Konstantinos Bartziokas

The impact of depressive symptoms on recovery and outcome of hospitalised COPD exacerbations.

The impact of depressive symptoms on outcomes of acute exacerbations of chronic obstructive pulmonary disease (AECOPD) has not been thoroughly evaluated in prospective studies. We prospectively enrolled 230 consecutive patients hospitalised for AECOPD, without previous diagnosis of depression. Depressive symptoms were evaluated with Becks depression inventory. Pulmonary function tests, arterial blood gases, COPD assessment test (CAT) and Borg dyspnoea scale were recorded on admission and on days 3, 10 and 40. Patients were evaluated monthly for 1 year. Patients with depressive symptoms required longer hospitalisation (mean±sd 11.6±3.7 versus 5.6±4.1 days, p<0.001). Clinical variables improved during the course of AECOPD, but depressive symptoms on admission had a significant impact on dyspnoea (p<0.001) and CAT score (p=0.012) improvement. Patients with depressive symptoms presented more AECOPD (p<0.001) and more hospitalisations for AECOPD (p<0.001) in 1 year. In multivariate analysis, depressive symptoms were an independent predictor of mortality (hazard ratio 3.568, 95% CI 1.302–9.780) and risk for AECOPD (incidence rate ratio (IRR) 2.221, 95% CI 1.573–3.135) and AECOPD hospitalisations (IRR 3.589, 95% CI 2.319–5.556) in 1 year. The presence of depressive symptoms in patients admitted for AECOPD has a significant impact on recovery and is related to worse survival and increased risk for subsequent COPD exacerbations and hospitalisations in 1 year.

Serum uric acid as a predictor of mortality and future exacerbations of COPD

Serum uric acid is increased in respiratory disease, especially in the presence of hypoxia and systemic inflammation. We evaluated serum uric acid as a biomarker for prediction of mortality and future acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Serum uric acid was measured in 314 eligible consecutive patients on admission for AECOPD. Patients were evaluated monthly for 1 year. Uric acid levels were higher in patients with more severe airflow limitation and in those experiencing frequent exacerbations. High uric acid levels (≥6.9 mg·dL−1) were an independent predictor of 30-day mortality in multivariate Cox regression analysis (HR 1.317, 95% CI 1.011–1.736; p=0.044), but not of 1-year mortality. Patients with high serum uric acid required more prolonged hospitalisation, and more often needed noninvasive ventilation and admission to the intensive care unit within 30 days. In addition, high uric acid levels were associated with increased risk and hospitalisation for AECOPD in 1 year in multivariate Poisson regression analysis (incidence rate ratio 1.184 (95% CI 1.125–1.246) and 1.190 (95% CI 1.105–1.282), respectively; both p<0.001). Serum uric acid is associated with increased 30-day mortality and risk for AECOPD and hospitalisations in 1-year follow-up. This low-cost biomarker may be useful in the identification of high-risk chronic obstructive pulmonary disease patients that could benefit from intensive management. Serum uric acid was linked with airflow limitation in COPD and predicted mortality and future exacerbations http://ow.ly/qflaZ

Cardiovascular comorbidities in hospitalised COPD patients: a determinant of future risk?

Cardiovascular disease (CVD), diabetes mellitus and arterial hypertension increase the risk of death and hospitalisations of chronic obstructive pulmonary disease (COPD) patients [1]. COPD patients with CVD are at increased risk of COPD-related hospitalisations [2]. Arterial hypertension is one of the most prevalent comorbidities, influencing 40–60% of COPD patients [1]. Diabetes mellitus is more prevalent in moderate to very severe COPD than in the general population [1] and hyperglycaemia during acute exacerbations of COPD (AECOPD) is associated with increased in-hospital mortality [3]. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has proposed a multidimensional classification for COPD management [4, 5] that includes symptoms and future risk of AECOPD, based on the severity of airflow limitation and previous exacerbation history. A recent study has shown that the risk of future hospital admission due to COPD and cardiovascular death is higher in the more symptomatic group B compared with group C, regardless the functional advantage of patients in the first group [6]. Our study assessed the effect of CVD, arterial hypertension and diabetes mellitus on the time to first AECOPD, and on exacerbation and hospitalisation risk in groups A–D of the GOLD 2011 and 2013 classification, in a cohort of patients admitted to hospital for AECOPD. Comorbidities are important determinants of future risk in COPD patients and should be considered in the assessment of future risk http://ow.ly/L2qJp

Duration of Hospitalization and Lung Function Deterioration as Predictors of Future Chronic Obstructive Pulmonary Disease Exacerbations

and CMV amend the intense respiratory muscle contractions. Accordingly, IL-6 and IL-10 levels after CMV are significantly lower compared with the levels before intubation. This effect is not observed in both control groups, excluding any drugor intubationrelated effect as the reason for the decrease in cytokine levels. Thus, the source of the augmented plasma IL-6 and IL-10 levels during AECOPD above the value observed after 6 hours of CMV could be the strenuously contracting respiratory muscles. The functional roles of respiratory muscle–derived IL-6 and IL-10 are not definitely established. Muscle-derived IL-6 might be signaling that the energy stores within the respiratory muscles are reaching critically low levels (glycogen depletion) and stimulate glycogenolysis in the liver to make glucose available to the strenuously contracting energy-depleted respiratory muscles (8). Thus, after attenuation of strenuous muscular contractions secondary to CMV application, IL-6 is being down-regulated, as the respiratory muscles are no longer energy depleted. Both IL-6 and IL-10 might be produced within the respiratory muscles secondary to oxidative stress development because of strenuous contractions (3, 5). Preliminary results from our laboratory suggest these cytokines are also affecting the control of breathing (9). Eotaxin and EGF are expressed in the COPD lung and are increased in AECOPD (11, 12). Increased bronchoalveolar lavage and plasma eotaxin (eosinophil chemotactic factor) during AECOPD may indicate airway eosinophilia, whereas the activation of the EGF receptor leads to gene expression for mucus secretion. The attenuation of the large negative swings in pleural pressure, and consequently the relief of lung stress after CMV, lead to decreased eotaxin and EGF levels in AECOPD. In conclusion, application of CMV in patients with AECOPD leads to decreased plasma levels for circulating IL-6, IL-10, eotaxin, and EGF. The origin of the augmented level of these cytokines during AECOPD could partly be the strenuously contracting respiratory muscles and/or the mechanically stressed lung. n