Incidence and risk factors of exacerbations among COPD patients in primary health care: APMPOC study.

BACKGROUND: Worldwide, chronic obstructive pulmonary disease (COPD) is the fourth cause of death. Exacerbations have a negative impact on the prognosis of COPD and the frequency and severity of these episodes are associated with a higher patient mortality. Exacerbations are the first cause of decompensation, hospital admission and death in COPD. The incidence of exacerbations has mainly been estimated in populations of patients with moderate-severe COPD requiring hospital care. However, little is known regarding the epidemiology of exacerbations in patients with less severe COPD forms. It is therefore possible that a high number of these less severe forms of exacerbations are underdiagnosed and may, in the long-term, have certain prognostic importance for the COPD evolution. The aim of this study was to know the incidence and risk factors associated with exacerbations in patients with COPD in primary care. METHODS AND DESIGN: A prospective, observational, 3-phase, multicentre study will be performed involving: baseline evaluation, follow up and final evaluation. A total of 685 smokers or ex-smokers from 40 to 80 years of age with COPD, without acute respiratory disease or any other long-term respiratory disease will be randomly selected among the population assigned to 21 primary care centres. The diagnosis of COPD and its severity will be confirmed by spirometry. Information regarding the baseline situation, quality of life and exposure to contaminants or other factors potentially related to exacerbations will be collected. A group of 354 patients with confirmed COPD of varying severity will be followed for one year through monthly telephone calls and daily reporting of symptoms with the aim of detecting all the exacerbations which occur. These patients will be evaluated again at the end of the study and the incidence of exacerbations and associated relative risks will be estimated by negative binomial regression. DISCUSSION: The results will be relevant to provide knowledge about natural history of the initial phases of the COPD and the impact and incidence of the exacerbations on the patients with mild-moderate forms of the disease. These data may be important to know the milder forms of exacerbation which are often silent or very little expressed clinically.

Efficacy of nebulized liposomal amphotericin B in treatment of experimental pulmonary aspergillosis.

The efficacy of therapeutic aerosolized amphotericin B (AMB) was studied in a steroid-immunosuppressed murine model of invasive pulmonary aspergillosis. Nebulized liposomal AMB can be a valid approach to the treatment of this infection, with subjects showing significantly improved survival relative to that of subjects given intravenous deoxycholate AMB, as well as lower lung weights and pulmonary glucosamine levels.

Lack of effect of glycoprotein IIb/IIIa blockade on myocardial platelet or polymorphonuclear leukocyte accumulation and on infarct size after transient coronary occlusion in pigs.

OBJECTIVES: We sought to assess the effect of glycoprotein (GP) IIb/IIIa blockade on myocardial platelet and polymorphonuclear leukocyte accumulation and on infarct size after coronary injury and transient coronary occlusion (CO) in pigs. BACKGROUND: It has been suggested that platelet GP IIb/IIIa blockade might reduce the severity of microvascular damage after reperfusion. METHODS: Sixteen thiopental-anesthetized, open-chest pigs, in whom platelets had been labeled with technetium-99m (99mTc) on the previous day, were submitted to catheter-induced left anterior descending coronary artery (LAD) injury followed by 55 min of CO and 5 h of reperfusion. Five minutes before reflow, the animals were blindly allocated to receive lamifiban (intravenous bolus of 250 microg/kg body weight and continuous infusion of 3 microg/kg per min) or saline. RESULTS: Lamifiban had a rapid and potent platelet anti-aggregatory effect, as demonstrated by significant prolongation of the bleeding time and profound (approximately 90%) inhibition of ex vivo platelet aggregation, and completely prevented the development of cyclic flow reductions of the LAD (0 vs. 5 +/- 1, one of them followed by re-occlusion, in control animals, p = 0.005). However, compared with animals receiving placebo, those treated with lamifiban had a similar (p = NS) content of (99m)Tc platelets in the reperfused myocardium (288 +/- 40% vs. 205 +/- 27% of the value in the control region, respectively) and similar myeloperoxidase activity (0.50 +/- 0.17 U/g vs. 0.47 +/- 0.17 U/g, respectively) and infarct size (46.8 +/- 12.0% vs. 49.8 +/- 10.5% of the area at risk, respectively). Arteriolar platelet thromboemboli were very rarely seen on histologic analysis. Lamifiban did not modify platelet P-selectin expression in additional studies. CONCLUSIONS: Platelet GP IIb/IIIa blockade has a potent antithrombotic effect at the culprit lesion, but does not significantly reduce the magnitude of microvascular platelet accumulation or myocardial damage after transient CO.