276 squamous-cell, 34 undifferentiated, 25 adenosquamous and 2 large-cell carcinomas. The TNM stage was IA in 52 patients, IB in 109, IIA in 20, IIB in 146, IIIA in 190, IIIB in 35 and IV in 5. The classification of disease was N0 in 240 (40.1%) patients, N1 in 179 (32.1%) and N2 in 138 (24.8%). Twenty-eight patients (5.03%) presented a skip metastasis to hilar lymph nodes, while 27 patients (4.85%) presented with skip metastasis to the mediastinum. The size of the primary tumors presenting with metastases was significantly smaller in adenocarcinomas compared to squamous-cell carcinomas (P = 0.046). Regarding the right lung, tumors originating in the upper lobe mainly metastasized to level No. 4, while tumors of the middle lobe spread to stations Nos. 4 and 7, and those in the lower lobe to level No. 7. Regarding the left lung, tumors originating in the upper lobe metastasized to level No. 5, while tumors within the lower lobe spread to stations, Nos. 7-9. CONCLUSIONS: Mediastinal lymph nodal dissection is necessary for the accurate determination of pTNM stage. It seems that there is no definite way for lymphatic spreading in relation to the location of the cancer. Skip metastasis to the mediastinal lymph nodes was present in 4.85% of our patients, while adenocarcinomas, even small-sized ones, are more aggressive than squamous-cell carcinomas.
Abstract: A case of a 30-year-old male with a fever, dry cough and associated abnormal findings in imaging modalities (bilateral hilar lymphadenopathy and nodular parenchymal opacities) is described. After a further and scrutinized work-up, the diagnosis of GLUS syndrome was made. Clinical, etiological, pathological and therapeutical aspects of the disease are discussed, demonstrating the paramount importance of the use of the immunohistochemical methods in the diagnosis of this disorder.
Abstract: OBJECTIVE: To evaluate the levels of hydrogen peroxide (H(2)O(2)) and 8-isoprostane in the expired breath condensate (EBC) of patients with COPD, and to assess the relationship between the above markers of oxidative stress and parameters expressing inflammatory process and disease severity. SETTING: Inpatient respiratory unit and outpatient clinic in tertiary care hospital. DESIGN: Cross-sectional study. PATIENTS: Thirty stable COPD patients (all smokers) with disease severity ranging from mild to severe. Ten subjects who were smokers with stage 0 disease (ie, at risk for COPD; mean [+/- SD] FEV(1), 88 +/- 5% predicted) were studied as a control group. METHODS: H(2)O(2) and 8-isoprostane levels were measured in EBC, and the values were correlated with variables expressing COPD severity (ie, FEV(1) percent predicted, dyspnea severity score (ie, Medical Research Council scale) and airway inflammation (ie, differential cell counts from induced sputum). RESULTS: The mean concentration of H(2)O(2) was significantly elevated in COPD patients compared to control subjects (mean, 0.66 micromol/L [95% confidence interval (CI), 0.54 to 0.68 micro mol/L) vs 0.31 micro mol/L [95% CI, 0.26 to 0.35 micromol/L], respectively; p < 0.0001). The difference was primarily due to the elevation of H(2)O(2) in patients with severe and moderate COPD, whose expired breath H(2)O(2) levels were significantly higher than those of patients with mild disease (mean, 0.96 micromol/L [95% CI, 0.79 to 1.13 micromol/L], 0.68 micromol/L [95% CI, 0.55 to 0.81 micromol/L], and 0.33 micromol/L [95% CI, 0.24 to 0.43 micromol/L], respectively, p < 0.0001). The mean concentration of 8-isoprostane was significantly elevated in patients with COPD compared to that of the control group (47 pg/mL [95% CI, 41 to 53 pg/mL] vs 29 pg/mL [95% CI, 25 to 33 pg/mL], respectively; p < 0.0001) but did not differ significantly among the different stages of the disease (p = 0.43). Repeatability and stability data within measurements showed that H(2)O(2) has a better repeatability and stability than 8-isoprostane. Furthermore, we observed significant correlations of H(2)O(2) with FEV(1), neutrophil count, and dyspnea score. Those correlations existed only in patients with moderate and severe disease. No correlations were found between levels of 8-isoprostane and the above parameters. CONCLUSIONS: We conclude that levels of H(2)O(2) and 8-isoprostane are elevated in the EBC of patients with COPD, but that H(2)O(2) seems to be a more repeatable and a more sensitive index of the inflammatory process and the severity of the disease.
