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PubMed2004

[Sulfhemoglobin].

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Biomarkers↗
PubMed2005

Exhaled breath condensate as a method of sampling airway nitric oxide and other markers of inflammation.

Most of the methods of investigating lung diseases have been invasive until the discovery that exhaled nitric oxide can be used as a surrogate marker of airway inflammation, particularly in asthma. Exhaled nitric oxide (NO) is now established as a marker of airway inflammation. It has been shown to correlate well with eosinophilic asthmatic airway inflammation, and to be able to predict decline in asthma control and airway function. Altered levels of NO are also associated with other inflammatory lung diseases. In addition, polymorphisms of the genes encoding the three nitric oxide synthases are associated with phenotypic differences associated with lung diseases. Exhaled NO is, however, non-specific. It is therefore of importance that collecting exhaled breath condensate (EBC) has emerged as a potential tool in the study of pulmonary diseases. The exhaled breath is collected in a cooling system which allows water vapour to condense. The EBC contains a number of mediators relating to the NO pathway, including nitrite as a metabolite of nitric oxide, nitrotyrosine, nitrosothiols plus small molecular mediators associated with oxidative stress, including hydrogen ions, and hydrogen peroxide. In addition, reports are emerging of the detection of larger molecules which not only include leukotrienes, prostaglandins, albumin and other proteins, such as cytokines, but also macromolecules, for example, DNA. EBC is becoming a technique which will allow repeated non-invasive sampling from the respiratory tract thus assisting pulmonary research and possibly the monitoring of lung diseases.

Animals↗
PubMed2005

[Comparison of oxidative stress markers in exhaled breath condensate and in serum of patients with tuberculosis and sarcoidosis].

UNLABELLED: Tuberculosis and sarcoidosis represent the granulomatous diseases. The aim of the study was to compare the markers of oxidative stress: in exhaled breath condensate (EBC) and in serum of patients with tuberculosis and sarcoidosis. MATERIAL AND METHODS: 19 patients with active lung tuberculosis and 15 patients with sarcoidosis were enrolled into the study. As a control served 15 healthy subjects. Hydrogen peroxide (H2O2) was measured in EBC and the ends products of lipid peroxidation (TBARs) were assessed in serum. RESULTS: The concentrations of H202 and TBARs (1022.96+/-186.02 nM and 4.22+/-0. 80 microM, respectively) were significantly higher in patients with tuberculosis as compared with the controls (398.15+/-37.10 nM and 0.48+/-0.17 microM, respectively). The patients with sarcoidosis revealed only the significantly elevated levels of hydrogen peroxide (963.30+/-105.77 nM) in breath condensate. CONCLUSIONS: It was found that local and systemic oxidative stress were present in patients with tuberculosis, while in those with sarcoidosis existed only the local reaction.

Adult↗
PubMedDate not supplied

[Antioxidant protection, metabolites of nitrogen oxide on the forming of oxidative stress in patients with bronchial asthma].

276 Patients with bronchial asthma of different degree of severity have been observed. An increase in processes of lipid peroxidation, depression of antioxidant protection, increase in oxide nitrogen metabolites in blood serum and condensate of exhaled air were detected. These pathological changes may be considered as manifestation of system oxidative stress more expressed in bronchi.

Adult↗
PubMed2005

[Measurement of airway inflammation in asthma].

Despite of the tremendous progress, which was made within the last few years in the diagnostics and treatment of asthmatic patients, there is a lack in a simple, non-invasive methods, which could be useful in the diagnostics and anti-inflammatory treatment monitoring. Invasive methods, such as bronchofiberoscopy (bronchoalveolar lavage fluid analysis and bronchial biopsy), enabled the better understanding of the pathophysiology of asthma and the elaboration of the grounds of pharmacological treatment of this disease. Unfortunately, these methods are less useful in the clinical practice due to their invasiveness. Spirometry, which is essential in diagnostics and treatment of asthmatics, is only indirect way of the airway inflammation assessment. Recent studies are focused on noninvasive methods of the evaluation of airway inflammation, such as measurements of exhaled nitric oxide (FENO) and allergic inflammation mediators in the inducible sputum. The higher degree of inducible form of nitric oxide synthase (iNOS) expression and higher levels of nitric oxide in exhaled air are observed in asthmatic patients. Many studies confirm, that the measurement of exhaled nitric oxide is a simple, non-invasive method in diagnostics and treatment monitoring in asthmatics, which does not intensify the symptoms of asthma.

