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G Caramori,
G Bettoncelli,
M Carone,
R Tosatto,
P Di Blasi,
A Pieretto,
G Invernizzi,
B Franco Novelletto, A Ciaccia,
I M Adcock,
A Papi
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ABSTRACT: It is important for the Italian National Health Service to obtain data on the degree of control of asthma and chronic obstructive pulmonary disease (COPD) in the general population in Italy in order for balanced planning of future investments in these diseases to be made. Currently, precise estimates of these parameters are not available in literature.
In collaboration with the Italian Academy of General Practitioners (SIMG; www.simg.it) we have investigated the degree of control of physician-diagnosed asthma and COPD in Italy.
A standardised questionnaire on asthma and COPD has been self-administered to a sample of 1937 Italian family physicians (representing around 5% of all the Italian doctors involved in general practice) chosen to cover all the Italian counties.
We have collected questionnaire data from 19,917 patients with asthma and COPD followed in their practice and 12,438 (62.4%) were correctly filled in enabling evaluation. We selected the number of emergency room visits, hospitalisations and intensive care unit admissions for asthma and COPD in the last 12 months as objective measures of the degree of asthma and COPD morbidity in these patients. The figures were respectively 12.4% (emergency room visits), 17.3% (hospitalisations) and 1.2% (intensive care unit admissions) of all patients with physician-diagnosed asthma and COPD.
This data suggests that in Italy the morbidity of asthma and COPD remains high; representing a significant burden for the Italian National Health Service. There is a clear necessity for further studies to investigate the causes of this incomplete control.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 04/2007; 67(1):15-22.
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G Caramori,
N Calia,
C Pasquini,
O Arar,
F Ravenna,
I Guzzinati,
A Boniotti,
L Cavazzini, A Ciaccia,
G Cavallesco,
A Papi
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ABSTRACT: We present a case of a 53 year old man with a thymoma near the pericardium, a rare ectopic localisation of thymoma. A round radiodensity found at the right cardiophrenic angle was initially suspected at the echocardiography to be a pericardial cyst. The diagnosis of thymoma was made only after histopathological examination of the surgically re-sected lesion.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 01/2006; 63(4):230-3.
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G Caramori,
M Fabbri,
D Paioli,
F Falcone,
C Severino,
G Felisatti,
O Arar,
I M Adcock,
K Fan Chung,
P J Barnes, A Ciaccia,
A Papi
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ABSTRACT: Little is known about the long-term natural history of asthma and the long-term clinical and functional consequences in non-smoking patients. From a functional point of view, non-smoking asthmatic patients may have a significantly greater decline in forced expiratory volume in one second (FEV1) compared with non-asthmatic subjects and may develop chronic irreversible (fixed) airflow limitation. This has been related to the physiological consequences of chronic airway inflammation causing airway remodeling. However these lesions are all potentially reversible and there is little radiological evidence indicating lung destruction (pulmonary emphysema), which is potentially irreversible, in non-smoking asthmatics. Severe chronic respiratory failure is the major cause of mortality in patients with severe chronic lung diseases. Domiciliary long-term oxygen therapy (LTOT) is an accepted treatment for patients with severe chronic respiratory failure. Our reasoning, therefore, was that if asthma is a cause of severe chronic respiratory failure in non-smokers we should be able to find non-smoking asthmatics within a large population of patients on LTOT. The aim of our study (Asthma and Long-term Oxygen Therapy, "ALOT") was to investigate the prevalence of non-smoking asthmatics in patients on LTOT in a multi-centre, cross-sectional study.
Between June and September 2003 we screened all subjects on long-term domiciliary oxygen therapy in three different hospitals in the North-East area of Italy (within the provinces of Ferrara and Bologna). Taken collectively, we have found one-hundred and eighty-four patients on LTOT. We have reviewed their clinical data (age, sex, smoking, history and physical examination, arterial blood gas analysis, pulmonary function).
114 patients (all smokers) fulfilled the diagnostic criteria for COPD. Seventy patients (all smokers) had other diseases. We were unable to find any non-smokers in our screened population of subjects on long-term domiciliary oxygen therapy. Furthermore, there was no past history of asthma and/or acute wheezing episodes in either of the patient groups.
This data suggests that asthma is an uncommon cause of severe chronic respiratory failure necessitating long-term domiciliary oxygen therapy in non-smokers and supports the current consensus that asthma and COPD are different diseases with differing stages of severity and the concept that long-term avoidance of active smoking is fundamental for the prevention of severe chronic respiratory failure.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 07/2005; 63(2):84-7.
