Background and objectiveSerum D-dimer is elevated in respiratory disease. The objective of our study was to investigate the effect of D-dimer on in-hospital and 1-year mortality after acute exacerbations of chronic obstructive pulmonary disease (AECOPD).MethodsUpon admission, we measured 343 AECOPD patients’ serum D-dimer levels and arterial blood gas analysis, and recorded their clinical characteristics. The level of D-dimer that discriminated survivors and non-survivors was determined using a receiver operator curve (ROC). The risk factors for in-hospital mortality were identified through univariate analysis and multiple logistic regression analyses. To evaluate the predictive role of D-dimer for 1-year mortality, univariate and multivariate Cox regression analyses were performed.ResultsIn all, 28 patients died, and 315 patients survived in the in-hospital period. The group of dead patients had lower pH levels (7.35±0.11 vs 7.39±0.05, P<0.0001), higher D-dimer, arterial carbon dioxide tension (PaCO2), C-reactive protein (CRP), and blood urea nitrogen (BUN) levels (D-dimer 2,244.9±2,310.7 vs 768.2±1,078.4 µg/L, P<0.0001; PaCO2: 58.8±29.7 vs 46.1±27.0 mmHg, P=0.018; CRP: 81.5±66, P=0.001; BUN: 10.20±6.87 vs 6.15±3.15 mmol/L, P<0.0001), and lower hemoglobin levels (118.6±29.4 vs 128.3±18.2 g/L, P=0.001). The areas under the ROC curves of D-dimer for in-hospital death were 0.748 (95% confidence interval (CI): 0.641–0.854). D-dimer ≥985 ng/L was a risk factor for in-hospital mortality (relative risk =6.51; 95% CI 3.06–13.83). Multivariate logistic regression analysis also showed that D-dimer ≥985 ng/L and heart failure were independent risk factors for in-hospital mortality. Both univariate and multivariate Cox regression analyses showed that D-dimer ≥985 ng/L was an independent risk factor for 1-year death (hazard ratio (HR) 3.48, 95% CI 2.07–5.85 for the univariate analysis; and HR 1.96, 95% CI 1.05–3.65 for the multivariate analysis).ConclusionD-dimer was a strong and independent risk factor for in-hospital and 1-year death for AECOPD patients.

ObjectiveTo 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.MethodsDemographics, 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.ResultsDuring the in-hospital period, 73 patients died and 679 patients recovered. Age, PaO2<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.ConclusionThe PSI score may be used to predict in-hospital mortality for hospitalized AECOPD patients, with a prognostic capacity superior to CURB65 and BAP65.

BACKGROUND: COPD is associated with cardiovascular and renal dysfunction. Cystatin C (CysC) is a biomarker of renal function and an independent risk factor for all-cause and cardiovascular mortality among elderly persons. The aim of the study was to examine the prognostic role of CysC for in-hospital mortality in subjects with a COPD exacerbation. METHODS: Upon admission, serum CysC levels and arterial blood gas analysis from 477 subjects with a COPD exacerbation were measured. Clinical characteristics were also recorded. A receiver operating characteristic curve analysis was used to determine the level of CysC that discriminated survivors from nonsurvivors. Univariate and multiple logistic regression analyses were used to identify the risk factors for in-hospital mortality. To reduce the influence of confounders, subgroup analyses were performed according to the comorbidities, including states of heart failure, renal dysfunction, and pH, P aCO 2 , and P aO 2 levels. RESULTS: During the in-hospital period, 59 subjects died, and 418 subjects recovered. The decedent group showed lower pH (7.27 ؎ 0.17 vs 7.38 ؎ 0.06, P < .001), higher CysC (2.21 ؎ 1.05 mg/L vs 1.39 ؎ 0.54 mg/L, P < .001), higher P aCO 2 (77 ؎ 39 mm Hg vs 48 ؎ 14 mm Hg, P < .001), and lower P aO 2 (74 ؎ 32 mm Hg vs 84 ؎ 26 mm Hg, P < .001) levels. The area under the receiver operating characteristic curve for the CysC prediction of death was 0.77 (95% CI 0.70 -0.84). CysC values >1.59 mg/L were associated with significantly higher inhospital mortality (relative risk ‫؍‬ 5.49, 95% CI 3.24 -9.32, P < .001). Multiple logistic regression analysis showed that pH <7.20, CysC >1.59 mg/L, and heart failure were independent predictors of in-hospital mortality. The subgroup analysis showed that the comorbid states of renal dysfunction, congestive heart failure, and the levels of pH, P aCO 2 , and P aO 2 did not alter the conclusion that CysC was a mortality risk factor for subjects with a COPD exacerbation. CONCLUSION: CysC was a strong and independent risk factor for hospital mortality secondary to COPD exacerbation.

The lowest SaO2, ESS index, and OSAHS were risk factors for uncontrolled hypertension.

This study was aimed to investigate the relationship between the interleukin-4-590C > T gene polymorphism and the susceptibility to asthma by meta-analysis. To explore the underlying relationship between the polymorphism of IL-4-590C > T and the susceptibility to asthma, this study systematically retrieved the literature including cohort studies and case-control studies published before June 2019 in PubMed, Embase, and Cochrane Library. Data on the odds ratio (OR) and 95% confidence interval (CI) of the literature were included in the relative studies. Subsequently, the included data were weighted by an inverse variance and then analyzed by the fixed or random effects model. Overall, 818 asthma patients and 831 healthy individuals participated in the 8 independent case-control studies in the current meta-analysis. There was no correlation between IL-4-590C > T TT genotype and the increased susceptibility to asthma (dominant model: OR = 1.31, 95% CI = 0.68–2.53). Subgroup analysis by ethnicity showed no significant results in the Asians (OR = 1.28, 95% CI = 0.24–6.80); however, IL-4-590C > T TT genotype significantly elevated the susceptibility to asthma in the Caucasians (OR = 1.43, 95%CI = 1.03–1.98). Meanwhile, subgroup analysis was performed by source of control. A statistically significant result was found in the population-based control group (OR = 1.33, 95% CI = 1.01–1.76), but not in the hospital-based control group (OR = 1.22, 95% CI = 0.27–5.46). The results demonstrated that IL-4-590C > T TT genotype could significantly enhance the susceptibility to asthma in Caucasians without increasing that in Asian populations. However, it still required a large sample of high-quality studies in multicentral hospital to further confirm its reliability.