BACKGROUND: Malignant Pleural Mesothelioma (MPM) is a tumour of the surface cells of the pleura that is highly aggressive and mainly caused by asbestos exposure. Electronic noses capture the spectrum of exhaled volatile organic compounds (VOCs) providing a composite biomarker profile (breathprint). OBJECTIVE: We tested the hypothesis that an electronic nose can discriminate exhaled air of patients with MPM from subjects with a similar long-term professional exposure to asbestos without MPM and from healthy controls. METHODS: 13 patients with a histology confirmed diagnosis of MPM (age 60.9±12.2 year), 13 subjects with certified, long-term professional asbestos exposure (age 67.2±9.8), and 13 healthy subjects without asbestos exposure (age 52.2±16.2) participated in a cross-sectional study. Exhaled breath was collected by a previously described method and sampled by an electronic nose (Cyranose 320). Breathprints were analyzed by canonical discriminant analysis on principal component reduction. Cross-validated accuracy (CVA) was calculated. RESULTS: Breathprints from patients with MPM were separated from subjects with asbestos exposure (CVA: 80.8%, sensitivity 92.3%, specificity 85.7%). MPM was also distinguished from healthy controls (CVA: 84.6%). Repeated measurements confirmed these results. CONCLUSIONS: Molecular pattern recognition of exhaled breath can correctly distinguish patients with MPM from subjects with similar occupational asbestos exposure without MPM and from healthy controls. This suggests that breathprints obtained by electronic nose have diagnostic potential for MPM.

Background: Sarcoidosis is a systemic granulomatous disease of unknown cause that affects the lungs in over 90% of cases. Breath analysis by electronic nose technology provides exhaled molecular profiles that have potential in the diagnosis of several respiratory diseases. Objectives: We hypothesized that exhaled molecular profiling may distinguish well-characterized patients with sarcoidosis from controls. To that end we performed electronic nose measurements in untreated and treated sarcoidosis patients and in healthy controls. Methods: 31 sarcoidosis patients (11 patients with untreated pulmonary sarcoidosis [age: 48.4 +/- 9.0], 20 patients with treated pulmonary sarcoidosis [age: 49.7 +/- 7.9]) and 25 healthy controls (age: 39.6 +/- 14.1) participated in a cross-sectional study. Exhaled breath was collected twice using a Tedlar bag by a standardized method. Both bags were then sampled by an electronic nose (Cyranose C320), resulting in duplicate data. Statistical analysis on sensor responses was performed off-line by principal components (PC) analyses, discriminant analysis and ROC curves. Results: Breathprints from patients with untreated pulmonary sarcoidosis were discriminated from healthy controls (CVA: 83.3%; AUC 0.825). Repeated measurements confirmed those results. Patients with untreated and treated sarcoidosis could be less well discriminated (CVA 74.2%), whereas the treated sarcoidosis group was undistinguishable from controls (CVA 66.7%) Conclusion: Untreated patients with active sarcoidosis can be discriminated from healthy controls. This suggests that exhaled breath analysis has potential for diagnosis and/or monitoring of sarcoidosis. (C) 2013 Elsevier Ltd. All rights reserved.

Pulmonary arterial hypertension (PAH) is a rare condition characterized by an increase in pulmonary arterial resistance leading to right heart failure and death. Arrhythmias are a growing problem in PAH; therefore, maintenance of sinus rhythm is considered to be an important treatment aim in these patients. We described the case of a 46-year-old woman with HIV-associated pulmonary arterial hypertension  who developed atrial flutter. After treatment with bosentan, it was observed a significant improvement in clinical and haemodynamic parameters. In addition, the AFL, which had previously persisted to both antiarrhythmic drug therapy and electrical stimulation, and had recurred after transthoracic electrical cardioversion, disappeared  in absence of any antiarrhythmic drug. Though the precise factors responsible for supraventricular arrhythmogenesis are still largely obscure, it is likely that initiation and maintenance of AFL may depend on all the conditions that can lead to increase in right atrial pressure, size, and wall stress, such as PAH. In our case, bosentan reduced both mean pulmonary artery pressure (mPAP) value and right heart chambers pressures. Therefore, it is conceivable that with the anatomical substrate needed for the maintenance of AFL being disappeared, sinus rhythm was restored.

A 57-year-old woman underwent an enucleoresection of her right kidney angiomyolipoma. Two weeks later she was admitted to our hospital because of dyspnea at rest with orthopnea. The chest x-ray showed the elevation of both hemidiaphragms and the measurement of the sniff transdiaphragmatic pressure confirmed the diagnosis of bilateral diaphragmatic paralysis. A diaphragm paralysis can be ascribed to several causes, i.e. trauma, compressive events, inflammations, neuropathies, or it can be idiopathic. In this case, it was very likely that the patient suffered from post-surgery neuralgic amyotrophy. To our knowledge, there are only a few reported cases of neuralgic amyotrophy, also known as Parsonage-Turner Syndrome, which affects only the phrenic nerve as a consequence of a surgery in an anatomically distant site.

