27 research outputs found

    Trattamento personalizzato dei pazienti con BPCO in fase stabile

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    Nella pratica clinica non esiste più alcuna giustificazione per un nichilismo terapeutico in quanto oggi il trattamento personalizzato farmacologico e non farmacologico dei pazienti con broncopneumopatia cronica ostruttiva (BPCO) in fase stabile, in accordo con le attuali linee guida dell’Organizzazione Mondiale della Sanità (OMS) del Progetto Mondiale BPCO, è sicuramente in grado di diminuire i sintomi respiratori, migliorare la capacità e la tolleranza allo sforzo e la qualità di vita del paziente, di prevenire in parte le riacutizzazioni, anche gravi, della malattia e di diminuirne la mortalità. Tuttavia, gli unici due provvedimenti terapeutici dimostratisi finora sicuramente efficaci nel diminuire la mortalità nei pazienti con BPCO in fase stabile sono: 1) la completa sospensione del fumo di tabacco, e 2) l’ossigenoterapia domiciliare a lungo termine limitatamente ai pazienti con BPCO e grave insufficienza respiratoria cronica refrattaria ad un trattamento ottimale con farmaci broncodilatatori ed antinfiammatori. Al contrario il trattamento farmacologico personalizzato della BPCO in fase stabile attualmente disponibile rimane in gran parte puramente sintomatico e modifica solo in parte la storia naturale della malattia. Sono quindi indispensabili ulteriori studi di medicina traslazionale umana per chiarire la patogenesi della malattia ed ulteriori studi clinici controllati a lungo termine con nuove terapie farmacologiche usando come misure primarie di efficacia clinica il decorso clinico e la mortalità della BPCO. Per accelerare la ricerca in questo settore, sono necessari investimenti significativi, sia a livello pubblico che privato, con lo scopo ambizioso di rendere nell’imminente futuro, la BPCO, una malattia pienamente prevenibile e trattabile

    Trattamento personalizzato dei pazienti con BPCO in fase stabile

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    In clinical practice there are no more justifications for the therapeutic nihilism because nowadays the personalised pharmacologic and non-pharmacologic treatment of the patients with stable chronic obstructive pulmonary disease (COPD), according to current Global initiative for chronic Obstructive Lung Disease (GOLD) guidelines is effective in decreasing respiratory symptoms, in increasing exercise tolerance and capacity, improving quality of life, preventing many COPD exacerbations (even the most severe) and decrease the mortality. However, smoking cessation and long-term oxygen therapy (in patients with advanced COPD and severe chronic hypoxemia refractory to maximal treatment with bronchodilator and anti-inflammatory drugs) are the only two interventions that have unequivocally shown to reduce COPD mortality. At the opposite the current pharmacologic personalised treatment of stable COPD is mainly symptomatic and modify only partially the natural history of the disease. This conclusion should reinforce the necessity of further human translational medicine research in order to promote a better understanding of the pathogenesis of COPD and also we need more long term controlled clinical studies of new drugs using as primary measures of clinical efficacy their effects on the lung function decline and the mortality. To accelerate research in this field, substantial investments are required at all levels, including the public and private sectors, with the ambitious aim of making in the near future COPD a preventable and fully treatable disease

    Embolization of a bronchial artery aneurysm in a chronic obstructive pulmonary disease (COPD) patient with non-massive hemoptysis

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    BACKGROUND: Bronchial artery aneurysm (BAA) is a rare condition with a reported prevalence of less than 1% of all selective bronchial arterial angiograms. Despite its low incidence, BAA represents a potential cause of hemoptysis. CASE REPORT: We describe the case of a 63-year-old man suffering from chronic obstructive pulmonary disease (COPD), who presented with non-massive hemoptysis. CT angiography revealed a single bronchial artery aneurysm of 9 mm in diameter, abutting the esophageal wall. Other CT findings included hypertrophy of the bronchial arteries along the mediastinal course, diffuse thickening of the walls of numerous bronchial branches and a "ground glass" opacity in the anterior segment of the right upper pulmonary lobe suggestive of alveolar hemorrhage. The final diagnosis was established based on selective angiography, which was followed by transcatheter arterial embolization (TAE) of the BAA and of the pathological bronchial circulation. Follow-up CT scans revealed a total exclusion of the aneurysm from the systemic circulation, resolution of the parenchymal "ground glass" opacity and absence of further episodes of hemoptysis over a period of two years. CONCLUSIONS: An incidental finding of a bronchial artery aneurysm necessitates prompt treatment. CT angiography and TAE represent the methods of choice for an appropriate diagnosis and treatment, respectively. In case of a BAA associated with chronic inflammatory diseases, such as COPD, in patients with hemoptysis, TAE of the BAA and of the pathological bronchial circulation, in association with the treatment of the underlying disease, represents a valid approach that can improve the pulmonary status and prevent further episodes of hemoptysis