Asthma↗
PubMed2006

[Exhaled nitric oxide: a new biomarker for respiratory pathologies].

There has been a growing interest for exhaled biomarkers. We review studies examining NO as a potential marker of airway inflammation, enabling noninvasive repeated monitoring of airway inflammation. The measurement technique has been standardized. We have determined the local normal levels for the Liège region. The exhaled NO level is elevated in asthma, and can predict asthma exacerbation. Exhaled NO has a value for the diagnosis of cystic fibrosis and primary ciliary dyskinesia.

Asthma↗
PubMed2005

Risk stratification in the patient with non ST segment elevation acute coronary syndrome.

Patients hospitalized with unstable angina (UA) or with a non-ST segment elevation myocardial infarct (NSTEMI) are at increased risk of suffering refractory angina, recurrent myocardial infarct (MI), and death. These patients need to be evaluated more aggressively. According to the last published guidelines (2002) of UA/NSTEMI by the ACC/AHA Task Force, these patients should be categorized in a risk scale as: low, intermediate or high. This should be done in the initial evaluation, which includes: medical history, physical exam, an electrocardiogram (ECG) and cardiac markers. The TIMI risk score should also be used as complementary in this risk assessment. High risk patients, without contraindications, should be managed more aggressively with coronary angiography. On the other end, low risk patients, and some intermediate, may be evaluated more conservatively with early non-invasive studies for further assessment of ischemia and prognosis.

Acute Disease↗
PubMed2005

[Exhaled hydrogen peroxide (H2O2) in allergic and non-allergic stable mild asthmatic children].

The evaluation of breath condensate (BC) composition is a new, non-invasive method studying inflammation processes in several respiratory diseases. Among many inflammation markers, hydrogen peroxide (H2O2) is the most common one, and its increased level was found in BC of cystic fibrosis and asthma patients. As in children's asthma, H2O2 is present and could correlates with the severity of the disease. The aim of our study was to check whether there exist differences between levels of H2O2 in children with allergic and non-allergic asthma. 83 allergic and 33 non-allergic children with mild asthma (50 girls and 66 boys, aged 7-17 years) were included in the study. All patients were clinically stable and used inhaled corticosteroids daily, and an inhaled bronchodilator on demand. Exhaled BC was obtained by spontaneously tidal volume breathing with EcoScreen (Jaeger, Germany). The content of H2O2 in the BC was measured spectrofluorometrically (homovanillic acid method). All subjects underwent flow-volume measurements immediately after collection of the condensate. Lung function in asthmatic allergic and non-allergic children showed near normal values and did not differ between groups. In the allergic group, the median H2O2 level in the expired condensate was 0.238 (0-1.86) microM, and in non-allergic 0.192 (0-0.78) microM (p > 0.05). We conclude that hydrogen peroxide in exhaled breath condensate of children with stable mild asthma does not differ significantly in allergic and non-allergic children and activity of airway inflammation seems to independent on allergic status of patients.

Adolescent↗
PubMedDate not supplied

Recent developments in human biomonitoring: non-invasive assessment of target tissue dose and effects of pneumotoxic metals.

Tobacco smoke and polluted environments substantially increase the lung burden of pneumotoxic chemicals, particularly pneumotoxic metallic elements. To achieve a better understanding of the early events between exposure to inhaled toxicants and the onset of adverse effects on the lung, the characterization of dose at the target organ would be extremely useful. Exhaled breath condensate (EBC), obtained by cooling exhaled air under conditions of spontaneous breathing, is a novel technique that could provide a non-invasive assessment of pulmonary pathobiology. Considering that EBC is water practically free of interfering solutes, it represents an ideal biological matrix for elemental characterization. Published data show that several toxic metals and trace elements are detectable in EBC, raising the possibility of using this medium to quantify the lung tissue dose of pneumotoxic substances. This novel approach may represent a significant advance over the analysis of alternative media (blood, serum, urine, hair), which are not as reliable (owing to interfering substances in the complex matrix) and reflect systemic rather than lung (target tissue) levels of both toxic metals and essential trace elements. Data obtained among workers occupationally exposed to either hard metals or chromium (VI) and in smokers with or without chronic obstructive pulmonary disease (COPD) are reviewed to show that--together with biomarkers of exposure--EBC also allows the simultaneous quantification of biomarkers of effect directly sampled from the epithelial lining fluid, thus providing novel insights on both kinetic and dynamic aspects of metal toxicology.