Can you diagnose the cause of this man's bilateral pulmonary nodules and acute respiratory failure? http://ow.ly/NfED30dDBzm.

MalignantPleuralMesothelioma(MPM)isanaggressiveneoplasm that isveryoftenassociatedwithasbestosexposure.MPMdiagnosisisdifficult, veryoftenrequiringinvasiveapproachessuchasthoracoscopy.Exhaledbreath containshundredsofdifferentvolatileorganiccompounds(VOCs)whichmaybe usedfordiagnosisofvariouspulmonaryandsystemicdisordersincludinglung cancer. Methods: Weenrolled13patientswithanestablisheddiagnosisofMPM,13 healthy controls(HC),and13subjectswithaprofessionalexposuretoasbestos without MPM(EXP).Tedlarbagswereusedtocollecthumanbreath.Samples werecollectedusingasorbent-trapfollowedbythermaldesorptionandanalysis by gaschromatographwithananalyticalmassspectrometer(GC-MS). Results: AnalysisshowedthatthemostabundantVOCs(>15 ng/L)inthein- vestigatedsampleswerecyclopentaneand cyclohexane.Thechemicalprofilewas differentforthesamplesclasses:EXPandMPM,showedalteredlevelsoftoluene, xylene, benzaldehyde,trimethylbenzene, limonene, 2-ethyl-1-hexanol,acetophe- none, cyclopentane.MPMpatientsshowed higherconcentrationofcyclohexane (meanvalue=339.31ng/L)comparedtoEXP(meanvalue=173.06ng/L)and controls(meanvalue=30.68ng/L).ByusingtheTukeyHSDtestitwasfound that cyclohexaneconcentrationforMPMwas significantlydifferentcomparedto HC (p=0.006)whereastheconcentrationforEXPwasnotsignificantlydifferent both comparedtoMPM(p=0.146)andcontrolgroup(p=0.285). Conclusions: BreathAnalysisbyGC-MSmayplayapotentialroleinthenon- invasiveassessmentofMPM.

COPD is currently recognized as a syndrome associated with a high prevalence of comorbidities and various phenotypes. Exacerbations are very important events in the clinical history of COPD because they drive the decline in lung function. In the present study, we aim to identify whether there are any clinical and functional specific features of frequent exacerbators in a population of patients with severe COPD.

In obese subjects with obstructive sleep apnea (OSA), chronic intermittent hypoxia (CIH) may be linked to systemic and adipose tissue inflammation.

Obstructive Sleep Apnea (OSA) is a sleep-related breathing disorder associated with the development of cardiovascular diseases and atherosclerosis. Systemic inflammation plays an important role in the development of cardiovascular complications in OSA patients. The aim of the study was to evaluate the relationship between carotid intima-media thickness (cIMT) and inflammatory markers plasma levels in OSA patients. We enrolled 80 OSA patients and 40 controls matched for age and body mass index (BMI). The presence and severity of sleep apnea was determined by in-laboratory portable monitoring (PM). Demographic data, blood pressure, heart rate, and cIMT were measured. High-sensitive C-Reactive Protein (hsCRP), interleukin (IL)-6, tumor necrosis factor (TNF)-α and pentraxin (PTX)-3 serum concentrations were detected. cIMT was higher in OSA patients than controls (0.89 ± 0.13 mm vs. 0.65 ± 0.1 mm, p < 0.01). Moderate-severe OSA patients (0.95 ± 0.09 mm) had significantly increased cIMT than mild OSA (0.76 ± 0.1 mm; p < 0.01) and control (0.65 ± 0.1 mm; p < 0.01). hsCRP, IL-6, TNF-α, and PTX-3 in patients with OSA (1.67 ± 0.66 mg/L, 2.86 ± 1.39 pg/mL, 20.09 ± 5.39 pg/mL, 2.1 ± 0.59 ng/mL, respectively) were significantly higher than in controls (1.08 ± 0.53 mg/L, p < 0.01; 1.5 ± 0.67 pg/mL, p < 0.01; 12.53 ± 3.48 pg/mL, p < 0.01; 1.45 ± 0.41 ng/mL, p < 0.01, respectively). Carotid IMT was significantly correlated to CRP (r = 0.44; p < 0.01), IL-6 (r = 0.42; p < 0.01), TNF-α (r = 0.53; p < 0.01), and PTX-3 (r = 0.49; p < 0.01). OSA patients showed increased cIMT, CRP, IL-6, TNF-α, and PTX-3 levels. Inflammatory markers levels are correlated to cIMT in OSA patients.

