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Background Acute appendicitis is a common abdominal emergency, while cerebral venous sinus thrombosis (CVST) is a rare cerebral vascular disease. Cases of CVST in patients with appendicitis have not been reported in the literature. We present a case of CVST in a patient with appendicular abscess. Case Description A 56-year old man presented to our department with a headache for 6 days; he had a history of abdominal pain 15 days before admission. Abdominal contrast-enhanced computed tomography revealed appendicular abscess. Head magnetic resonance venography and contrast-enhanced magnetic resonance imaging showed thrombosis in the left transverse and sigmoid sinus. Antithrombotic treatments were administered, and antibiotic treatments and puncture and drainage were used to treat the appendicular abscess. The patient's headache disappeared after 10 days of treatment, and he had recovered well clinically at 3-month follow-up. Conclusions CVST after acute appendicitis is rare, and clinicians should be aware of this complication when suspicious symptoms occur. The underlying mechanisms require further investigation.

Background Platelet activation is implicated in secondary brain injury following traumatic brain injury (TBI). C-type lectin-like receptor 2 (CLEC-2) is extensively expressed on platelets and participates in platelet activation. We investigate dthe prognostic significance of plasma CLEC-2 in TBI patients. Methods One hundred and six patients with isolated severe blunt TBI and 106 healthy controls were prospectively investigated. Plasma CLEC-2 concentrations were detected and Glasgow coma scale (GCS) scores were recorded. The relationship between plasma CLEC-2 concentrations and 30-day mortality in addition to overall survival was determined using multivariate models. Results Patients exhibited a substantially higher concentration of plasma CLEC-2 than healthy controls. Among patients, plasma CLEC-2 concentrations were remarkably increased in the GCS scores- and Rotterdam computerized tomography classification- dependent manner. As compared with survivors within posttraumatic 30 days, plasma CLEC-2 concentrations were remarkably raised in non-survivors. Rising plasma CLEC-2 concentration was independently associated with an enhanced risk of 30-day mortality and short overall survival time. Plasma CLEC-2 concentrations had a significantly high area under receiver operating characteristic curve for predicting 30-day mortality. Conclusions Incremental plasma CLEC-2 concentrations are intimately related to increasing trauma severity, in close association with increased 30-day death, indicating the prognostic role of plasma CLEC-2 in TBI.

Secreted protein acidic and rich in cysteine-like 1 (SPARCL1) regulates synaptic stability with upregulation throughout axonal regeneration. Our study aims to determine the correlation of serum SPARCL1 concentrations with the severity and in-hospital mortality of severe traumatic brain injury (sTBI).A total of 102 consecutively recruited patients admitted for sTBI and 102 randomly selected healthy controls were included in this observational prospective study. Serum SPARCL1 concentrations were measured and correlated with Glasgow coma scale (GCS) scores and in-hospital mortality using multivariate analysis.Compared with controls (median, 0.22 ng/ml; interquartile range, 0.19-0.41 ng/ml), patients had significantly higher SPARCL1 concentrations (median, 3.29 ng/ml; interquartile range, 1.88-4.37; P 0.001). There was an independently correlation between SPARCL1 concentrations and GCS scores (t = -7.011, P 0.001). We found a high area under receiver operating curve (AUC) of serum SPARCL1 concentrations to predict in-hospital mortality (AUC, 0.822; 95% confidence interval, 0.734-0.891). In the multiple logistic regression analysis, serum SPARCL1 concentrations3.29 ng/ml was independently associated with in-hospital mortality (odds ratio = 10.052, 95% confidence interval = 1.918-52.686, P = 0.006).The novel findings of our study are that sTBI patients had an increase of serum SPARCL1 concentrations, and that there is an association between high serum SPARCL1 concentrations and sTBI mortality or trauma severity.

BACKGROUND To investigate the correlation between plasma D-dimer level and severity and prognosis of patients admitted to the emergency department with trauma. METHODS A total of 168 trauma patients admitted to the department of emergency surgery of Shengzhou People's Hospital were included in this study. The general information was collected, and the plasma D-dimer level was measured within 24 hours after admission. Patients were divided into the mild traumatic group (ISS ≤ 16 points), the moderate traumatic group (16 25 points) according to the Injury Severity Score (ISS) evaluation. According to the results from a 28-day follow-up, plasma D-dimer levels were compared between the survival group and the death group. The correlation between plasma D-dimer levels and severity of trauma patients admitted to the emergency department (according to the ISS) was analyzed. The receiver operating characteristic (ROC) curve evaluated the predictive value of plasma D-dimer levels for prognosis in patients admitted to the emergency department with trauma. RESULTS Plasma D-dimer levels successively increased from the mild traumatic group (2.51 ± 0.46 mg/L), the moderate traumatic group (4.09 ± 1.00 mg/L) to the severe traumatic group (6.58 ± 1.14 mg/L) (F = 0.659, p < 0.05). Plasma D-dimer levels were significantly and positively correlated with ISSs (r = 0.720, p < 0.001). The plasma D-dimer level in the survival group (3.72 ± 1.26 mg/L) was significantly lower than that in the death group (5.19 ± 0.87 mg/L) (t = 6.251, p < 0.001). According to the Youden index, the optimal cutoff value of plasma D-dimer was 4.00 mg/L, the AUC was 0.849, the standard error was 0.034, the 95% CI was 0.783 - 0.915, the sensitivity was 0.938, and the specificity was 0.603. CONCLUSIONS Plasma D-dimer levels were positively correlated with the severity of patients with trauma admitted to the department of emergency surgery and can predict poor prognosis.

