BackgroundThis 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.MethodsThe 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.ResultsThe 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).ConclusionsWe 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.
The purpose of this study was to assess the plasma neutrophil gelatinase-associated lipocalin (NGAL) for early detection of acute kidney injury (AKI) and prediction of mortality in severely burned patients. From January 2014 to September 2015, 76 consecutive patients with more than 20% of TBSA burned were enrolled. Blood samples for plasma NGAL were collected at 0, 7, 14, 21, and 28 days after admission and analyzed with injury severity, clinical outcome, and AKI development. Plasma NGAL was significantly affected by the TBSA burned, AKI, and mortality, and it was significantly increased after operation and septic shock. Plasma NGAL was significantly increased within 7 days before AKI development in total patients (P < .001) and septic shock patients (P < .001) but not significantly increased in patients without septic shock (P = .167). Though, in a receiver operating characteristic curve analysis for predicting AKI, continuous renal replacement therapy application, and mortality, plasma NGAL was statistically significant; plasma NGAL was not independently associated with mortality in a multivariate logistic regression analysis. Plasma NGAL should be interpreted carefully in the major burn patients because it can reflect both inflammatory condition and AKI.
Rationale: Procalcitonin (PCT) is used as a biomarker for identifying the occurrence of sepsis. Previous studies have reported high levels of PCT with acetaminophen intoxication without evidence of infection. Here, we report two patients with acetaminophen intoxication with high levels of PCT without showing any symptoms of bacterial infection. Patient concerns: This case study examined two unrelated patients with acetaminophen intoxication admitted to emergency at different times. The first patient was admitted to the emergency department after ingesting approximately 8000 mg (153.8 mg/kg) of acetaminophen. On admission, C-reactive protein (CRP), glutamic oxaloacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT) were normal. PCT and acetaminophen levels were 31.89 ng/mL and below 0.5 μg/mL, respectively. The second patient was admitted to the emergency department 8 h after ingesting ∼23,600 mg (280.6 mg/kg) of acetaminophen. By the second day of admission, GOT and GPT increased to 2508 and 1473 IU/L, respectively. PCT was 45.66 ng/mL with acetaminophen level at 116.9 μg/mL. Both patients were clear of symptoms associated with bacterial infection. Diagnosis: Acetaminophen intoxication. Interventions: N-acetylcysteine was given intravenously to both patients for 20 h per protocol. Outcomes: Both patients were discharged without complications. Lessons: Observations suggests that elevated levels of PCT in patients intoxicated with acetaminophen may be associated with involvement of other organs impacted by cytokine stimuli from sterile inflammation resulting from hepatic damage rather than PCT secretion directly caused by hepatic cell damage.
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