Mortality after admission with pneumonia is higher than after admission with an exacerbation of COPD.
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ABSTRACT:
SUBMITTER: Vestbo J
PROVIDER: S-EPMC9117732 | biostudies-literature | 2022 May
REPOSITORIES: biostudies-literature
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Mortality after admission with pneumonia is higher than after admission with an exacerbation of COPD.
Vestbo Jørgen J Waterer Grant G Leather David D Crim Courtney C Diar Bakerly Nawar N Frith Lucy L Jacques Loretta L Harvey Catherine C Satia Imran I Woodcock Ashley A
The European respiratory journal 20220519 5
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Project description:BackgroundLow handgrip strength (HGS) is independently associated with a higher exacerbation risk in stable chronic obstructive pulmonary disease (COPD); however, the relationship between HGS while being admitted for COPD exacerbation and further exacerbation risk after discharge remains unclear.MethodsWe enrolled patients admitted for COPD exacerbation between January 2018 and June 2019. HGS tests were done within 3 days after admission. The primary endpoint was exacerbations within 12 months after the index admission, which needed emergency room visits or hospital admission. We analyzed the relationships among demographics, HGS, pulmonary function parameters, and acute exacerbation events.ResultsAmong 43 enrolled patients, 31 (72.1%) participants (HGSw) had HGS weakness (22.1 ± 4.1 kg). The other 12 (27.9%) participants (non-HGSw) had the strength of handgrips 33.7 ± 3.1 kg. HGSw group showed a significantly higher rate of emergency room visits within 6, 9, and 12 months after the index admission than non-HGSw group (0.81 ± 1.30 vs. 0.08 ± 0.29, p = 0.045; 1.26 ± 1.59 vs. 0.17 ± 0.38, P = 0.019; 1.48 ± 1.86 vs. 0.25 ± 0.62, P = 0.027, respectively). There was a trend to have higher admission rate within 9 and 12 months in HGSw group, which did not achieve statistical significance (0.77 ± 1.38 vs. 0.08 ± 0.29, P = 0.064; 0.94 ± 1.56 vs. 0.08 ± 0.29, P = 0.062, respectively).ConclusionsHGS weakness measured upon admission for COPD exacerbation was associated with a higher risk of exacerbation in the next year. Trial registration ClinicalTrials.gov Identifier: NCT04885933.
| S-EPMC8296662 | biostudies-literature
Project description:PBMCs were isolated from patients suffering from Community Acquired Pneumonia (CAP) or acute exacerbating chronic obstructive pulmonary disease (AECOPD) or from healthy donors. RNA was extracted from these samples. 400 ng RNA per sample were then reverse transcribed with the Life Technologies miR RT kit with megaplex primers. Reverse transcribed RNA was then loaded on the human Taqman Low Density Array (TLDA) Cards and run according to manufacturer´s recommendations
2020-05-26 | GSE136390 | GEO
Project description:Limited data are available on the impact of time to ICU admission and outcomes for patients with severe community acquired pneumonia (CAP). Our objective was to examine the association of time to ICU admission and 30-day mortality in patients with severe CAP.A retrospective cohort study of 161 ICU subjects with CAP (by International Classification of Diseases, 9th edition, codes) was conducted over a 3-year period at two tertiary teaching hospitals. Timing of the ICU admission was dichotomized into early ICU admission (EICUA, direct admission or within 24 h) and late ICU admission (LICUA, >or= day 2). A multivariable analysis using Cox proportional hazard model was created with the primary outcome of 30-day mortality (dependent measure) and the American Thoracic Society (ATS) severity adjustment criteria and time to ICU admission as the independent measures.Eighty-eight percent (n = 142) were EICUA patients compared with 12% (n = 19) LICUA patients. Groups were similar with respect to age, gender, comorbidities, clinical parameters, CAP-related process of care measures, and need for mechanical ventilation. LICUA patients had lower rates of ATS severity criteria at presentation (26.3% vs 53.5%; P = .03). LICUA patients (47.4%) had a higher 30-day mortality compared with EICUA (23.2%) patients (P = .02), which remained after adjusting in the multivariable analysis (hazard ratio 2.6; 95% CI, 1.2-5.5; P = .02).Patients with severe CAP with a late ICU admission have increased 30-day mortality after adjustment for illness severity. Further research should evaluate the risk factors associated and their impact on clinical outcomes in patients admitted late to the ICU.