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ABSTRACT: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) underlines that spirometry is the gold standard as the most reproducible, standardised, and objective way of measuring airflow limitation in the diagnosis and assessment of Chronic Obstructive Pulmonary Disease (COPD). However, studies undertaken in different countries have suggested a widespread underuse of spirometry by general practitioners to establish the diagnosis of COPD. Precise estimates of the prevalence of physician-diagnosed COPD in Italy are not currently available. In collaboration with the Italian Academy of General practitioners (SIMG) we have investigated the degree of use of spirometry to establish the diagnosis of COPD in Italy.
A standardised questionnaire has been self-administered to a sample of 2425 Italian general practitioners (representing 5% of all the Italian doctors involved in general practice). They have been chosen to cover each of the Italian counties.
The prevalence of physician-diagnosed COPD was found to be approximately 4%. However, 30% of general practitioners do not use spirometry to establish the diagnosis of COPD. The main reasons given for the failure to use spirometry are (i) that spirometry is not necessary for the diagnosis of COPD or (ii) there are logistical limitations to the access of the patients to lung function laboratories.
This data suggests that contrary to GOLD Guidelines, in Italy, as with other countries, spirometry is not always used in the diagnosis of COPD. There is a clear necessity for further education initiatives targeted to this group of physicians.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 04/2005; 63(1):6-12.
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G Caramori,
C Di Gregorio,
I Carlstedt,
P Casolari,
I Guzzinati,
I M Adcock,
P J Barnes, A Ciaccia,
G Cavallesco,
K F Chung,
A Papi
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ABSTRACT: To study the expression of mucins in peripheral airways in patients with chronic obstructive pulmonary disease (COPD).
Peripheral lung sections from smokers with COPD (n = 9) and age-matched controls including smokers (n = 11) and lifelong non-smokers with normal lung function (n = 6) were stained with alcian blue, periodic acid-Schiff (PAS) and by immunohistochemistry of mucins (MUC): MUC2, MUC4, MUC5AC, MUC5B and MUC6. Histochemical staining and immunoreactivity of bronchiolar epithelium were graded and the presence or absence of stained mucus in the bronchiolar lumen was evaluated. There were no differences in alcian blue and PAS epithelial staining between the three groups. Intraluminal PAS staining was significantly more frequent among COPD subjects (P < 0.05). The expression of MUC5AC was significantly higher in the bronchiolar epithelium of patients with COPD (P < 0.05). Within the bronchiolar lumen, the predominant mucin was MUC5B. Intraluminal MUC5B was significantly more frequent among COPD patients (P < 0.05).
COPD is specifically associated with increased expression of MUC5B in the bronchiolar lumen and of the mucin MUC5AC in the bronchiolar epithelium. These changes in mucin production in the peripheral airways may contribute to the pathophysiology of COPD.
Histopathology 12/2004; 45(5):477-84. · 3.08 Impact Factor
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A Papi,
G Casoni,
G Caramori,
I Guzzinati,
P Boschetto,
F Ravenna,
N Calia,
S Petruzzelli,
L Corbetta,
G Cavallesco,
E Forini,
M Saetta, A Ciaccia,
L M Fabbri
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ABSTRACT: Squamous cell carcinoma has a stronger association with tobacco smoking than other non-small cell lung cancers (NSCLC). A study was undertaken to determine whether chronic obstructive pulmonary disease (COPD) is a risk factor for the squamous cell carcinoma histological subtype in smokers with surgically resectable NSCLC.
Using a case-control design, subjects with a surgically confirmed diagnosis of squamous cell carcinoma were enrolled from smokers undergoing lung resection for NSCLC in the District Hospital of Ferrara, Italy. Control subjects were smokers who underwent lung resection for NSCLC in the same hospital and had a surgically confirmed diagnosis of NSCLC of any histological type other than squamous cell.
Eighty six cases and 54 controls (mainly adenocarcinoma, n = 50) were enrolled. The presence of COPD was found to increase the risk for the squamous cell histological subtype by more than four times. Conversely, the presence of chronic bronchitis was found to decrease the risk for this histological subtype by more than four times. Among patients with chronic bronchitis (n = 77), those with COPD had a 3.5 times higher risk of having the squamous cell histological subtype.
These data suggest that, among smokers with surgically resectable NSCLC, COPD is a risk factor for the squamous cell histological subtype and chronic bronchitis, particularly when not associated with COPD, is a risk factor for the adenocarcinoma histological subtype.