Background The C-reactive protein to albumin ratio (CAR) is a novel inflammation index that has recently been used as a marker for poor prognosis or mortality in various patient groups. This study aimed to evaluate the association between the CAR and 30-day mortality in patients with hepatitis B virus-related decompensated cirrhosis (HBV-DeCi). Methods This was a retrospective cohort study of 113 patients who had been diagnosed with HBV-DeCi. Univariate and multivariate regression models were used to determine risk factors for mortality. Results The CAR was observed to be significantly higher in the non-surviving patients compared to the surviving patients. Moreover, the CAR was positively correlated with the model for end-stage liver disease (MELD) score and Child-Pugh score. In multivariate analysis, the CAR and the MELD score were independent prognostic factors for HBV-DeCi patients. Conclusions A high CAR value at admission can serve as an independent predictor of 1-month mortality in patients with HBV-DeCi.

Lipocalin-2 is related to acute brain injury. We assessed the prognostic value of serum lipocalin-2 in head trauma.Blood samples were collected from 115 controls and 115 patients with severe traumatic brain injury. Trauma severity was assessed by Glasgow Coma Scale (GCS) scores at baseline. Thirty-day mortality and overall survival time were recorded.Compared with the controls, serum lipocalin-2 concentrations were significantly increased in the patients. Lipocalin-2 concentrations were independently associated with GCS scores (t=-7.271, P0.001) and serum C-reactive protein concentrations (t=4.325, P0.001). Under receiver operating characteristic curve for 30-day mortality, sensitivity and specificity were 85.7% and 63.2% respectively for lipocalin-2 concentrations at a cutoff value of 591ng/ml. Additionally, area under curve (AUC) of lipocalin-2 concentrations [AUC, 0.825; 95% confidence interval (95% CI), 0.743-0.889] was equivalent to that of GCS scores (AUC, 0.869; 95% CI, 0.793-0.925; P=0.413). Moreover, serum lipocalin-2 concentrations591ng/ml emerged as an independent predictor for 30-day mortality (odds ratio, 4.360; 95% CI, 1.908-12.430) and overall survival (hazard ratio, 3.820; 95% CI, 1.935-10.500).Enhanced serum concentration of lipocalin-2 at admission is associated with trauma severity and neuroinflammation as well as is a predictor of mortality after head trauma.

Adiponectin plays an important role in the regulation of tissue inflammation. There is a paucity of data on circulating plasma adiponectin concentrations in human traumatic brain injury. This study is designed to investigate the potential associations between plasma adiponectin levels and clinical outcomes after traumatic brain injury.Plasma adiponectin levels of 86 patients with severe traumatic brain injury and 86 healthy subjects were determined. Clinical outcomes included in-hospital mortality, 6-month mortality and 6-month unfavorable outcome (Glasgow Outcome Scale score of 1-3).Plasma adiponectin levels were significantly higher in patients compared to controls (20.5±5.9 vs. 7.7±2.0μg/ml; P0.001) and emerged as an independent predictor of in-hospital mortality [odds ratio (OR), 1.318; 95% confidence interval (CI), 1.049-1.629; P=0.008], 6-month mortality (OR, 1.328; 95% CI, 1.082-1.657; P=0.007) and 6-month unfavorable outcome (OR, 1.240; 95% CI, 1.066-1.443; P=0.005) in a multivariate analysis. For predicting these clinical outcomes, areas under receiver operating characteristic curve of plasma adiponectin level were similar to those of Glasgow Coma scale scores (all P0.05). However, adiponectin did not improve predictive values of Glasgow Coma scale scores (all P0.05).Plasma adiponectin level may represent a novel biomarker for predicting clinical outcomes of traumatic brain injury.

Introduction Recently, we reported that high levels of resistin are present in the peripheral blood of patients with intracerebral hemorrhage and are associated with a poor outcome. However, not much is known regarding the change in plasma resistin and its relation with mortality after traumatic brain injury (TBI). Thus, we sought to investigate change in plasma resistin level after TBI and to evaluate its relation with disease outcome. Methods Fifty healthy controls and 94 patients with acute severe TBI were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5 and 7 after TBI. Its concentration was measured by enzyme-linked immunosorbent assay. Results Twenty-six patients (27.7%) died from TBI within 1 month. After TBI, plasma resistin level in patients increased during the 6-hour period immediately after TBI, peaked within 24 hours, plateaued at day 2, decreased gradually thereafter and was substantially higher than that in healthy controls during the 7-day period. A forward stepwise logistic regression selected plasma resistin level (odds ratio, 1.107; 95% confidence interval, 1.014-1.208; P = 0.023) as an independent predictor for 1-month mortality of patients. A multivariate linear regression showed that plasma resistin level was negatively associated with Glasgow Coma Scale score (t = -6.567, P < 0.001). A receiver operating characteristic curve identified plasma resistin cutoff level (30.8 ng/mL) that predicted 1-month mortality with the optimal sensitivity (84.6%) and specificity (75.0%) values (area under curve, 0.854; 95% confidence interval, 0.766-0.918; P < 0.001). Conclusions Increased plasma resistin level is found and associated with Glasgow Coma Scale score and mortality after TBI.