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Background: Haemoptysis is a challenging symptom that can be associated with potentially life-threatening medical conditions. Follow-up is key in these patients to promptly detect new or misdiagnosed pathologic findings. Few prospective studies have evaluated long-term prognostic outcomes in patients with haemoptysis. Furthermore, the role played by antiplatelet and anticoagulant drugs on mortality and recurrence rates is unclear. The aim of this study was to assess mortality after 18 months of follow-up. Furthermore, the incidence of recurrence and the risk factors for recurrence and death were evaluated (including the role played by anticoagulant and antiplatelet drugs).Methods: Observational, prospective, multicentre, Italian study.Results: 451/606 (74.4%) recruited patients with haemoptysis completed the 18 months follow-up. 22/604 (3.6%) diagnoses changed from baseline to the end of the follow-up. 83/604 (13.7%) patients died. In 52/83 (62.7%) patients, death was the outcome of the disease which caused haemoptysis at baseline. Only the diagnosis of lung neoplasm was associated with death (OR (95%CI): 38.2 (4.2-347.5); p-value: 0.0001). 166 recurrences were recorded in 103/604 (17%) patients. The diagnosis of bronchiectasis was significantly associated with the occurrence of a recurrence (OR (95% CI): 2.6 (1.5-4.3)); p-value < 0.0001). Anticoagulant, antiaggregant, and anticoagulant plus antiaggregant drugs were not associated with an increased risk of death and recurrence.Conclusions: Our study showed a low mortality rate in patients with haemoptysis followed-up for 18 months. Pulmonary malignancy was the main aetiology and the main predictor of death, whereas bronchiectasis was the most frequent diagnosis associated with recurrence. Antiplatelet and/or anticoagulant therapy did not change the risk of death or recurrence. Follow-up is recommended in patients initially diagnosed with lower airways infections and idiopathic bleeding.Trial Registration: NCT02045394. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a progressive condition characterized by airflow limitation associated with an abnormal inflammatory response of the lungs to noxious particles and gases, caused primarily by cigarette smoking. Increased oxidative burden plays an important role in the pathogenesis of COPD. There is a delicate balance between the toxicity of oxidants and the protective function of the intracellular and extracellular antioxidant defense systems, which is critically important for the maintenance of normal pulmonary functions. Several biomarkers of oxidative stress are available and have been evaluated in COPD. In this review, we summarize the main literature findings about circulating oxidative stress biomarkers, grouped according to their method of detection, measured in COPD subjects. [ABSTRACT FROM AUTHOR]

Background: Few population-based studies have assessed the prevalence and the risk factors of non-allergic rhinitis (NAR) in comparison to allergic rhinitis (AR). Moreover, epidemiologic data on rhinitis in the elderly subjects and in southern Europe are scarce. Objective: This study aimed at estimating the prevalence and at comparing the risk factor distribution of AR and NAR in a general population sample aged 20-84 years in Italy. Methods: A questionnaire on respiratory symptoms and risk factors was administered to random samples of the Italian population aged 20-44 (n = 10,494) 45-64 (n = 2167) and 65-84 (n = 1030) in the frame of the Gene Environment Interactions in Respiratory Diseases (GEIRD) study. Current AR and NAR were defined according to the selfreported presence of nasal allergies or of nasal symptoms without a cold or the flu. Results: NAR showed a significant descending pattern in females from 12.0 % (95 % CI 11.1, 13.1) in the 20-44 year age class, to 7.5 % (5.4, 10.3) in the 65-84 year age class (p = 0.0009), and a roughly stable pattern in males, from 10.2 % (9.3, 11.2) to 11.1 % (8.4, 13.9) (p = 0.5261). AR decreased from 26.6 % (25.7, 27.6) in 20-44 years age class to 15.6 % (13.3, 18.0) in the 65-84 years age class (p < 0.0001), without gender difference. Subjects living near industrial plants and ex- and current smokers had a higher risk of NAR. Current smokers had a lower risk and subjects living in a Mediterranean climate a higher risk of AR. Conclusion: AR and NAR are fairly distinct conditions, as they have a different age, gender and risk factor distribution. [ABSTRACT FROM AUTHOR]

Introduction: Idiopathic pulmonary fibrosis (IPF), a fatal lung disease of unknown origin, is characterized by chronic and progressive fibrosing interstitial pneumonia which progressively impairs lung function. Oxidative stress is one of the main pathogenic pathways in IPF. The aim of this systematic review was to describe the type of markers of oxidative stress identified in different biological specimens and the effects of antioxidant therapies in patients with IPF.Methods: We conducted a systematic search of publications listed in electronic databases (Pubmed, Web of Science, Scopus and Google Scholar) from inception to October 2017. Two investigators independently reviewed all identified articles to determine eligibility.Results: After a substantial proportion of the initially identified articles (n = 554) was excluded because they were duplicates, abstracts, irrelevant, or did not meet the selection criteria, we identified 30 studies. In each study, we critically appraised the type, site (systemic vs. local, e.g. breath, sputum, expired breath condensate, epithelial lining fluid, bronchoalveolar lavage, and lung tissue specimens), and method used for measuring the identified oxidative stress biomarkers. Furthermore, the current knowledge on antioxidant therapies in IPF was summarized.Conclusions: A number of markers of oxidative stress, with individual advantages and limitations, have been described in patients with IPF. Nevertheless, trials of antioxidant treatments have been unable to demonstrate consistent benefits, barring recent pharmacogenomics data suggesting different results in specific genotype subgroups of patients with IPF. [ABSTRACT FROM AUTHOR]