Thorax 09/2004; 59(8):679-81. · 6.84 Impact Factor
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ABSTRACT: Oxidants are involved in many respiratory disorders, including asthma and chronic obstructive pulmonary diseases. Reduced glutathione (GSH), one of the most important antioxidant compounds against oxidant free radicals, is particularly abundant in the respiratory epithelial lining fluid, where its concentration is increased in inflammatory disorders.
We hypothesized that reducing agents may have a direct effect on airway smooth muscle. Therefore, we studied the effects of GSH on airway smooth muscle contractility in guinea-pig main bronchi. In parallel, we evaluated superoxide anion generation associated with in vitro bronchial smooth muscle contraction.
Guinea-pig main bronchi were mounted in organ baths filled with Krebs-Henseleit solution. Concentration-response curves to acetylcholine (Ach) (10(-9)-10(-3) M), carbachol (10(-9)-10(-4) M), or histamine (10(-9)-10(-3) M) were performed in the presence or absence of either reduced or oxidized glutathione (GSSG) (10(-5)-10(-3) M). We also evaluated the effects of GSH and GSSG on allergen-induced contraction in main bronchi obtained from ovalbumin-sensitized guinea-pig. Superoxide dismutase (SOD)-inhibited cytochrome c reduction kinetics was performed to evaluate superoxide anion (O2-) production during Ach-induced contraction.
Reduced but not oxidized glutathione significantly decreased smooth muscle contraction induced by Ach, carbachol, and histamine. Similarly, only the reduced form of glutathione attenuated the bronchoconstriction induced by allergen exposure in bronchi from sensitized animals. Finally, SOD-inhibited cytochrome c reduction kinetics demonstrated increased O2- production following bronchial smooth muscle contraction. This production was not affected by epithelium removal.
Our findings show that GSH decreases bronchial smooth muscle contraction to different stimuli and that oxidant free radicals are produced during bronchial smooth muscle contraction. We suggest that oxidants are involved in the mechanisms of bronchoconstriction and that reducing agents could be a possible therapeutic option for airway obstruction sustained by bronchospasm.
Clinical & Experimental Allergy 08/2003; 33(7):999-1004. · 5.03 Impact Factor
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G Caramori,
M Romagnoli,
P Casolari,
C Bellettato,
G Casoni,
P Boschetto,
K F Chung,
P J Barnes,
I M Adcock, A Ciaccia,
L M Fabbri,
A Papi
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ABSTRACT: Exacerbations represent an important feature of the clinical manifestation and natural history of chronic obstructive pulmonary disease (COPD). Nuclear localisation of p65 is a signal of nuclear factor-kappaB (NF-kappaB) activation. A study was undertaken to evaluate whether NF-kappaB activation is modified in sputum cells during COPD exacerbations.
Total and nuclear p65 immunoreactivity was measured by immunocytochemistry in the sputum cells of 11 smokers with moderate COPD during an exacerbation and after 6-8 weeks of clinical stability.
Total sputum cell count was significantly increased during exacerbations from a median (IQR) of 880 (510-1865) to 1914.5 (1065-3205) x 10(3)/ml (p<0.05). The main inflammatory cells in the sputum were neutrophils (83.2 (75.4-92.3)%) and macrophages (14.7 (2.6-21.6)%) and their relative proportion did not change during exacerbations. Nuclear staining for p65 was absent in sputum neutrophils, both during exacerbations and in the stable phase. In contrast, the percentage of macrophages expressing nuclear p65 increased significantly during exacerbations from a median (IQR) of 16 (7-24)% to 41.4 (6-69)% (p<0.05).