Abstract: BACKGROUND: Cardiac tamponade as the initial manifestation of metastatic cancer is a rare clinical entity. Furthermore, a thoraco-biliary fistula is another rare complication of echinococcosis due to rupture of hydatid cysts located at the upper surface of the liver to the pleural or pericardial cavity. We report a case of non-small cell lung cancer with a coexisting hepatic hydatid cyst presenting as a bilious pericardial effusion. CASE REPORT: A 66-year-old patient presented with cardiac tamponade of unknown origin. Chest CT-scan demonstrated a left central lung tumor, a smaller peripheral one, bilateral pleural effusions and a hydatid cyst on the dome of the liver in close contact to the diaphragm and pericardium. Pericardiotomy with drainage was performed, followed by bleomycin pleurodesis. The possible mechanism for the bilious pericardial effusion might be the presence of a pericardio-biliary fistula created by the hepatic hydatid cyst. CONCLUSIONS: This is the first case of a bilious pericardial effusion at initial presentation in a patient with lung cancer with coexisting hepatic hydatid cyst.
Abstract: Inhaled prostaglandin (PG)E2 has been found to cause bronchodilation in asthmatics, although it does not have bronchodilative effects in normal subjects. The aim of this study was to investigate the levels of PGE2 in the expired breath condensate of patients with asthma, the possible contribution of smoking habit to its levels and the possible relationship between PGE2 and the degree of bronchial hyperresponsiveness, as assessed by the provocation dose of histamine causing a 20% fall in forced expiratory volume in one second (FEV1) (PD20). A total of 30 mild asthmatics (15 smokers, all steroid-naive, FEV1 88+/-6 (%+/-SD)) and 20 healthy control subjects (10 smokers) were studied. Histamine challenge testing was performed in all subjects and the PD20 was determined. The results showed that asthmatic smokers had significantly higher values of PGE2 compared to asthmatic nonsmokers and control subjects (40+/-21 versus 14.5+/-4.5 versus 11.7+/-3 pg x mL(-1), respectively). Further analysis showed that PGE2 levels were significantly higher in asthmatic smokers compared to smoker and nonsmoker controls (40+/-21 versus 11.6+/-2 versus 11.7+/-4 pg x mL(-1), respectively). No significant difference was observed between asthmatic nonsmokers and both control smokers and control nonsmokers. No significant correlation was found between PGE2 levels and PD20 in all groups of asthmatics, irrespective of smoking habit. In conclusion, the elevation of prostaglandin E2 in the expired breath condensate of patients with asthma is mainly attributed to smoking habit and prostaglandin E2 levels do not predict the degree of bronchial hyperresponsiveness.
Abstract: Endogenous airway acidification, as assessed by pH in expired breath condensate, has been implicated in asthma pathophysiology. We measured pH in breath condensate of patients with inflammatory airway diseases in stable condition and examined its relationship with the inflammatory process (as assessed by differential cell counts in induced sputum), oxidative stress (as assessed by H(2)O(2) and 8-isoprostane), and nitric oxide metabolism (as assessed by total nitrate/nitrite). We studied 40 patients with bronchial asthma (20 with moderate disease, forced expiratory volume in 1 second 60 [10]% SD predicted), 20 patients with bronchiectasis, 20 patients with chronic obstructive pulmonary disease (COPD), and 10 normal subjects. Mean (95% confidence intervals) pH values were significantly lower in patients with COPD and bronchiectasis compared with patients with asthma and control subjects (7.16, 7.09-7.23 and 7.11, 7.04-7.19 versus 7.43, 7.35-7.52 and 7.57, 7.51-7.64, respectively, p < 0.0001). Patients with moderate asthma had significantly lower values compared with mild and control subjects. In patients with COPD and bronchiectasis, the values of pH were significantly correlated with both sputum neutrophilia and oxidative stress. Respectively, in patients with moderate asthma, a significant correlation was observed between pH and sputum eosinophilia, total nitrate/nitrite, and oxidative stress. The pH of the expired breath condensate might be a simple, noninvasive, inexpensive, and easily repeatable procedure for the evaluation of the inflammatory process in airway diseases.