    Recumbent deoxygenation in mild/moderate liver cirrhosis: the “Clinodeoxia”. The ortho-clino paradigm

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    BACKGROUND: While the effects of postural change on arterial oxygenation have been well documented in normal subjects, and attributed to the relationship of closing volume (CV) to the tidal volume, in liver cirrhosis such postural changes have been evaluated mainly in a rare, peculiar clinical end-stage condition which is characterized by increased dyspnea shifting from supine to upright position ("platypnea"). The latter is associated with worsening of PaO2 ("orthodeoxia"). We evaluated the effects of postural changes on arterial oxygenation in patients affected by mild/moderate liver cirrhosis. METHODS: We performed pulmonary function tests and arterial blood gas evaluation in sitting and supine positions in 22 patients with mild/moderate liver cirrhosis, biopsy-proved, and 22 matched non-smokers control subjects. RESULTS: Recumbency elicited a decrease of PaO2 (Δ(sup-sit)PaO2) in 19 out of 22 controls and in all but one cirrhotics. The magnitude of this postural change was significantly (p = 0.04) greater in cirrhotics (9.6 ± 5.3%) compared to controls (6.7 ± 3.7%). In the subset of cirrhotics younger than 60 yrs and with PaO2 greater than 80 mmHg in sitting position, the Δ(sup-sit)PaO2 in recumbency further increased to 12 ± 5.8%, significantly (p = 0.014) greater than in same subgroup of controls (7.1 ± 3.8%). CONCLUSIONS: In mild/moderate liver cirrhosis the postural variations in PaO2 follow the normal trends, but are of greater magnitude probably as a consequence of hypoventilated units of lung for postural and disease-linked tidal airway closure, resulting in more pronounced recumbent hypoxemia ("clinodeoxia")

    Obstructive sleep apnoea syndrome and endothelial function: potential impact of different treatment strategies-meta-analysis of prospective studies.

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    PURPOSE Previous studies have shown an association between obstructive sleep apnoea syndrome (OSAS) and cardiovascular events. Whether this association is mediated by an impairment of endothelial function, which is itself a driver of elevated cardiovascular risk, has yet to be clarified, as it is the eventual protective role of several OSAS treatments. The aim of our meta-analysis is to evaluate the effect of various OSAS treatments on endothelial function calculated by means of flow-mediated dilatation (FMD). METHODS We conducted a meta-analysis of prospective studies including patients affected by mild to severe OSAS treated with continuous positive airway pressure (CPAP), surgery, oral appliance and medical treatments. FMD was measured before and after treatment RESULTS: After pooling results from different treatment strategies, OSAS treatment showed a positive impact on endothelial function (Mean Difference [MD] = 2.58; 95% CI 1.95-3.20; p < 0.00001). CONCLUSIONS Our study supports the hypothesis that several modalities of treatment for OSAS positively impact endothelial function. Whether this effect also associates with an improvement of clinical outcomes remains to be ascertained

    Tiotropium and salmeterol/fluticasone combination do not cause oxygen desaturation in COPD

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    It has been documented that tiotropium is less likely to induce oxygen desaturation in stable COPD patients compared to long-acting beta(2)-agonists (LABAs) and combined administration of a LABA and an inhaled corticosteroid (ICS) reduces the potential for acute effects of LABA on blood-gas tensions. In this study, we have compared the acute effects of tiotropium 18 mu g and salmeterol/fluticasone combination (SFC) 50/250 mu g on arterial blood gases in 20 patients with stable COPD. Each subject was studied on 2 days, separated from one another by at least 4 days. Blood specimens were taken just before the inhalation and at 15, 30, 60, 180 and 360 min after inhalation of each treatment, and spirometry was performed at the same time points. As expected, both treatments significantly improved FEV1 (greatest changes were 0.20 L, 95% CI: 0.13-0.27 at 360 min after tiotropium; and 0.13 L, 95% CI: 0.06-0.19 at 180 min after SFC). The greatest mean changes from baseline in PaO2 were -1.7 (95% CI: -4.0 to 0.6) mmHg, p = 0.134, after tiotropium; -0.8 (95% CI: -2.2 to 0.6) mmHg, after SFC. Both changes were observed after 15 min. Both drugs caused a small decrease in PaCO2 (greater changes: -1.9 (95% CI -3.2 to -0.6) mmHg, p = 0.005 at 60 min after tiotropium; and -2.4 (95% CI: -3.5 to -1.3) mmHg, p = 0.0002 at 180 min after SFC). These results indicate that both tiotropium and SFC are able to induce a significant long-last bronchodilation without affecting arterial blood gases. Moreover, they confirm that the impact of tiotropium on PaO2 is small and without clinical significance and the addition of a LABA to an ICS can reduce the potentially dangerous acute effect of the LABA on blood gases. (C) 2008 Published by Elsevier Ltd
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