NF-kappaB appears to be activated in sputum macrophages but not in sputum neutrophils during exacerbations of COPD
Thorax 05/2003; 58(4):348-51. · 6.84 Impact Factor
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ABSTRACT: In chronic obstructive pulmonary disease (COPD) there is decreased vascularity of the bronchi and inflammation of the airways that may have opposite effects on the regulation of heat loss. Exhaled air temperature increase (delta(e) T) was measured in 23 patients with moderate COPD (18 male, mean age +/- SEM 70 +/- 1 yrs; forced expiratory volume in one second (FEV1) 45 +/- 3%, FEV1/forced vital capacity 54 +/- 4%) and 16 normal volunteers (64 +/- 4 yr) and compared to exhaled nitric oxide (eNO) and inflammatory cells in induced sputum as a marker of airway inflammation. Delta(e) T was measured during a flow- and pressure-controlled single exhalation with a fast-response thermometer. delta(e) T was reduced in patients with COPD (1.86 +/- 0.15 delta C x s(-1)) compared to normal subjects (4.00 +/- 0.26 delta C x s(-1)). There was no difference in delta(e) T between patients treated with inhaled steroids and those who were steroid naïve. Delta(e) T was correlated with eNO (r=0.60) but not with sputum neutrophilia. In COPD patients, delta(e) T was increased (2.26 +/- 0.16 delta C x s(-1)) after the inhalation of 200 microg of albuterol, which is a known vasodilator, indicating that delta(e) T and bronchial blood flow may be correlated. Exhaled temperature increase is reduced in chronic obstructive pulmonary disease patients and is increased by the inhalation of vasodilators and therefore may be related to changes of bronchial blood flow and tissue remodelling.
European Respiratory Journal 04/2003; 21(3):439-43. · 5.89 Impact Factor
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ABSTRACT: Case reports of a short trachea with early branching of the main bronchi are uncommon. The case is presented of a 64 year old woman with upper airway obstruction due to this anatomical abnormality which caused breathlessness and wheezing that was misdiagnosed (and treated) as bronchial asthma for many years.
Thorax 05/2002; 57(4):372-3. · 6.84 Impact Factor
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ABSTRACT: Reactive oxygen radicals are involved in many respiratory diseases, including chronic obstructive pulmonary disease (COPD). Carbocysteine lysine salt monohydrate (CLS) is a mucoactive drug effective in the treatment of bronchopulmonary diseases characterized by mucus alterations, including COPD. In the present study, the antioxidant activity of CLS was studied in vitro in three different oxygen radical producing systems, i.e. bronchoalveolar lavages (BAL) from patients affected by COPD, ultrasound treated human serum and cultured human lung endothelial cells challenged with elastase.
BAL, exposed or not to different concentrations of CLS (1.5-30 mM), was assayed for free radical content by fluorometric analysis of DNA unwinding (FADU) or by cytochrome c reduction kinetics. Human serum was treated with ultrasound in the presence or absence of CLS (1.5, 2.5 mM) or N-acetyl cysteine (NAC; 4, 5 mM) and assayed for free radical content by FADU. Human endothelial cells cultured in vitro from pulmonary artery were incubated with elastase (0.3 IU/mL), in the presence or absence of glutathione (GSH; 0.65 mM) or CLS (0.16 mM). The supernatant was tested for cytochrome c reduction kinetics whereas cell homogenates were assessed for xanthine oxidase (XO) content by SDS-PAGE.
Results showed that CLS is more effective as an in vitro scavenger in comparison to GSH and NAC. CLS reduced the damage of DNA from healthy donors exposed to COPD-BAL and was able to quench clastogenic activity induced in human serum by exposure to ultrasound at concentrations as low as 2.5 mM. NAC protect DNA from radical damage, starting from 5 mM. In human lung endothelial cells cultured in presence of elastase, CLS (0.16 mM) decreased xanthine oxidase activity.
These results suggest that CLS could act by interfering with the conversion of xanthine dehydrogenase into superoxide-producing xanthine oxidase. The antioxidant activity of CLS could contribute to its therapeutic activity by reducing radical damage to different lung structures.
Panminerva medica 10/2001; 43(3):215-20. · 1.11 Impact Factor
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ABSTRACT: We report the case of a 32-year-old man with the onset of exercise-related dyspnea, chest pain and chest radiography simulating a pleural effusion. The computed tomography of the chest showed signs suggesting pleural liposarcoma. Because of these findings, a videothoracoscopy was performed which surprisingly showed the presence in the left pleural space of intrapleural omentum and spleen. This report underlines that the clinical manifestations of Bochdalek hernia in adults are variegate and in most cases preoperative diagnosis is not possible.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 05/2001; 56(2):121-3.
