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Risk factors for pulmonary embolism in patients preliminarily diagnosed with community-acquired pneumonia: a prospective cohort study.

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Risk factors for pulmonary embolism in patients preliminarily diagnosed with community-acquired pneumonia: a prospective cohort study.

J Thromb Thrombolysis. 2015 Sep 14;

Authors: Zhang Y, Zhou Q, Zou Y, Song X, Xie S, Tan M, Zhang G, Wang C

Abstract
D-dimer levels are increased in patients with acute pulmonary embolism (PE). However, D-dimer levels are also increased in patients with community-acquired pneumonia (CAP). The aim of this prospective cohort study was to examine the incidence and clinical features of patients preliminarily diagnosed with CAP and with increased D-dimer levels, and who finally were diagnosed with PE. Patients diagnosed with CAP and hospitalized in the Respiratory Department of the Tenth People's Hospital Affiliated to Tongji University between May 2011 and May 2013 were enrolled. D-dimer levels were measured routinely after admission. For patients with increased D-dimer levels, those suspected with PE underwent computed tomography pulmonary angiography (CTPA). A total of 2387 patients with CAP was included: 724 (30.3 %) had increased D-dimer levels (median of 0.91 mg/L). CTPA was performed for 139 of the 724 patients (median D-dimer levels of 1.99 mg/L). Among the 139 patients, 80 were diagnosed with PE, and 59 without PE; D-dimer levels were 2.83 and 1.41 mg/L, respectively (p < 0.05). Multivariate analysis showed that age, coronary heart disease, chronic obstructive pulmonary disease (COPD), lower limb varicosity, chest pain, shortness of breath, hemoptysis, fever, and increased levels of troponin I were independent risk factors for PE. Presentation of PE and CAP are similar. Nevertheless, these results indicated that for hospitalized patients with CAP and elevated D-dimer levels, PE should be considered for those >60 years; with CHD, COPD, or lower limb varicosity; with chest pain, shortness of breath, hemoptysis, increased troponin I, or low fever.

PMID: 26370200 [PubMed - as supplied by publisher]

Determinants of bacteriological outcomes in exacerbations of chronic obstructive pulmonary disease.

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Changes in sputum microbiology following antibiotic treatment of acute exacerbations of chronic obstructive pulmonary disease (AECOPD), including patterns of bacteriological relapse and superinfection are not well understood. Sputum microbiology at exacerbation is not routinely performed, but pathogen presence and species are determinants of outcomes. Therefore, we determined whether baseline clinical factors could predict the presence of bacterial pathogens at exacerbation. Bacterial eradication at end of treatment (EOT) is associated with clinical resolution of exacerbation. We determined the clinical, microbiological and therapeutic factors that were associated with bacteriological eradication in AECOPD at EOT and in the following 8 weeks.

METHODS: Sputum bacteriological outcomes (i.e., eradication, persistence, superinfection, reinfection) from AECOPD patients (N = 1352) who were randomized to receive moxifloxacin or amoxicillin/clavulanate in the MAESTRAL study were compared. Independent predictors of bacterial presence in sputum at exacerbation and determinants for bacteriological eradication were analyzed by logistic regression and receiver operating characteristic (ROC) analyses.

RESULTS: Significantly greater bacteriological eradication with moxifloxacin was mainly driven by superior Haemophilus influenzae eradication (P = 0.002, EOT). Baseline clinical factors were a weak predictor of the presence of pathogens in sputum (AUCROC = 0.593). On multivariate analysis, poorer bacterial eradication was associated with antibiotic resistance (P = 0.0001), systemic steroid use (P = 0.0024) and presence of P. aeruginosa (P = 0.0282).

CONCLUSIONS: Since clinical prediction of bacterial presence in sputum at AECOPD is poor, sputum microbiological analysis should be considered for guiding antibiotic therapy in moderate-to-severe AECOPD, particularly in those who received concomitant systemic corticosteroids or are at risk for infection with antibiotic-resistant bacteria.

Right ventricular diastolic function and exercise capacity in COPD.

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Decreased exercise capacity in chronic obstructive pulmonary disease (COPD) is incompletely explained by pulmonary pathologic and physiologic abnormalities. We evaluated the extent to which right ventricular diastolic function (RVDF) is associated with exercise capacity in COPD.

