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Anastasios Kallianos,1 Athanasios Panoutsopoulos,1 Christoforos Mermigkis,2 Konstantinos Kostopoulos,1 Chrysanthi Papamichail,1 Ioannis Kokkonouzis,3 Christoforos Kostopoulos,1 Ioannis Nikolopoulos,4 Antonis Papaiwannou,5 Sofia Lampaki,5 John Organtzis,5 Georgia Pitsiou,5 Paul Zarogoulidis,5 Georgia Trakada1 1Sleep Disorders Unit, Department of Clinical Therapeutics, “Alexandra” General Hospital, Athens School of Medicine, 2Sleep Disorders Unit, Pulmonary Department, 401 General Army Hospital, 3Pulmonary Department, 251 Hellenic Air Force General Hospital, 4Sleep Disorders Unit, “Sotiria” Regional Chest Diseases Hospital of Athens, Athens, Greece; 5Pulmonary Department – Oncology Unit, George Papanikolaou General Hospital of Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, GreeceIntroduction: There is growing research evidence suggesting the presence of endothelial dysfunction and systemic inflammation in patients with obstructive sleep apnea syndrome (OSAS). Continuous positive airway pressure (CPAP) is the most effective method for treating OSAS; nonetheless, the effects of CPAP on the aforementioned pathophysiologic pathways as well as on the systemic disease that result or coexist with the OSAS remain elusive.Aim: To assess the effect of 3-month CPAP therapy on endothelial-dependent dilation, plasma levels of inflammatory markers, blood pressure (BP), and glucose control on male and female patients with OSAS.Methods: Our study group consisted of 40 (24 males and 16 females) patients with no prior history of cardiovascular disease, with an apnea–hypopnea index ≥15, who were assigned to receive CPAP treatment. Measurements of flow-mediated dilation (FMD), 24-hour ambulatory BP, and blood analysis were performed at baseline and 3months after CPAP therapy.Results: Baseline FMD values were negatively correlated with the apnea–hypopnea index (r=−0.55, P=0.001). After 3months of CPAP, there was an increase in the FMD values (5.40%±2.91% vs 3.13%±3.15%, P

Anastasios Kallianos,1 Paul Zarogoulidis,2 Fotini Ampatzoglou,2 Georgia Trakada,2,3 Elias Gialafos,4 Georgia Pitsiou,2 Athanasia Pataka,2 Lemonia Veletza,2 Konstantinos Zarogoulidis,2 Wolfgang Hohenforst-Schmidt,5 Dimitris Petridis,6 Ioannis Kioumis,2 Aggeliki Rapti112nd Pulmonary Department, Sotiria Chest Diseases Hospital, Athens, 2Pulmonary Department-Oncology Unit, “G Papanikolaou” General Hospital, Aristotle University of Thessaloniki, Thessaloniki, 3Pulmonary Laboratory, Therapeutic Clinic Alexandra Hospital, University of Athens, Athens, 4Heart Diseases Department Aiginitio Hospital, University of Athens, Athens, Greece; 5Medical Clinic I, “Fuerth” Hospital, University of Erlangen, Fuerth, Germany; 6Department of Food Technology, School of Food Technology and Nutrition, Alexander Technological Educational Institute, Thessaloniki, GreeceIntroduction: Pulmonary function tests (PFTs) do not always predict functional limitations during exercise in sarcoidosis. Cardiopulmonary exercise testing (CPET) may facilitate the recognition of exercise intolerance in these patients.Aim: As relevant data in sarcoid patients are limited, the aim of the study reported here was to assess exercise capacity impairment during a maximal CPET and to evaluate potential correlations with PFT measurements and radiological stages of the disease.Method: A total of 83 sarcoid patients consecutively referred for evaluation of exertional dyspnea over a 3-year period were studied retrospectively with PFTs, including spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) and lung volumes, and CPET using standard protocol. Patients were grouped according to their radiological stages: Stage I (n=43), Stages II–III (n=31), and Stage IV (n=9).Results: Forced expiratory volume in 1 second, forced vital capacity, and total lung capacity were mildly impaired only in Stage IV (means ± standard deviation: 72.44±28.00, 71.33±26.70, and 59.78±21.72, respectively), while DLCO was mildly and moderately reduced in Stages II–III and IV (72.68±14.13 and 51.22±18.50, respectively) and differed significantly between all stages (I vs II–III: P=0.003, I vs IV: P=0.003, and II–III vs IV: P=0.009). Exercise capacity (as expressed by peak oxygen consumption