Aerosols↗
PubMed2006

[Exhaled nitric oxide in patients with obstructive sleep apnea syndrome].

UNLABELLED: Exhaled nitric oxide has been extensively investigated as a non-invasive marker of airway inflammation. Some authors have suggested that morning FE(NO) in obstructive sleep apnea syndrome (OSAS) patients is elevated due to inflammation of upper airways, while others have not found any differences between patients and healthy subjects. The purpose of this study was to analyze concentration of exhaled nitric oxide (FE(NO)) in OSAS patients. METHODS: 119 (99 M, 20 F) consecutive patients of sleep laboratory participated in this study. Standard overnight sleep studies with polysomnography or portable screening device were carried out in the whole group: OSAS was diagnosed in 66 patients and 53 no-OSAS served as controls. FE(NO) was measured on-line with a flow rate kept at 0.045 - 0.055 l/s, according to the recommendations of ATS using a chemiluminescence analyzer twice: before the sleep study (8-10 p.m.) and after termination of data collection (6 - 8 a.m.). There were no differences in age between patients and controls. Respiratory disturbance index (RDI) was 40.3+/-24.9 in patients and 3.7+/-2.8 in controls (p<0.001). In OSAS patients both evening and morning FE(NO) was significantly higher compared to controls (23.1+/-14.8 ppb vs. 16.8+/-9.8 ppb and 22.4+/-13.2 ppb vs. 15.3+/-8.1 ppb respectively, p<0.05). Weak but statistically significant correlations for the whole group between morning FE(NO) and mean and minimum arterial oxygen saturation (SaO2) during sleep and number of study minutes with SaO2<90% were observed. Lower evening FE(NO) in OSAS patients with coexisting arterial hypertension when compared to normotensive OSAS patients was also noticed (19.1+/-10.8 ppb vs. 27.1+/-19.1 ppb; p<0.05). CONCLUSIONS: The increase in FE(NO) in OSAS patents may be caused by repetitive apneas and hypoxemia during sleep.

Adult↗
PubMed2006

[Influence of bronchoscopy on nitric oxide in exhaled air].

UNLABELLED: Nitric oxide has been extensively studied as a noninvasive marker of airway inflammation, especially in asthma. Assuming, bronchoscopy can produced not only systemic but also local inflammatory response we hypothesized that bronchofiberoscopy can be responsible for an increase in nitric oxide synthesis with resulting increase in fractional concentration of exhaled nitric oxide (FE(NO)). Seventeen subjects (10 M, 7 F), at mean age of 53.8+/-14.1 yrs undergoing diagnostic bronchoscopy participated in the study. The indications for bronchoscopy were as follows: lung cancer (n=5; 29%), interstitial lung diseases (n=3; 18%), slowly resolving pneumonia (n=3; 18%), hemoptysis (n=3; 18%), differential diagnosis of asthma/ dyspnea (n=3; 18%). During bronchoscopy bronchial washing (n=7) and bronchoalveolar lavage (BAL) (n=10) has been performed. FE(NO) has been analyzed on-line with chemiluminescence analyzer (NIOX, Aerocrine, Sweden) according to American Thoracic Society guidelines, before and at 1, 2, 3 and 24 hours after bronchoscopy. Mean FE(NO) before bronchoscopy was 19.7+/-4.5 ppb (mean +/- SEM), post - bronchoscopy a decrease with a nadir at second hour (12.1+/-1.5 ppb, p<0.05) was observed, FE(NO) 24 hours after bronchoscopy was not different than baseline (18.4+/-2.5 ppb). There were no differences in the FE(NO) profile in BAL patients when compared to those in whom only the bronchial washing has been performed. CONCLUSIONS: Bronchoscopy leads to a significant decrease in exhaled nitric oxide. The underlying mechanisms are unclear. Future studies including analysis of other inflammatory markers are needed to explain these changes.

Asthma↗
PubMed1991

DNA adducts and other biological markers in risk assessment for environmental carcinogens.

In order to validate a number of biologic markers as indicators of effective dose or potential risk, we have applied them in related cross-sectional, longitudinal and case-control studies. Biologic markers such as carcinogen-DNA adducts and activated oncogenes have already provided insights into mechanisms of chemical carcinogenesis. They have also given information regarding the extent of interindividual variation in biologic response within the human population. These results are directly relevant to quantitative risk assessment. However, more research is needed to establish quantitative links between biologic markers and human risk of cancer.

Biomarkers↗