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ABSTRACT: We investigated the relationship between the reversibility of airflow limitation, the concentration of nitric oxide (NO) in exhaled air, and the inflammatory cells in the sputum of patients with stable chronic obstructive pulmonary disease (COPD). We examined nine normal healthy control subjects and 20 nonatopic patients with COPD. Ten patients had no reversibility of airflow limitation (increase in FEV(1) of < 12% and < 200 ml after 200 microg of inhaled salbutamol), and 10 patients had partial reversibility of airflow limitation (increase in FEV(1) of < 12% but > 200 ml after 200 microg of inhaled salbutamol). Exhaled NO levels were higher in COPD patients with partial reversibility of airflow limitation than in those with no reversibility of airflow limitation (median 24 [interquartile range 15.3 to 32] ppb versus 8.9 [4.6 to 14.7] ppb; p < 0.01). Compared with healthy control subjects, only COPD patients with partial reversibility of airflow limitation had increased concentrations of sputum eosinophils. We conclude that, in patients with stable COPD, even a partial bronchodilator response to inhaled salbutamol is associated with increased exhaled NO and sputum eosinophilia, suggesting that these patients may have a different response to treatment than do those without reversible airflow limitation.
American Journal of Respiratory and Critical Care Medicine 12/2000; 162(5):1773-7. · 11.08 Impact Factor
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M Saetta,
S Baraldo,
L Corbino,
G Turato,
F Braccioni,
F Rea,
G Cavallesco,
G Tropeano,
C E Mapp,
P Maestrelli, A Ciaccia,
L M Fabbri
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ABSTRACT: Previous studies have shown an increased number of inflammatory cells and, in particular, CD8+ve cells in the airways of smokers with chronic obstructive pulmonary disease (COPD). In this study we investigated whether a similar inflammatory process is also present in the lungs, and particularly in lung parenchyma and pulmonary arteries. We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: nonsmokers (n = 8), asymptomatic smokers with normal lung function (n = 6), and smokers with COPD (n = 10). Alveolar walls and pulmonary arteries were examined with immunohistochemical methods to identify neutrophils, eosinophils, mast cells, macrophages, and CD4+ve and CD8+ve cells. Smokers with COPD had an increased number of CD8+ve cells in both lung parenchyma (p < 0.05) and pulmonary arteries (p < 0.001) as compared with nonsmokers. CD8+ve cells were also increased in pulmonary arteries of smokers with COPD as compared with smokers with normal lung function (p < 0.01). Other inflammatory cells were no different among the three groups. The number of CD8+ve cells in both lung parenchyma and pulmonary arteries was significantly correlated with the degree of airflow limitation in smokers. These results show that an inflammatory process similar to that present in the conducting airways is also present in lung parenchyma and pulmonary arteries of smokers with COPD.
American Journal of Respiratory and Critical Care Medicine 09/1999; 160(2):711-7. · 11.08 Impact Factor
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ABSTRACT: Chronic infections such as those caused by Helicobacter pylori, Chlamydia pneumoniae, and cytomegalovirus have been epidemiologically related to coronary heart disease (CHD). Other studies place H. pylori in relation to other extradigestive diseases. We carried out an epidemiologic pilot study to evaluate the prevalence of H. pylori in patients with chronic bronchitis, a respiratory disease characterized by persistent chronic inflammation, in comparison with a matched control group.
An enzyme-linked immunosorbent assay IgG test for H. pylori diagnosis was performed in 60 consecutive patients with chronic bronchitis (15 women and 45 men; age range, 50-89 years; mean age, 70.38 years) and in 69 control subjects, well matched for age and social status (19 women and 50 men: age range, 52-90 years; mean age, 71.3 years).
Foty-nine of 60 patients with chronic bronchitis (81.6%) and 40 of 69 subjects in the control group (57.9%) were H. pylori-positive (P = 0.0079). The odds ratio, calculated by simple analysis (3.2) and confirmed by logistic regression analysis (3.399), indicated that H. pylori infection greatly increases the risk of chronic bronchitis.
To date, CHD is the only convincing association between H. pylori infection and an extradigestive disease. The main conclusion of this pilot study is that H. pylori infection seems to increase the risk of developing of chronic bronchitis. An important step in this field will be to evaluate the possible change in the clinical conditions after successful eradication therapy in H. pylori-positive patients with chronic bronchitis.
Scandinavian Journal of Gastroenterology 09/1999; 34(8):828-30. · 2.02 Impact Factor
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ABSTRACT: We investigated whether acute exposure to nitrogen dioxide (NO2) causes major inflammatory responses (inflammatory cell recruitment, oedema and smooth muscle hyperresponsiveness) in guinea pig airways. Anaesthetised guinea pigs were exposed to 18 ppm NO2 or air for 4 h through a tracheal cannula. Bronchoalveolar lavage was performed and airway microvascular permeability and in vitro bronchial smooth muscle responsiveness were measured. Exposure to NO2 induced a significant increase in eosinophils and neutrophils in bronchoalveolar lavage fluid, microvascular leakage in the trachea and main bronchi (but not in peripheral airways), and a significant in vitro hyperresponsiveness to acetylcholine, electrical field stimulation, and neurokinin A, but not to histamine. Thus, this study shows that in vivo exposure to high concentrations of NO2 induces major inflammatory responses in guinea pig airways that mimic acute bronchitis induced by exposure to irritant gases in man.