| S-EPMC3021366 | biostudies-other
Project description:BackgroundChronic obstructive pulmonary disease (COPD) exacerbation (ECOPD) alters the natural course of the disease. To date, only C-reactive protein has been used as a biomarker in ECOPD, but it has important limitations. The mitochondria release peptides (Humanin (HN), FGF-21, GDF-15, MOTS-c and Romo1) under certain metabolic conditions. Here, we aimed to evaluate the pathophysiologic, diagnostic and prognostic value of measuring serum mitochondrial peptides at hospital admission in patients with ECOPD.MethodsA total of 51 consecutive patients admitted to our hospital for ECOPD were included and followed for 1 year; in addition, 160 participants with stable COPD from our out-patient clinic were recruited as controls.ResultsSerum FGF-21 (p < .001), MOTS-c (p < .001) and Romo1 (p = .002) levels were lower, and GDF-15 (p < .001) levels were higher, in patients with ECOPD than stable COPD, but no differences were found in HN. In receiver operating characteristic analysis, MOTS-c (AUC 0.744, 95% CI 0.679-0.802, p < .001) and GDF-15 (AUC 0.735, 95% CI 0.670-0.793, p < .001) had the best diagnostic power for ECOPD, with a diagnostic accuracy similar to that of C-RP (AUC 0.796 95% IC 0.735-0.848, p < .001). FGF-21 (AUC 0.700, 95% CI 0.633-0.761, p < .001) and Romo1 (AUC 0.645 95% CI 0.573-0.712, p = .001) had lower diagnostic accuracy. HN levels did not differentiate patients with ECOPD versus stable COPD (p = .557). In Cox regression analysis, HN (HR 2.661, CI95% 1.009-7.016, p = .048) and MOTS-c (HR 3.441, CI95% 1.252-9.297, p = .016) levels exceeding mean levels were independent risk factors for re-admission.ConclusionsMost mitochondrial peptides are altered in ECOPD, as compared with stable COPD. MOTS-c and GDF15 levels have a diagnostic accuracy similar to C-RP for ECOPD. HN and MOTS-c independently predict future re-hospitalization.
| S-EPMC10734331 | biostudies-literature
Project description:Purpose:It is a challenge to control oxygen saturation (SpO2) in patients with exacerbations of COPD during admission. We tested a newly developed closed-loop system, O2matic®, and its ability to keep SpO2 within a specified interval compared with manual control by nursing staff. Patients and methods:We conducted a crossover trial with patients admitted with an exacerbation of COPD and hypoxemia (SpO2 ?88% on room air). Patients were monitored with continuous measurement of SpO2. In random order, they had 4 hours with manually controlled oxygen and 4 hours with oxygen delivery controlled by O2matic. Primary outcome was time within a prespecified SpO2 target interval. Secondary outcomes were time with SpO2 <85%, time with SpO2 below target but not <85%, and time with SpO2 above target. Results:Twenty patients were randomized and 19 completed the study. Mean age was 72.4 years and mean FEV1 was 0.72 L (33% of predicted). Patients with O2matic-controlled treatment were within the SpO2 target interval in 85.1% of the time vs 46.6% with manually controlled treatment (P<0.001). Time with SpO2 <85% was 1.3% with O2matic and 17.9% with manual control (P=0.01). Time with SpO2 below target but not <85% was 9.0% with O2matic and 25.0% with manual control (P=0.002). Time with SpO2 above target was not significantly different between treatments (4.6% vs 10.5%, P=0.2). Patients expressed high confidence and a sense of safety with automatic oxygen delivery. Conclusion:O2matic was able to effectively control SpO2 for patients admitted with an exacerbation of COPD. O2matic was significantly better than manual control to maintain SpO2 within target interval and to reduce time with unintended hypoxemia.