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We read with great interest the article of Dr. Blomster H and colleagues entitled:“Endothelial function is well preserved in obese patients with mild obstructive sleep apnea”[1]. In the manuscript, the authors clearly show that mild obstructive sleep apnea (OSA) does not correlate with endothelial dysfunction, measured by brachial artery flow-mediated dilatation (FMD), assuming that in mild OSA, endothelial function is still preserved. The data are very interesting, although the authors did not analyze the time of onset of symptoms, as well as ...

Abstract Background: Tremolite is one of the six recognized types of asbestos, whose toxicity and carcinogenity is welldocumented. Resident population in the area of Lagonegro (Basilicata, Italy) has been shown to be exposed to enviromental tremolite pollution, deriving from superficial rocks and asbestos caves. A branch of the ongoing health surveillance program for residents is evaluating the prevalence of pulmonary functional abnormalities. Methods: The study group was composed by 655 long-term residents in the tremolite-exposed area of Lagonegro (age 49.35 ± 16.68, current smokers 109, ex-smokers 126) . The control group was composed by 653 individuals living in areas not tremolite-exposed (age 54.45 ± 17.16, current smokers 128, ex-smokers 137). All the participants to the study performed a lung function test. Results: Prevalence of obstructive and restrictive diseases did not show significant differences between the two groups. Tremolite-exposed group showed a higher prevalence of small-airways disease compared to the nonexposed group (p&lt;0.01). Odds Ratio for small-airways obstruction was 3.46 (95% CI, lower limit 2.55, upper limit 4.69). irrespective of smoking status. Conclusions: According to our data, tremolite exposure may be a risk factor for small airways disease. It is mandatory to follow these subjects longitudinally by repeated measurements

Recently, it has been clearly described an independent relationship between obstructive sleep apnea syndrome (OSAS) and cardiovascular risk, with underlying mechanisms also including endothelial dysfunction. We enrolled 32 consecutive non-obese patients (mean age of 39.5±11.5 years), of which 16 with mild OSAS and 16 snoring without OSAS. Mild OSAS is defined by an AHI index between 5 and 15. We have investigated if whether there was a relationship between mild OSAS, endothelial function and carotid intima-media thickness (C-IMT). The population was divided into two groups: Group 1 (16 simple snorer patients with an average age of 39.4±12.1 years) and Group 2 (16 subjects with mild OSAS with an average age of 39.6±11.2 years). Each group underwent cardiovascular investigation including measurement of flow-mediated dilation (FMD) of the brachial artery and C-IMT. Both groups comprised non-obese subjects. Patients with mild OSAS had serum total cholesterol values statistically significantly higher than simple snores patients (178.6±24.9 vs 159.2±25.3; p=0.038). OSAS patients had also a trend towards higher values of maximum C-IMT compared to simple snorer patients (0.70±0.15 vs 0.65±0.16), although below the level of significance. Between the two groups, no difference was found for FMD values. The present results on mild OSAS strengthen the importance of a diagnosis of OSAS as soon as possible, in order to encourage all primary prevention interventions to correct risk factors responsible for disease progression and the occurrence of cardiovascular diseases, not excluding the use of therapies of non-invasive ventilation even in the early stages of the disease.

Abstract Interest in cypress allergy is widely rising: an increasing number of studies have pointed out the efficacy of immunotherapy to reduce cypress-related symptoms and drug use. Cypress immunotherapy is well tolerated, but there are few studies dealing with its sub-clinical effects on the airways. The aim of this investigation is to assess the effects of immunotherapy on airways by the analysis of exhaled breath condensate (EBC), nasal lavage fluid (NAL) and nasal cytology. Fifteen mono-sensitized to cypress pollen patients have been observed, among them 9 have been treated with sub-cutaneous immunotherapy (SCIT), 3 with sub-lingual immunotherapy (SLIT) and 3 which were not treated underwent EBC, NAL and nasal cytology out of the pollen season. 8-isoprostane in EBC, Eosinophil cationic protein (ECP) and inflammatory cells in nasal cytology were also evaluated. The median value of 8-isoprostane in EBC was 18.58 pg/ml in patients who did not undergo immunotherapy, 49.38 pg/ml in SCIT patients and 13.41 pg/ml in SLIT subjects. The median value of ECP in nasal lavage was higher in non- treated subjects (27.3 mg/l) than in those treated with SCIT (1 mg/l)(p less than 0,05) or SLIT (2.6 mg/l). All nasal cytology specimens did not show any sign of inflammation. In conclusion SLIT seems to be well tolerated and to reduce significantly the levels of ECP in nasal lavage. In addition the levels of 8-isoprostane in EBC among SCIT patients were unexpectedly high and need to be further evaluated.

