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  • SUMMARY. Morbidly obese subjects are characterized by important changes in respiratory function both during spontaneous breathing as well as during general anesthesia and mechanical ventilation. The most characteristic abnormalities consist of decreased functional residual capacity (FRC), reduced expiratory reserve volume, decreased compliance and increased resistance of the respiratory system. Breathing at low lung volume promotes airway closure in the dependent lung zones with consequent gas exchange abnormalities. Furthermore, the decreased expiratory reserve as a result of decreased FRC and the higher ventilatory requirements of these patients due to increased metabolic demands may promote expiratory flow limitation (EFL) in the tidal volume range. The presence of peripheral airway closure and EFL during tidal breathing promotes peripheral airway injury and may accelerate the abnormalities of lung function. The risk of injury is expected to be higher during mechanical ventilation due to the high pressure transients, which develop under this condition. Consequently, external positive endexpiratory pressure must be applied to these subjects in order to increase the end-expiratory lung volume above the closing volume as well as the flow limitation volume and thus, decrease the risk of peripheral airway injury. Pneumon 2007; 20(3):230-234.
  • SUMMARY. Background: Obstructive sleep apnoea syndrome (OSAS) and metabolic syndrome share common pathogenetic mechanisms such as central obesity, insulin resistance, dyslipidaemia, inflammation, and cardiovascular disease. Objectives: The aim of this study was to investigate the prevalence of metabolic syndrome in patients with OSAS referred to the sleep laboratory of the Department of Pneumonology of the Medical School of the Democritus University of Thrace. Population and Method: Seventy-nine (79) subjects were studied, with medical history, clinical examination, laboratory biochemical tests and full polysomnography. Results: Twenty-one subjects (27%) did not suffer from OSAS and served as controls, while 58 subjects (73%) suffered from mild (n=17), moderate (n=8) or severe (n= 33) OSAS. In the control group 15/21 subjects (71.43%) met the diagnostic criteria for metabolic syndrome. In the OSAS group, 16/17 patients (94.18%) with mild disease, 7/8 patients (87.5%) with moderate disease and 25/33 patients (75.75%) with severe disease suffered from metabolic syndrome. No statistically significant difference in the prevalence of metabolic syndrome was detected between the groups. Conclusions: The prevalence of metabolic syndrome, although high in patients with OSAS, did not differ significantly from that in subjects without OSAS. Pneumon 2007; 20(3):240-244.
  • Summary. The case is reported of pulmonary actinomycosis in a middle-aged woman, a smoker, who had clinical and radiological findings of a tumour-like lesion. The diagnosis was made by CTguided fine needle aspiration biopsy, which revealed tissue rich in actinomycetes. Treatment with a course of penicillin was effective, with complete resolution of the pulmonary lesions and with no relapse four years after the completion of treatment. Pneumon 2007; 20(3):249-252.
  • SUMMARY. The case is presented of a patient with two thoracic tumours. The diagnostic approach included the use of conventional chest X-ray, thoracic CT scan, 3D CT and an FNA core biopsy. The management was based on surgical excision of the tumours. The histological examination of the surgical tissue biopsy revealed two schwannomas and excluded malignancy. Pneumon 2007; 20(3):258-262
  • SUMMARY. The lung is directly and continuously exposed to the environment and has therefore developed strong defense mechanisms, which, as those of other organs, include innate and adaptive immune responses. Mechanical barriers, secretions of the bronchial mucosa, antimicrobial constituents of the blood, such as the complement system, and the leukocytes and phagocytes of the pulmonary system are all part of the innate defense. Adaptive immunity is deployed through delayed mechanisms, which are mediated mainly by T-cells, B-cells and the antibodies they produce. Adaptive immunity is specific for each virulent factor; it leads to the development of immune memory and therefore leads to successful and rapid response against that specific pathogen in future encounters. The balance between all these immune mechanisms is crucial for the deployment of a successful defense against infectious agents, cancer cells and autoimmune disorders, and for minimization of collateral lung tissue damage. Disorders of immune response may occur, leading either to reduced response and immune deficiency (serious infections) or to overreaction of the immune response, with allergy or autoimmune disease. Such disorders can characteristically be observed in diseases such as bronchial asthma, pulmonary emphysema, granulomatous inflammation, idiopathic pulmonary fibrosis and acute respiratory distress syndrome. Pneumon 2007; 20(3):274-278
  • SUMMARY. Due to its large surface area and its rich blood supply, the lung is susceptible to oxidative injury by many reactive oxygen species and free radicals. The main sources of oxidants affecting the lung include external agents (smoke, radiation, carcinogens, drugs, ozone, hyperoxia) and cellular mechanisms (inflammatory cells such as neutrophils, eosinophils, macrophages, fibroblasts, endothelial cells, xanthine and NADPH oxidases). Via these sources oxygen and nitrogen reactive species are produced, which exert the final harmful effect of cell damage. The major oxidative agents are the superoxide anion, hydrogen peroxide, the hydroxyl radical, nitric oxide, etc. Antioxidants help the lung to ward off the consequences of the oxidative injury. Antioxidant defenses include non-enzymatic agents (vitamins C and E, beta-carotene, uric acid) and enzymes (dismutase, catalases and peroxidases). New research has revealed the activity in antioxidant defense at a more subtle level of low molecular weight proteins such as oxygenase-heme, thioredoxins, etc. The susceptibility of the lung to oxidant injury depends mainly on the degree of its ability to upregulate the antioxidant defenses, which means that the various lung diseases attributed to oxidative injury could possibly be controlled by the antioxidant mechanisms at the cellular level or even at the level of gene expression. Antioxidant defense may be present at both cell and mRNA expression level, but antioxidant activity is the critical factor in the development and progression of lung disease. Pneumon 2007; 20(3):289-292
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