European Journal of Pharmacology 07/1999; 374(2):241-7. · 2.52 Impact Factor
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ABSTRACT: Asthma (Greek word that means "breathlessness" or "open-mouth breath") is a chronic inflammatory disorder of the airways, with extensive infiltration of the airway lumen and wall with eosinophils, mast cells, activated T-lymphocytes. Airway inflammation is associated with airway hyperresponsiveness, recurrent episodes of reversible airflow limitation and respiratory symptoms such as wheezing, chest tightness, breathlessness and cough with mucus production. Curiously, asthma worsens particularly at night and in the early hours of the morning. The current consensus on asthma therapy suggests that pharmacological control of asthma can be achieved with antiinflammatory "controller" medications such as inhaled glucocorticoids and cromones. Short-acting bronchodilators act as "reliever" medications and rapidly reverse acute manifestations of asthma. Asthmatic exacerbations require the repetitive administration of inhaled short-acting beta-2-agonist and the early introduction of oral glucocorticoids. Rarely the severity of exacerbation requires the administration of oxygen (that, if available, is not contraindicated), intravenous bronchodilators, glucocorticoids and epinephryne and mechanical ventilation.
Recenti progressi in medicina 06/1999; 90(5):271-9.
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S Pinamonti,
M Leis,
A Barbieri,
D Leoni,
M Muzzoli,
S Sostero,
M C Chicca,
A Carrieri,
F Ravenna,
L M Fabbri, A Ciaccia
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ABSTRACT: Xanthine oxidase (xanthine: oxygen oxidoreductase, EC 1.1.3.22), a molybdenum-containing hydroxylase that produces superoxide and uric acid from purine substrates and molecular oxygen, is involved in the oxidative stress underlying several human pathologies including lung diseases. An enzymatic activity similar to xanthine oxidase was previously reported in bronchoalveolar lavage fluid of patients with chronic obstructive pulmonary disease (COPD-BAL), by fluorometric analysis of DNA unwinding and cytochrome c reduction kinetics. Here we report the detection of xanthine oxidase activity products by electron paramagnetic resonance (EPR) in presence of the spin-trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) and reversed-phase high-performance liquid chromatography (RP-HPLC) in COPD-BAL (n = 14, average age of patients 65 years, range 38-81) and BAL from healthy nonsmoker controls (n = 6, average age 64 years, range 44-73). Superoxide DMPO adducts were detected in COPD-BAL and in an in vitro system containing xanthine and xanthine oxidase (XA/XO), but not in BAL controls and when superoxide dismutase (SOD, 1000 I.U./ml) was added to COPD-BAL. The HPLC analyses after addition of xanthine showed production of uric acid in COPD-BAL and in the XA/XO system but not in BAL controls. These results support the involvement of xanthine oxidase in the mechanisms of superoxide production by BAL supernatant, which increases oxidative stress in chronic obstructive pulmonary disease.
Free Radical Biology and Medicine 12/1998; 25(7):771-9. · 5.42 Impact Factor
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American Journal of Respiratory and Critical Care Medicine 06/1998; 157(5 Pt 2):S195-8. · 11.08 Impact Factor
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ABSTRACT: Although chronic obstructive pulmonary disease (COPD) has a public health importance similar to asthma, it has received less attention. The first guideline on the management of COPD was released in 1987 by the American Thoracic Society. In 1992 the Canadian Thoracic Society released its guidelines. In 1995 the European Respiratory Society and the Thoracic Society of Australia and New Zealand released their guidelines and the American Thoracic Society updated and expand its COPD guidelines. All these documents were followed in 1997 by the guidelines developed by the British Thoracic Society. These COPD guidelines show many similarities but also have some interesting differences. The aim of this paper is to review these similarities and discrepancies. Like all guidelines, COPD guidelines suffer from the limited amount of evidence-based medicine supporting them, a limitation that, however, provides a strong stimulus for further research.
Current opinion in pulmonary medicine 04/1998; 4(2):76-84. · 3.08 Impact Factor