METHODS: Fifty-one patients with COPD were evaluated by echocardiography, spirometry, and the 6 min walk test (6MWT). RVDF was assessed using 4 echocardiographic parameters: 1) the ratio of tricuspid valve (TV) early (E) and late (A) inflow velocities (TV E/A) 2) TV early tissue Doppler velocity (TV e') 3) TV deceleration time (DT) and 4) the ratio of TV E and e' velocities (TV E/e'). Multiple linear regression was used to examine the extent to which these parameters were associated with 6MWT distance. All models adjusted for age, sex, post-bronchodilator FEV1/FVC, resting heart rate, and use of supplemental O2 during 6MWT. A regression model was calculated for each of the 4 markers of RVDF.

RESULTS: Forty-seven percent of the sample had GOLD stage III or IV COPD. All 51 subjects had preserved left ventricular ejection fraction (LVEF, mean = 71.7%, SD = 7.8%). A higher TV E/A ratio was associated with increased 6MWT distance (p = 0.001). TV e', TV DT and TV E/e' did not have a statistically significant association with 6MWT distance in regression models.

CONCLUSIONS: In a cohort with moderate to severe COPD and normal LVEF, TV E/A was associated with 6MWT distance after adjusting for relevant demographic and medical covariates. RV diastolic dysfunction may independently contribute to exercise intolerance in COPD.

COPD and its comorbidities: Impact, measurement and mechanisms.

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Chronic obstructive pulmonary disease (COPD) frequently coexists with other conditions often known as comorbidities. The prevalence of most of the common comorbid conditions that accompany COPD has been widely reported. It is also recognized that comorbidities have significant health and economic consequences. Nevertheless, there is scant research examining how comorbidities should be assessed and managed in the context of COPD. Also, the underlying mechanisms linking COPD with its comorbidities are still not fully understood. Owing to these knowledge gaps, current disease-specific approaches provide clinicians with little guidance in terms of managing comorbid conditions in the clinical care of multi-diseased COPD patients.

This review discusses the concepts of comorbidity and multi-morbidity in COPD in relation to the overall clinical outcome of COPD management. It also summarizes some of the currently available clinical scores used to measure comorbid conditions and their prognostic abilities. Furthermore, recent developments in the proposed mechanisms linking COPD with its comorbidities are discussed.

Airway exposure to e-cigarette-vapors impairs autophagy and induces aggresome-formation.

e-cigAIMS: Electronic(e)-cigarettes are proposed to be a safer alternative to tobacco-cigarettes. Hence, we evaluated if e-cigarette-vapors (eCV) impair cellular proteostasis similar to cigarette-smoke (CS)-exposure.

RESULTS: First, we evaluated the impact of eCV-exposure (2.5mg or 7.5mg) on Beas2b cells that showed significant increase in accumulation of total polyubiquitinated-proteins (ub, insoluble-fractions) with time-dependent decrease in proteasomal-activities from 1 r (p<0.05), 3hr (p<0.001) to 6hrs (p<0.001) of eCV-exposure as compared to room-air control. We verified that even minimal eCV-exposure (1hr) induces valosin containing protein (VCP; p<0.001), sequestosome-1/p62 (aberrant-autophagy marker; p<0.05) and aggresome-formation (total poly-ub-accumulation; p<0.001) using immunoblotting (IB), fluorescence microscopy and immunoprecipitation (IP). The inhibition of protein synthesis by 6 hr cyclohexamide (50µg/ml) treatment significantly (p<0.01) alleviates eCV-induced (1 hr) aggresome-bodies. We also observed that eCV (1hr) induced protein-aggregation can activate oxidative stress, apoptosis (caspase-3/7) and senescence (p<0.01) as compared to room-air controls. We verified by using an autophagy inducer carbamazepine (20 µM, 6 hrs) or cysteamine (250μM; 6 hrs, anti-oxidant), that eCV induced changes in oxidative stress, poly-ub-accumulation, proteasomal activity, autophagy, apoptosis and/or senescence could be controlled by autophagy induction. We further confirmed the role of acute eCV-exposure on autophagy impairment in murine lungs (C57BL/6 and CD1) by IB (Ub, p62, VCP) and IP (VCP, p62), similar to in-vitro experiments.

INNOVATION: In this study, we report for the first time that eCV-exposure induces proteostasis/autophagy impairment leading to oxidative stress, apoptosis and senescence that can be ameliorated by an autophagy inducer.

CONCLUSION: eCV-induced autophagy-impairment and aggresome-formation suggests its potential role in COPD-emphysema pathogenesis.

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