37 research outputs found

    The Pneumonia Severity Index as a Predictor of In-Hospital Mortality in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

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    <div><p>Objective</p><p>To determine whether the pneumonia severity index (PSI) can predict in-hospital mortality for AECOPD patients and compare its usefulness with the CURB65 and BAP65 indexes to predict mortality.</p><p>Methods</p><p>Demographics, clinical signs and symptoms, comorbidities, and laboratory and radiographic findings of hospitalized AECOPD patients were obtained. Univariate and multiple logistic regression analyses were used to identify the risk factors for in-hospital mortality. The PSI, CURB65 and BAP65 scores were calculated. Receiver operating characteristic (ROC) curve analysis was used to identify the PSI, CURB65 and BAP65 scores that could discriminate between non-survivors and survivors. To control for the confounding factor of invasive mechanical ventilation (IMV) regarding the mortality of AECOPD, subgroup analysis was performed when excluded patients who had met the criteria of IMV but who had not received the cure of IMV according to their wishes.</p><p>Results</p><p>During the in-hospital period, 73 patients died and 679 patients recovered. Age, PaO<sub>2</sub><60 mmHg, pH < 7.35, PaCO2≥50 mmHg, nursing home residency, congestive heart failure, liver disease, sodium<130 mmol/L, lower FEV1% and altered mental status were risk factors for in-hospital mortality. The areas under the ROC curves (AUCs) of the PSI for death were 0.847 (95% CI: 0.799-0.895). The cut-off value was 116.5 with a sensitivity of 82.2% and a specificity of 77.6%. However, the AUCs of the CURB65 and BAP65 for death were only 0.744 (95% CI: 0.680-0.809) and 0.665 (95% CI: 0.594-0.736), respectively. Subgroup analysis also showed that the PSI score could predict the mortality of AECOPD patients with an AUC = 0.857 (95% CI: 0.802-0.913), with exclusion of the patients who met the criteria of IMV but who did not receive the cure of IMV.</p><p>Conclusion</p><p>The PSI score may be used to predict in-hospital mortality for hospitalized AECOPD patients, with a prognostic capacity superior to CURB65 and BAP65.</p></div

    Sub-group analysis of in-hospital mortality by the PSI, CURB65 and BAP65 score and risk groups for AECOPD when the patients who had met the criteria but did not receive the cure of IMV were excluded.

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    <p>PSI: pneumonia severity index.</p><p>Sub-group analysis of in-hospital mortality by the PSI, CURB65 and BAP65 score and risk groups for AECOPD when the patients who had met the criteria but did not receive the cure of IMV were excluded.</p

    Mortality Risk in Patients with AECOPD.

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    <p>PaO<sub>2</sub>: partial pressure of arterial oxygen; PaCO<sub>2</sub>: partial pressure of arterial carbon dioxide; FEV1%, predicted forced expiratory volume in one second.</p><p>Mortality Risk in Patients with AECOPD.</p

    Baseline characteristics and survival of patients hospitalized with AECOPD.

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    <p>NHR: nursing home resident, PaO<sub>2</sub>: partial pressure of arterial oxygen; PaCO<sub>2</sub>: partial pressure of arterial carbon dioxide. FEV1%, predicted forced expiratory volume in one second; FEV1/FVC, forced expiratory volume in one second/forced vital capacity; CHF: congestive heart failure; SBP: systolic blood pressure; NIV: noninvasive mechanical ventilation; IMV: invasive mechanical ventilation.</p><p>Baseline characteristics and survival of patients hospitalized with AECOPD.</p

    Comparison of in-hospital mortality according to the PSI risk group in COPD exacerbation and community-acquired pneumonia.

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    <p>Comparison of in-hospital mortality according to the PSI risk group in COPD exacerbation and community-acquired pneumonia.</p

    In-hospital mortality according to the PSI, CURB65 and BAP65 score and risk groups for AECOPD.

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    <p>PSI: pneumonia severity index.</p><p>In-hospital mortality according to the PSI, CURB65 and BAP65 score and risk groups for AECOPD.</p

    An efficient method to genotype the polymorphisms of cholinergic nicotinic receptor subunit genes and their associations with COPD onset risk

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    <p><b>Background:</b> Single-nucleotide polymorphisms (SNPs) in the cholinergic nicotinic receptor subunit genes on chromosome 15q25.1, including <i>CHRNA3</i>, <i>CHRNB4</i> and <i>CHRNA5</i>, are well-established biomarkers of chronic obstructive pulmonary disease (COPD) and lung cancer. Thus, there is great demand for a rapid, easy and inexpensive method to detect these variations for purpose of risk prediction in large populations. <b>Aim of the Study:</b> The aim of this study was to establish an accurate and efficient method for genotyping <i>CHRN</i> SNPs and testing their association with age at onset of COPD in Chinese population as well as the clinical stage in COPD patients. <b>Materials and Methods:</b> We designed a method to specifically genotype 5 SNPs of <i>CHRN</i> genes based on a modified high-resolution melt (HRM) method and then validated the genotyping results by direct sequencing of 120 samples. We further used the HRM method to genotype these 5 SNPs in 1,013 COPD patients. <b>Results:</b> Requiring little time, few material costs and only a simplified protocol, the modified HRM method could accurately distinguish the genotypes of <i>CHRN</i> SNPs, demonstrating kappa coefficients >0.96 based on the results from direct sequencing. Furthermore, the data showed that the GG genotype of SNP rs56218866 was associated with a significantly earlier age of COPD onset than A (AA+AG) genotypes (61.0 ± 8.93 vs. 67.8 ± 9.88; <i>P</i> = 0.031), which was not found for the other SNPs. No significant association was observed between the COPD stages and any of the above SNPs. <b>Conclusion:</b> A simple, rapid and efficient HRM method was introduced for <i>CHRN</i> SNP genotyping and a suggestion that the SNP rs56218866A>G is associated with early-onset COPD in a Chinese population was found.</p

    Increased fibroblasts in small airway walls in rats induced by wood smoke exposure.

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    <p>Immunostaining for FSP1 and spindle-shaped cells in small airway walls following smoke exposure for 7 months is shown in (A). (B) Graph showing that the number of fibroblasts increased significantly in small airway walls exposed to WS or CS for 4 to 7 months. Data are shown as the mean ± SEM. n = 8 animals/group. Scale bar  = 50 µm.</p
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