Background:The clinical presentation of hemoptysis often raises a number of diagnostic possibilities. Objectives:This study was designed to evaluate the relative frequency of different causes of hemoptysis and the value of chest radiography, computed tomography (CT) scanning and fiber-optic bronchoscopy in the evaluation of a Greek cohort population. Methods:We prospectively followed a total of 184 consecutive patients (137 males/47 females, 145 smokers/39 nonsmokers) admitted with hemoptysis between January 2001 and December 2003 to the University Hospital of Heraklion. Follow-up data were collected on August 2005. Results:The main causes of hemoptysis were bronchiectasis (26%), chronic bronchitis (23%), acute bronchitis (15%) and lung cancer (13%). Bronchiectasis was significantly more frequent in nonsmokers (p < 0.02). Among nonsmokers, patients with moderate/severe bleeding or a history of tuberculosis were more likely to have bronchiectasis (OR 8.25; 95% CI 1.9–35.9, p = 0.007 and OR 16.5; 95% CI 1.7–159.1, p = 0.007, respectively). Nonsmokers with normal or abnormal X-rays were equally likely to have bronchiectasis (OR 2.5; 95% CI 0.66–9.39, p = 0.2). Lung cancer was only found in smokers. Smokers with normal X-rays were less likely to have lung cancer compared to smokers with abnormal X-ray (OR 5.4; 95% CI 1.54–19.34, p = 0.004). There were no smokers with normal CT and lung cancer. Follow-up data were collected in 91% of patients. Lung cancer did not develop in any patient assumed to have hemoptysis of another origin than lung cancer on initial evaluation. Conclusions:Bronchiectasis is the main diagnosis in patients admitted with hemoptysis to a Greek University Hospital and it is more frequent among nonsmokers with moderate/severe bleeding and/or previous tuberculosis infection. Nonsmokers with moderate/severe hemoptysis and/or a history of tuberculosis should be evaluated with high-resolution CT. Smokers with hemoptysis are at increased risk for lung cancer and need to be extensively evaluated with chest CT and bronchoscopy.

CD8+ve T-cell responses play a primary role in chronic obstructive pulmonary disease (COPD), but there is little information regarding COPD exacerbations. Sputum induction is a relatively non-invasive and safe method to study airway inflammation. The aim of the study was to investigate changes in airway T-lymphocyte subpopulations at the onset of severe COPD exacerbations via analysis of sputum. Induced sputum samples were collected from 12 COPD patients aged (mean±sd) 69±7 years, ex-smokers (68±23 pack-years), mean FEV1 (%predicted) 40±14 at the onset of an acute severe exacerbation requiring hospital admission and 16 weeks after remission of the exacerbation. Inflammatory cells and T-lymphocyte subpopulations (CD4, CD8, Tc1, Tc2) were measured using chemical and double immunocytochemical methods. Increased percentages of sputum neutrophils (P=0.002) and decreased CD4/CD8 and CD8-IFNγ/CD8-IL4+ve (Tc1/Tc2) cell ratios (P=0.03,P=0.02, respectively) were found at the onset of exacerbation compared to stable state. We conclude that a CD8+ve type-2-mediated immune response is induced at the onset of severe COPD exacerbation.

STUDY OBJECTIVES:The aim of this study was to examine the relationship between airway inflammation, nitrosative stress, heme-oxygenase expression, and acute severe exacerbations of COPD.DESIGN:We measured heme oxygenase (HO)-1, inducible nitric oxide (NO) synthase expression and nitrotyrosine formation, as well as eosinophilic cationic protein, myeloperoxidase (MPO), interleukin (IL-8), and granulocyte macrophage-colony stimulating factor levels in induced sputum samples from 12 COPD patients (mean +/- SD; FEV1 40 +/- 14% predicted) at the onset of an acute severe exacerbation of COPD requiring hospital admission and 16 weeks after remission.RESULTS:We demonstrated increased percentages (p = 0.001) and absolute numbers (p = 0.028) of total nitrotyrosine positive (+ve) inflammatory cells (ie, polymorphonuclear cells and macrophages), increased percentages (p = 0.04) and absolute numbers (p = 0.05) of total HO-1 +ve inflammatory cells, and increased MPO (p = 0.005) and IL-8 levels (p = 0.028) during severe exacerbation compared with the stable state.CONCLUSIONS:Our results support the hypothesis of an involvement of inflammatory and nitrosative stress in severe COPD exacerbations. Future therapeutic strategies may aim at regulating inflammation and NO synthesis during COPD exacerbations.

