The aim of this study was to determine the impact of HRCT-confirmed emphysema on biomarkers evaluating airway and systemic inflammation in COPD patients. Forty-nine consecutive male COPD outpatients with stable COPD were divided in two groups according to the presence or absence of emphysema on HRCT. Patients underwent pulmonary function tests, plus assessment of exercise capacity, body composition and quality of life. Biomarkers were measured in serum (CRP, interleukin-6, TNF-alpha, leptin, adiponectin, osteocalcin, insulin growth factor-1, and systemic oxidative stress), in plasma (fibrinogen and VEGF) and in whole blood (B-type natriuretic peptide). TNF-alpha, 8-isoprostane and pH were additionally measured in exhaled breath condensate. Patients with emphysema had more severe lung function impairment, lower body-mass index and fat-free mass index, and poorer quality of life. Additionally, they presented increased systemic oxidative stress and plasma fibrinogen and lower BNP compared to patients without emphysema. After proper adjustment for disease severity, all differences remained with the exceptions of body-mass index, fat-free mass index and BNP. COPD patients with HRCT-confirmed emphysema present increased systemic oxidative stress and fibrinogen, suggesting that they may be more prone to the systemic consequences of COPD compared to patients without emphysema.

BackgroundThe aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients.MethodsThis was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the University Hospital of Larissa, Greece. Patients with stable renal function, who underwent non urgent contrast-enhanced computed tomography for diagnostic purposes, were included in the study. Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline. All patients received additional hydration. Contrast-induced nephropathy was defined as relative increase by 25% of the baseline values of serum creatinine.ResultsContrast-induced nephropathy in NacA and CG were 18.33% and 15.6%, respectively (p = 0.81). The percentage change median (interquartile range (IR)) of serum cystatin-C (mg/L) from baseline in patients who underwent contrast-induced tomography, were 37.23% (28.53) and 93.20% (46.90) in NacA and in CG, respectively (p = 0.03). The 8-isoprostane serum levels in NacA were significantly lower compared to CG at 2 hours (p = 0.012) and 24 hours (p = 0.006) following radiocontrast infusion. Multivariate analysis revealed that contrast-induced nephropathy was independently associated with a higher baseline ratio of serum urea/creatinine (odds ratio, 1.02; 95 CI%, 1.00–1.05) and with the use of nephrotoxic medications (odds ratio, 0.24; 95 CI%, 0.06–0.94).ConclusionIntravenous administration of N-acetylcysteine and ascorbic acid failed to reduce contrast-induced nephropathy in critically ill patients who underwent contrast-enhanced computed tomography, despite a significant reduction of 8-isoprostane levels in treated patients.Trial registrationClinicalTrials.gov, NCT01017796. Registered on 20 November 2009.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-017-1862-3) contains supplementary material, which is available to authorized users.

Osteopontin (OPN) is a multifunctional cytokine involved in carcinogenesis. Serum levels of OPN, vascular endothelial growth factor (VEGF), and matrix metalloproteinase-9 (MMP-9) were measured by ELISA in 90 lung cancer patients. OPN levels were elevated in patients compared to controls (p <.0001). Smokers, patients with worse performance status, and weight loss exhibited higher OPN levels (p =.0012,.00036, and.0003, respectively). Increased OPN levels were associated with worse survival (p =.0018). Finally, OPN levels were positively correlated with both VEGF (p =.0008) and MMP-9 (p <.0001). OPN might serve as a prognostic biomarker, and the positive correlation between OPN and both VEGF and MMP-9 could implicate new insights in tumor angiogenesis.

Background This study was conducted to investigate whether high-tidal-volume mechanical ventilation is associated with increased lung inflammation compared with low-tidal-volume mechanical ventilation in critically ill patients with no evidence of lung injury. Methods In this prospective, single-blind, randomized (1:1), parallel-group study, 18 critically ill patients with normal lungs were randomly assigned to receive mechanical ventilation with a tidal volume of either 6 mL/kg (low tidal volume) or 12 mL/kg (high tidal volume) during the first 4 days in the intensive care unit. Results At baseline and at 24, 48, and 96 hours, exhaled breath condensate was collected to measure interleukin 1β, interleukin 10, tumor necrosis factor α, and total nitric oxide metabolites. Interleukin 1β levels in exhaled breath condensate were significantly increased at 24 hours compared with baseline in the high-tidal-volume group but not in the low-tidal-volume group. The interleukin 1β increase in the high-tidal-volume group was transient. Exhaled breath condensate levels of interleukin 1β, interleukin 10, tumor necrosis factor α, and total nitric oxide metabolites did not differ significantly between the high-tidal-volume and low-tidal-volume groups at any time point. Conclusion Short-term mechanical ventilation with a tidal volume of 12 mL/kg may trigger inflammatory responses in the lungs of intensive care unit patients without preexisting lung injury.