| S-EPMC6300382 | biostudies-literature
Project description:IntroductionOne-year mortality in COPD patients is reported to be between 4% and 43%, depending on the group examined.AimTo examine the one-year mortality in COPD patients after severe exacerbation and the correlation between mortality and patients' characteristics and comorbidities.MethodsA total of 152 COPD patients hospitalized for severe exacerbation were assessed for vitamin D status, diabetes mellitus (DM), arterial hypertension (AH), and metabolic syndrome (MS). Data were gathered about smoking status and number of exacerbations in previous year. CAT and mMRC questionnaires were completed by all patients. Pre- and post-bronchodilatory spirometry was performed. One-year mortality was established from national death register.ResultsOne-year mortality is 7.2%. DM, MS, and VD are not predictors for one-year mortality. However there is a trend for increased mortality in patients with AH (9.5% vs. 2.1%, p = 0.107). There is increased mortality in patients with mMRC > 2 (11.1 vs. 0%, p = 0.013). The presence of severe exacerbation in the previous year is a risk factor for mortality (12.5% vs. 1.4%, p = 0.009). There is a trend for increased mortality in the group with FEV1 < 50% (11.5 vs. 4.4%, p = 0.094). Cox regression shows 3.7% increase in mortality rate for 1% decrease in FEV1, 5.2% for 1% decrease in PEF, 7.8% for one year age increase and 8.1% for 1 CAT point increase (all p < 0.05).ConclusionsThis study finds relatively low one-year mortality in COPD patients after surviving severe exacerbation. Grade C and FEV1 > 80% may be factors for good prognosis. Risk factors for increased mortality are age, FEV1 value, severe exacerbation in previous year and reduced quality of life.
| S-EPMC5157192 | biostudies-literature
Project description:Patients admitted for chronic obstructive pulmonary disease (COPD) commonly continue to smoke. The utilization and effectiveness of tobacco cessation medications after discharge is largely unknown. We sought to examine whether pharmacologic treatment of tobacco use following admission for COPD was associated with smoking cessation at 6 to 12 months.Multivariable logistic regression analysis of a cohort of 1334 smokers, discharged from hospital with a COPD exacerbation between 2005 and 2012, identified administratively within the Veterans Affairs Veterans Integrated Service Network-20, adjusted for variables chosen a priori. Our primary exposure was treatment with any 1 or combination of smoking cessation medications within 90 days of discharge determined from pharmacy records, with the outcome of smoking cessation at 6 to 12 months after discharge.Four hundred fifty (33.7%) of the patients were dispensed a smoking cessation medication, with 53.4% receiving a nicotine patch alone. Overall, 19.8% of patients reported quitting smoking at 6 to 12 months. Compared to those not receiving medications, the odds of quitting were not greater among patients dispensed any single or combination of smoking cessation medications within 90 days of discharge (odds ratio [OR]: 0.88, 95% confidence interval [CI]: 0.74-1.04). Among patients treated with medications compared to nicotine patch alone, varenicline (OR: 2.44, 95% CI: 1.48-4.05) was associated with increased odds of cessation, and short-acting nicotine replacement therapy alone (OR: 0.66, 95% CI: 0.51-0.85) was associated with decreased odds of cessation.Treatment was provided to a minority of subjects and was not associated with cessation, with potential differences observed in effectiveness between medications. Systems-based changes may improve delivery of this key intervention.