Disagreement exists between different COPD guidelines considering classification of severity of the disease. The aim of our study was to determine whether there is any correlation between severity scales of various COPD guidelines (ATS, BTS, ERS and GOLD) and the frequency of hospitalisations for COPD exacerbation. A cohort of 67 COPD patients (65 male–2 female, 45 ex-smokers, 22 current smokers, aged (69.4±1.1)) was recruited from those admitted in the pulmonary clinic of the University Hospital of Heraklion, Crete for an acute exacerbation. Lung function tests and arterial blood gases analyses were performed during stable conditions at a scheduled visit 2 months after discharge. The patients were stratified using the FEV1 percent-predicted measurement of this visit into mild, moderate and severe in accordance to the ATS, BTS, ERS and GOLD scales of severity. The number of hospitalisations for acute exacerbation was recorded for the following 18 months. A total of 165 exacerbations were recorded. The correlation between the severity of COPD and the number of hospitalisations per year was statistically significant using the GOLD classification system of severity (P=0.02 and r=0.294). A weak correlation was also found between the number of hospitalisations and the ERS classification system (P=0.05 and r=0.24). No statistically significant correlation was found between the number of hospitalisations and the ATS or BTS severity scales. In conclusion the GOLD and ERS classification systems of severity of COPD correlated to exacerbations causing hospitalisation. The same was not true for the ATS and BTS severity scales. Better correlation was achieved with the GOLD scale.

BACKGROUND Previous studies have shown that the inflammatory response to cigarette smoking differs between smokers who acquire COPD and those who do not, and the CD8(+) T- lymphocytes have been identified as a key player in this response. OBJECTIVE To investigate the cytotoxic activity and perforin expression of CD8(+) lymphocytes in the airway lumen of patients with COPD. METHODS Thirty-six male smokers with COPD, 25 male smokers without COPD, and 10 healthy nonsmokers participated in the study. T-lymphocytes of induced sputum samples were labeled with appropriate monoclonal antibodies and measured using flow cytometry. The cytotoxic activity of CD8(+) cells was defined by incubating them with specific target cells (K562). RESULTS The percentage and the total number of CD8(+) lymphocytes were significantly higher in COPD smokers compared to non-COPD smokers (p = 0.01 and p = 0.005, respectively) or to healthy nonsmokers (p = 0.02 and p = 0.01, respectively). Perforin expression in CD8(+) cells was significantly higher in smokers with COPD compared to the other two groups (p = 0.001). Increased cytotoxic activity of T cells was also observed in induced sputum of patients with COPD in comparison to the other two groups. CONCLUSION CD8(+) cells are not only increased in number in sputum samples of smokers with COPD but are highly activated, expressing high levels of perforin. These findings suggest that CD8(+) T-lymphocytes play a significant role in the inflammatory process of COPD.

Background Severe persistent asthma (SPA) and chronic obstructive pulmonary disease (COPD) are both associated with non-reversible airflow limitation and airway neutrophilia.Objective To compare inflammatory cell profiles and T lymphocyte subsets between SPA and COPD patients with similar severity of airflow limitation.Methods Sputum induction and lung function tests were performed in 15 COPD patients aged (mean+/-SD) 68+/-8 years, ex-smokers, mean forced expiratory volume in 1 s (FEV1) 45% of predicted (%pred) and 13 SPA aged 55+/-10 years, non-smokers, mean FEV1 49%pred. All patients were on inhaled steroid treatment. Eight asthmatics exhibited irreversible airflow limitation. Differential cell count, metachromatic cell count and double immunocytochemistry for the analysis of T lymphocyte subsets were performed on sputum slides.Results COPD patients had increased sputum neutrophils in comparison with SPA (P<0.03), but similar to SPA with fixed obstruction. In COPD sputum neutrophils negatively correlated with the lung transfer factor for carbon monoxide (K-CO) (r=-0.462, P=0.04). SPA showed significantly increased eosinophils and metachromatic cells vs. COPD patients (P<0.04, P<0.007, respectively). Increased CD4/CD8 and decreased CD4-IFN-gamma/CD4-IL4(+) cell ratio (P<0.001) were found in SPA vs. COPD. In SPA, CD4/CD8(+) cell ratio correlated with sputum eosinophils (r=0.567, P=0.04).Conclusion In spite of treatment with inhaled steroids, SPA and COPD exhibit distinct sputum inflammatory cell patterns, although SPA with fixed airflow limitation and COPD patients have similar numbers of neutrophils.

