Delta neutrophil index as an early predictor of acute appendicitis and acute complicated appendicitis in adults.

BACKGROUND: This retrospective study aimed to evaluate the ability of the delta neutrophil index (DNI) to predict histologically normal appendicitis preoperatively and to differentiate between simple and complicated appendicitis. METHODS: The data from 650 patients were divided into positive and negative appendectomy groups (histologically normal appendicitis). The patients in the acute appendicitis group were further sub-divided into simple and complicated appendicitis groups. RESULTS: The DNI was significantly higher in the positive group than in the negative appendectomy group (0.4 vs. -0.4, p < 0.001) as well as in the complicated group compared with that in the simple appendicitis group (1.2 vs. 0.3, p < 0.001). The DNI independently predicted a positive appendectomy and an acute complicated appendicitis in multivariate logistic regression analysis [odds ratio (OR) 2.62, 95% confidence interval (CI) (1.11~6.16), p = 0.028 and odds ratio (OR) 4.10, 95% confidence interval (CI) (2.94~5.80), p < 0.001]. The optimum cut-off for a positive appendectomy and acute complicated appendicitis were 0.2 [area under curve (AUC) 0.709] and 0.6 (AUC 0.727). CONCLUSIONS: We suggest that obtaining a preoperative DNI is a useful parameter to aid in the diagnosis of histologically normal appendicitis and to differentiate between simple and complicated appendicitis.

Plasma neutrophil gelatinase-associated lipocalin as an early predicting biomarker of acute kidney injury and clinical outcomes after recovery of spontaneous circulation in out-of-hospital cardiac arrest patients.

AIMS: To determine whether the level of plasma neutrophil gelatinase-associated lipocalin (NGAL) can predict acute kidney injury (AKI) and clinical outcomes after recovery of spontaneous circulation (ROSC) in patients with out-of-hospital cardiac arrest (OHCA). METHODS: We conducted a prospective observational study of consecutive admitted patients with ROSC after OHCA between January 2013 and March 2015. Plasma was collected within 4h of ROSC to determine the level of NGAL. Outcome variables were AKI, 30-day survival, and good neurological outcome (GNO). We evaluated the association between NGAL and outcomes. RESULTS: Fifty-four patients were included. AKI occurred in 26 (48.0%); 15 (27.7%) survived over 30 days and 8 had GNO (14.8%). NGAL was significantly lower in the group with non-AKI, 30-day survival, and GNO. To predict AKI, 30-day survival, and GNO, the area under the receiver operating characteristic curve for NGAL was 0.810, 0.728, and 0.875, respectively. In a logistic regression model, NGAL >189 ngml(-1) was strongly associated with AKI (odds ratio [OR] 7.01, 95% confidence interval [CI]: 1.89-26.01) in a multivariate model. A lower level of NGAL was strongly associated with 30-day survival (OR 6.12, 95% CI: 1.64-23.42 at NGAL <153.5 ngml(-1)) and GNO (OR 19.83, 95% CI: 2.21-178.32 at NGAL <129.5 ngml(-1)) in a univariate model, but was not significantly associated with outcomes in a multivariate model. CONCLUSIONS: Plasma NGAL is a strong predictor of AKI in patients exhibiting OHCA at ICU admission. Lower levels of NGAL are associated with greater chance of 30-day survival and GNO.

Changes in immunoreactivity of HSP60 and its neuroprotective effects in the gerbil hippocampal CA1 region induced by transient ischemia.

Heat shock proteins act as molecular chaperones and are involved in protein folding, refolding, transport, and translocation. In the present study, we observed changes in heat shock protein 60 (HSP60) immunoreactivity and protein level in the gerbil hippocampal CA1 region after 5 min of transient forebrain ischemia and its neuroprotective effect against ischemic damage. HSP60 immunoreactivity in the CA1 region began to increase in the stratum pyramidale at 30 min after ischemia/reperfusion, and peaked 24 h after ischemia/reperfusion. Thereafter, HSP60 immunoreactivity was decreased in the CA1 region with time. Seven days after ischemia/reperfusion, HSP60 immunoreactivity was increased again in the CA1 region: at this time point after ischemia/reperfusion, HSP60 immunoreactivity was expressed in glial cells in the ischemic CA1 region. HSP60 immunoreactive glial cells were astrocytes containing glial fibrillar acidic protein. In contrast, change in HSP60 immunoreactivity in the ischemic CA2/3 region was not significant compared with that in the ischemic CA1 region. In Western blot study, HSP60 protein level in the CA1 region was increased after ischemia/reperfusion and highest 24 h after ischemia/reperfusion. Animals treated with recombinant adenoviruses expressing Hsp60 (Ad-Hsp60) showed the neuroprotection of CA1 pyramidal neurons from ischemic damage. These results suggest that HSP60 may be associated with delayed neuronal death of CA1 pyramidal neurons after transient ischemia, and the induction of HSP60 protects the neurons from ischemic damage.