Anastasios Kallianos,1 Sotirios Tsimpoukis,2 Paul Zarogoulidis,3 Kaid Darwiche,4 Andriani Charpidou,2 Ilias Tsioulis,3 Georgia Trakada,5 Konstantinos Porpodis,3 Dionysios Spyratos,3 Athanasios Panoutspoulos,5 Lemonia Veletza,5 Konstantinos Kostopoulos,5 Charalampos Kostopoulos,4 Ilias Karapantzos,6 Kosmas Tsakiridis,7 Wolfgang Hohenforst-Schmidt,8 Konstantinos Zarogoulidis,3 Aggeliki Rapti,1 Konstantinos Syrigos21Second Pulmonary Clinic, Sotiria Hospital, 2Oncology Unit, Sotiria Hospital, Athens, Greece; 3Oncology Unit, G Papanikolaou General Hospital, Thessaloniki, Greece; 4Interventional Unit, Ruhrland Clinic, Essen, Germany; 5Pulmonary Laboratory, Alexandra Hospital, Athens, Greece; 6Ear, Nose, and Throat Department, Saint Luke Private Hospital, 7Cardiothoracic Department, Saint Luke Private Hospital, Thessaloniki, Greece; 8II Medical Clinic, Hospital of Coburg, Coburg, GermanyAbstract: Nitric oxide (NO) is a marker of airway inflammation and indirectly a general indicator of inflammation and oxidative stress. NO is a contributing factor in lung cancer at an early stage and also after chemotherapy treatment of lung cancer. We studied whether exhaled NO levels were altered by three cycles of chemotherapy at diagnosis and after chemotherapy, and whether, directly or indirectly, these changes were related to the course of disease. Also, a correlation of NO levels with other markers of inflammation was performed. We studied 42 patients diagnosed early: 26 men and 16 women with lung cancer. We analyzed blood tests for control of inflammatory markers, functional pulmonary tests, and alveolar exhaled NO. We recorded a decrease in exhaled NO after three cycles of chemotherapy in all patients, regardless of histological type and stage: there were 42 patients with mean 9.8 NO after three cycles (average 7.7). Also, a strong correlation appeared between NO measurements before and after chemotherapy and C-reactive protein (P < 0.05, r = 0.42, before) and (P < 0.045, r = 0.64, after). NO alveolar measurement as an indicator of airway inflammation indicates response to chemotherapy in lung cancer. Also, the inflammatory process in lung cancer was confirmed and indicated response to chemotherapy through an index that is sensitive to inflammatory disease of the airways.Keywords: nitric oxide, lung cancer, inflammation

Nikolaos Papanas1, Paschalis Steiropoulos2, Evangelia Nena2, Argyris Tzouvelekis2, Efstratios Maltezos1, Georgia Trakada2, Demosthenes Bouros21Outpatient Clinic of Obesity, Diabetes and Metabolism at the 2nd Department of Internal Medicine, 2Department of Pneumonology, Democritus University of Thrace, Alexandroupolis, GreeceAbstract: The aim of this study was to examine the potential correlation of sleep characteristics with glucose metabolism in nondiabetic men with obstructive sleep apnea syndrome (OSAS). Included were 31 male patients (mean age 46.7 ± 11 years), recently diagnosed with OSAS by full polysomnography. There was a significant correlation of fasting glucose and glycosylated hemoglobin (HbA1c) levels with arousal index (P = 0.047 and P = 0.014, respectively). Moreover, HbA1c levels were correlated with apnea hypopnea index (P = 0.009), a widely accepted marker of the severity of OSAS, and with percentage of sleep time with saturation of hemoglobin with oxygen as measured by pulse oximetry (SpO2)