| S-EPMC5926808 | biostudies-other
Project description:IntroductionPatients suffering from chronic obstructive pulmonary disease (COPD) are prone to acute exacerbations (AECOPD) or community acquired pneumonia (CAP), both posing severe risk of morbidity and mortality. There is no available biomarker that correctly separates AECOPD from COPD. However, because CAP and AECOPD differ in aetiology, treatment and prognosis, their discrimination would be important.MethodsThis study analysed the ability of selected candidate transcripts from peripheral blood mononuclear cells (PBMCs) to differentiate between patients with AECOPD, COPD & CAP, and CAP without pre-existing COPD.ResultsIn a previous study, we identified differentially regulated genes between CAP and AECOPD in PBMCs. In the present new cohort, we tested the potential of selected candidate PBMC transcripts to differentiate at early time points AECOPD, CAP+COPD, and CAP without pre-existing COPD. Expression of YWHAG, E2F1 and TDRD9 held predictive power: This gene set predicted diseases markedly better (model accuracy up to 100%) than classical clinical markers like CRP, lymphocyte count and neutrophil count (model accuracy up to 82%).DiscussionIn summary, in our cohort expression levels of YWHAG, E2F1 and TDRD9 differentiated with high accuracy between COPD patients suffering from acute exacerbation or CAP.
| S-EPMC10995291 | biostudies-literature
Project description:Lower respiratory infections, such as community-acquired pneumonia (CAP), and chronic obstructive pulmonary disease (COPD) rank among the most frequent causes of death worldwide. Improved diagnostics and profound pathophysiological insights are urgent clinical needs. In our cohort, we analysed transcriptional networks of peripheral blood mononuclear cells (PBMCs) to identify central regulators and potential biomarkers. We investigated the mRNA- and miRNA-transcriptome of PBMCs of healthy subjects and patients suffering from CAP or AECOPD by microarray and Taqman Low Density Array. Genes that correlated with PBMC composition were eliminated, and remaining differentially expressed genes were grouped into modules. One selected module (120 genes) was particularly suitable to discriminate AECOPD and CAP and most notably contained a subset of five biologically relevant mRNAs that differentiated between CAP and AECOPD with an AUC of 86.1%. Likewise, we identified several microRNAs, e.g. miR-545-3p and miR-519c-3p, which separated AECOPD and CAP. We furthermore retrieved an integrated network of differentially regulated mRNAs and microRNAs and identified HNF4A, MCC and MUC1 as central network regulators or most important discriminatory markers. In summary, transcriptional analysis retrieved potential biomarkers and central molecular features of CAP and AECOPD.
| S-EPMC6959367 | biostudies-literature
Project description:Introduction:Chronic obstructive pulmonary disease (COPD) may, in some patients, be characterized by recurring acute exacerbations. Often these exacerbations are associated with airway infections. As immunoglobulins (Ig) are important parts of the immune defence against airway infections, the aim of this study was to relate the levels of circulating immunoglobulins to clinical features in unselected patients with COPD included in a Norwegian multicenter study. Methods:Clinical and biological data, including circulating levels of immunoglobulins, were assessed in 262 prospectively included patients with COPD GOLD stage II-IV at five hospitals in south-eastern Norway. A revisit was done after one year, and survival was assessed after five years. Clinical features and survival of those with immunoglobulin levels below reference values were compared to those with normal levels. Results:In total, 11.5% of all COPD patients and 18.5% of those with GOLD stage IV had IgG concentrations below reference values. These patients were more likely to use inhaled or oral steroids, had lower BMI, and lower FEV1%. Moreover, they had significantly more COPD-related hospital admissions (2.8 vs 0.6), number of prednisolone courses (3.9 vs 1.2), and antibiotic treatments (3.7 vs 1.5) in the preceding year. Importantly, hypogammaglobulinemia was significantly associated with reduced survival in a log-rank analysis. In multivariate regression analysis, we found that the higher risk for acute exacerbations in these patients was independent of other risk factors and was associated with impaired survival. Conclusion:In conclusion, our study suggests that hypogammaglobulinemia may be involved in poor outcome in COPD and may thus be a feasible therapeutic target for interventional studies in COPD.
| S-EPMC7173948 | biostudies-literature