Background: Obstructive Sleep Apnea Syndrome (OSAS) is a common airways disease recognized as an independent cardiovascular risk factor. It is often associated with obesity, diabetes and dyslipidemia. Its pathophysiological consequences (hypoxia, hypercapnia, micro-arousals, sympathetic hyperactivity, oxidative stress, systemic inflammation and hyper-coagulability) are implicated in the development of hypertension, endothelial dysfunction and higher intima-media thickness (IMT) values, all elements known to lead to atherosclerosis. The study aim was to demonstrate a relationship between OSAS duration and IMT values and to confirm how OSAS severity could influence IMT (a marker of atherosclerosis). Methods: We enrolled 156 patients (125 men, mean age: 60 ± 12 years) affected by OSAS of different severity: 111 (71%) were in CPAP therapy; some of the population were also affected by hypertension [102 (65%)], dyslipidemia [52 (33%)] and diabetes [38 (24%)]. Patients underwent evaluation of carotid artery IMT and answered a questionnaire investigating the time of onset (confirmed by a person aware of the patient's previous sleeping habits) and the duration of the disease. Results: We found a statistically significant higher IMT value in patients with longer-lasting disease (OSAS duration in IMT < 0.9 mm: 120 (60-192) months versus OSAS duration in IMT ≥ 0.9 mm: 200 (120-310) months; p < 0.001). OSAS severity is positively related to IMT values. We found a positive relationship between IMT and OSAS duration [r = 0.34; p < 0.001] and between AHI and IMT [r = 0.51; p < 0.001]. Conclusions: Our study shows that the duration of OSAS and its severity are important factor related with higher values of IMT and hence with a higher risk of atherosclerosis.

Background: The obstructive sleep apnoea syndrome (OSAS) is a common airways disease which often involves cardiovascular structures, causing vessel inflammation as well as hypoxia, induced by difficulties in the passage of air through the upper airways. Aim of our research is to evaluate the effects of Continuous Positive Airway Pressure (CPAP) on the syndrome itself and the patients cardiovascular risk profile, practically adopting Flow-Mediated Vasodilation (FMD) technique to evaluate endothelial function. Methods and results: We enrolled 63 patients (49 males and 14 female, mean age: 54 ± 10 years) subdivided into four groups: high cardiovascular risk factors, no CPAP therapy, CPAP therapy started less- and more than 3 months before. The patients underwent FMD of the brachial artery using a high resolution ultrasonograph connected to an image analysis system. The maximum recovery value was calculated as the ratio (maximum-baseline) of the change in diameter over the baseline value. Data obtained from this study demonstrate the significant reversibility of FMD in patients treated for more than 3 months with CPAP therapy (Group 4). Conclusions: Our study shows the importance of administering CPAP therapy for more than 3 months in patients suffering from OSAS to improve EF to a level equal to high cardiovascular risk subjects probably due to a recovery from the systemic hypoxia. Besides, our work points out the importance of FMD as a clinical tool able to point out any improvement or regression after therapies.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive loss of central and peripheral motor neurons. Some studies have found discordant data in the presence of sleep apnea in ALS patients. An obstructive component also occurs with upper airways hypotonia and muscle weakness that may result in an excessive reduction of airway lumen, leading to obstructive sleep apnea (OSA). The aim of this study was to assess the role of obstructive apneic events at disease onset in the ALS prognosis.

Leptin plays a key role in obstructive sleep apnea syndrome (OSAS). Leptin production in human airways has been previously evaluated by measuring leptin concentration in the exhaled breath condensate and in the induced sputum. The aim was to study leptin expression in the cells of induced sputum and in exhaled breath condensate of subjects with OSAS. Moreover, leptin concentrations in the blood were measured in the same groups of subjects. We enrolled four groups of patients: (1) obese patients with OSAS (OO); (2) non-obese patients with OSAS (NOO); (3) obese patients without OSAS (ONO); and (4) non-obese subjects without OSAS (C). Leptin expression was evaluated by immunocytochemistry in the sputum cells of the enrolled subjects. The concentrations of leptin in the exhaled breath condensate and plasma were measured by using a specific enzyme immunoassay. Leptin protein expression and the percentage of macrophages and neutrophils expressing leptin were higher in the induced sputum of OO, NOO and ONO patients than in C. Leptin concentrations in the exhaled breath condensate were significantly higher in OO patients (5.12 (3.8-6.6) ng ml(-1)) than in NOO (4.1 (3.9-5.2) ng ml(-1)) and ONO (4.2 (3.6-5.0) ng ml(-1)) patients. The concentration of leptin in plasma was significantly more elevated in OO (36 (24-65.9) ng ml(-1)) than in NOO (30.2 (12.4-51.4) ng ml(-1)), whereas it was not significantly different in ONO patients. This study showed that leptin in sputum and in the exhaled breath condensate is higher in obese patients with OSAS than in obese subjects without OSAS. Moreover, different mechanisms for determining leptin concentrations in the exhaled breath condensate and the blood are suggested.