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Purpose: The diagnosis and treatment of secondary infection of pancreatic necrotic tissue remain a major challenge. The level of soluble triggering receptor expressed on myeloid cells (sTREM-1) in fine needle aspiration (FNA) fluid may be a good marker of infected necrosis. Methods: Patients with a clinical suspicion of secondary infection of necrotic tissue were enrolled. The serum levels of C-reactive protein, amylase, procalcitonin (PCT), and sTREM-1 and the fluid levels of sTREM-1, PCT, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and amylase were examined. When infected necrosis was defined, the first step was percutaneous or endoscopic drainage. If there was no improvement after 72 h, an open necrosectomy was performed. Results: In 30 patients with suspected infection, 18 patients were diagnosed as having secondary infection of necrotic tissue. The levels of sTREM-1 and PCT in FNA fluid were found to have the closest correlation with the diagnosis of infected necrosis [sTREM-1: area under the receiver operating characteristic curve (AUC) 0.972; 95% confidence interval (95%CI) 0.837-1.000; PCT: AUC 0.903; 95%CI 0.670-0.990, P > 0.05]. A fluid sTREM-1 cutoff value of 285.6 pg/ml had a sensitivity of 94.4% and a specificity of 91.7%. In a multiple logistic regression analysis, an sTREM-1 level of more than 285 pg/ml and a PCT level of more than 2.0 ng/ml in FNA fluid were independent predictors of infected necrosis. Conclusions: The fluid level of sTREM-1 will help in the rapid and accurate diagnosis of secondary infection of necrotic tissue in patients with severe acute pancreatitis (SAP). [ABSTRACT FROM AUTHOR]

Serial measurement of exhaled nitric oxide (eNO) has been shown to be a good noninvasive marker of asthma control. Active smoking decreases eNO levels. The effect of real-life environmental exposure to tobacco smoke (ETS) on eNO levels is not known. Our objective was to study the impact of environmental tobacco exposure on eNO levels in asthmatic and non-asthmatic children. Single breath off-line collection of eNO was performed in asthmatic and non-asthmatic children with and without ETS. Urine was collected for cotinine/nicotine analysis. Fifty-seven children were enrolled, of which 25 were asthmatic and 32 had smoke exposure. One active smoker was excluded from the data analysis. The mean eNO was 11.1 ppb (n = 31; SD = 18.5) in those passively exposed vs. 11.1 ppb (n = 25; SD = 19.9) among the unexposed (not statistically significant). The mean eNO was 6.1 (n = 32; SD = 4.4) among the non-asthmatics and 17.8 (n = 24; SD = 27.4) among the asthmatics (p = 0.02; CI: 1.9–21.6). Real-life environmental tobacco exposure does not appear to decrease eNO levels in asthmatic children. Off-line collection of exhaled nitric oxide with a Mylar collection device helps differentiate asthmatics from non-asthmatics. [ABSTRACT FROM AUTHOR]