Background: Previous studies have shown that the inflammatory response to cigarette smoking differs between smokers who develop chronic obstructive pulmonary disease (COPD) and those who do not and that the CD8(+) T-tymphocytes have been identified as a key player in this process. The aim of this study was to investigate further the role of CD8(+) cells and their subtypes in sputum cells.Methods: Sputum induction was performed in 36 COPD patients, 25 smokers without COPD and 10 non-smoking healthy controls. After stimulation of sputum lymphocytes with phorbol-myristate-acetate, we used double immunocytochemical methods to identify CD4(+), CD8(+) cells and CD8(+) INFgamma or IL4 cells (Tc1, Tc2).Results: COPD patients had an increased number of CD8(+) cells in sputum as compared with smokers without COPD (P = 0.0001) and control subjects (P = 0.001). CD8(+)-IL4 cells were reduced both in COPD and in smokers without COPD compared to controls (P = 0.0001), while CD8(+)-IFNgamma cells were significantly reduced only in COPD (P = 0.001) as compared with controls. A significant (P = 0.02) relationship between the CD8(+)-IL4/CD8(+)-IFNgamma ratio and FEV1 (% pred) was found only in COPD patients.Conclusion: These findings suggest that an imbalance both in T-lymphocyte subpopulation (CD4/CD8) and in CD8(+) cell subsets (Tc1/Tc2) characterizes the inflammatory responses of smokers with established COPD. (C) 2003 Elsevier Ltd. All rights reserved.

Chronic obstructive pulmonary disease (COPD) constitutes an enormous and growing health problem, the treatment of which has been less than satisfactory so far. It is a disease state characterized by an abnormal inflammatory process in the airway wall of the large and peripheral airways as well as in the parenchyma as a response to inhalation of several noxious agents including mainly the smoking. This inflammatory response is characterized by an increase in macrophages, neutrophils and T-lymphocytes with a predominance of CD8(+) cells. Several inflammatory mediators are likely to play a role in COPD including LTB4, IL-8 and TNF-alpha. The inflammatory process in COPD is markedly different from that in asthma and requires different therapy. A diagnosis of COPD should be considered in any patient who has cough, sputum production, dyspnea and a history of current or ex-smoking or exposure to several risk factors. The diagnosis should be confirmed by an obstructive ventilatory disorder with spirometry. The effective management of COPD includes the assessment and monitoring of the disease, reducing risk factors with emphasis to smoking cessation, managing stable COPD and effective treatment of the exacerbations. Improved methods for early detection, new medication through targeted pharmacotherapy and possible means to identify the susceptible smokers could be new therapy and to prevent modalities against this epidemic.

BACKGROUND AND AIM Induced sputum (IS) has been proposed as a useful non-invasive method mainly for the assessment of airway diseases. The aim of this study was to evaluate IS cellular composition and T-lymphocyte subpopulations and to compare them with those of bronchoalveolar lavage fluid (BALF) in patients with sarcoidosis. METHODS We studied prospectively 20 patients (12 female, 8 male) of median age 46 yr (range 25-65) with sarcoidosis and 10 normal subjects (5 female, 5 male) of median age 39 yr (range 26-60). IS was performed with hypertonic saline solution using an ultrasonic nebulizer (De Vilbis 2000). BALF was performed by conventional procedure using fiberoptic bronchoscopy. May-Giemsa-Grunewald stained preps were differentially counted and T-lymphocyte subsets were analyzed by flow activated cell sorter (FACS). RESULTS The percentage of macrophages was significantly lower in IS than in BALF (p < 0.0001), the percentage of neutrophils was significantly lower in BALF than in IS (p < 0.0001), while there was no difference in the percentage of lymphocytes (p = 0.693) and eosinophils (p = 0.25) in IS vs BALF in patients with sarcoidosis. A significant correlation was found between BALF and IS lymphocyte counts (r = 0.61, p = 0.004), macrophages (r = 0.51, p = 0.02), and CD4+/CD8+ ratio (r = 0.700, p = 0.001). CONCLUSIONS These results suggest that the inflammation in sarcoidosis could be effectively and non-invasively determined by the analysis of cell differential counts and T-lymphocyte subsets in IS. Further studies are needed to explore the role of IS vs BALF in the follow-up of these patients.