ObjectiveTo explore the correlation of serum lipocalin-2 (LCN2) with inflammation and the predictive value of LCN2 for detecting acute kidney injury (AKI) in acute pancreatitis (AP).MethodsNighty-one patients with AP, who were admitted to Bazhong Municipal Hospital of Traditional Chinese Medicine between June 2016 and June 2018, were enrolled in the present study. Clinical paramaters were analyzed between patients with AKI (n=29) and patients without AKI (n=62). The correlation of serum LCN2 with inflammation was assessed with Pearson’s correlation analysis. The area under the receiver operating characteristic curve (ROC AUC) for serum LCN2 predicting AKI in AP patients was assessed.ResultsCompared with the patients without AKI, the patients with AKI showed increased serum levels of C-reactive protein [(64.8±10.5) vs. (148.3±21.6) mg/L], procalcitonin [(3.5±2.3) vs. (4.8±3.9) μg/L], urea nitrogen [(5.5±2.1) vs. (6.6±2.8) mmol/L], creatinine [(80.3±28.1) vs. (107.3±30.8) μmol/L], interleukin-6 [(10.1±3.7) vs. (16.2±4.6) pg/mL], and LCN2 [(155.0±37.6) vs. (394.8±53.1) mg/mL], as well as decreased level of calcium [(2.6±1.3) vs. (2.0±1.0) mmol/L], the differences were all statistically significant (P<0.05). The serum level of LCN2 was correlated with C-reactive protein (r=0.694, P<0.05), interleukin-6 (r=0.762, P<0.05), and procalcitonin (r=0.555, P<0.05) in patients with AP. The ROC AUC of LCN2 for predicting AKI was 0.844 (P<0.05) , with a sensitivity of 81.3% and a specificity of 81.4% when the cut-off value was 210.2 ng/mL.ConclusionsSerum LCN2 concentration is elevated in patients with AKI. In patients with AP, serum LCN2 level is positively correlated with C-reactive protein, interleukin-6, and procalcitonin. It can be regarded as a reliable indicator for predicting AKI.
ObjectiveTo analyze the risk factors of acute pancreatitis (AP) associated with hepatic dysfunction. MethodsWe collected the clinical data of AP patients from June 2012 to December 2014. According to the hepatic function, patients were divided into normal or mildly abnormal group (A), moderately abnormal hepatic function group (group B) and hepatic failure group (group C). We comparatively analyzed the relationship of abnormal hepatic function with causes (biliary, alcoholic, hypertriglyceridemia, and the others), age, gender, abdominal CT findings, laboratory test results, Ranson scores and the severity of acute pancreatitis bedside index (BISAP). ResultsA total of 117 AP patients were included in the study, including 75 males and 42 females aged from 28 to 71 years with the mean age of (53.21±1.35) years. There were 73 patients with mild AP (MAP), 28 with moderately severe AP (MSAP) and 16 with severe AP (SAP). There were 64 patients in group A, 37 in group B, and 16 in group C, in whom 73 patients were with hepatic dysfunction. The ratio of SAP and MSAP in group C was 75.0%, and MAP was 25.0%. There were 52 patients with bilious AP, 39 with alcoholic AP, 19 with hypertriacylglycerolemia AP, and 7 with others; the difference in causes among the three groups were not significant (P > 0.05). The differences in serum amylase, prothrombin time, white blood cells count, serum creatinine, triglycerides, total cholesterol, hemoglobin, and blood urea nitrogen among the three groups were not significant (P > 0.05). ConclusionsAP associated with hepatic dysfunction or failure may be caused by a various of factors. Whether the changes of serum amylase, prothrombin time, white blood cell count, serum creatinine, triglycerides, total cholesterol, hemoglobin, blood urea nitrogen, and BISAP scores can be the indexes of the judgment of AP with hepatic dysfunction needs more researches. Proper assessment of the related risk factors helps to prevent serious hepatic dysfunction or even failure.
Objective To summarize the change in the cytokine network, the classification of various cytokines, interaction, and systemic impact on patients with acute pancreatitis (AP). Methods The recently published literatures in domestic and abroad about advancement of cytokines in AP were reviewed. Results Cytokines had a complex network and interactions. There were a variety of regulatory mechanisms. The tumor necrosis factor-α (TNF-α) and interleukin cytokines played important roles in the progress of AP. Conclusions Change of cytokines during AP is a complex process. Any separate regulation for the release of sigle factor has no significant effect on the disease. The treatment according to immune balance should be a better direction.
Objective To investigate the significance of urinary trypsinogen-2 dipstick test and the ratio of urinary amylase to urinary creatinine for the diagnosis of acute pancreatitis(AP).Methods A total of 57 consecutive patients who were suspected as AP presenting with abdominal pain at the emergency department experienced the test of serum and urinary amylase, urinary creatinine assay, urinary trypsinogen-2 dipstick and ultrasonography. Results There were 18 patients diagnosed as acute pancreatitis, the serum amylase assay had a sensitivity of 88.9 percent (cutoff value, 300 U per liter) and a specificity of 87.2 percent, the sensitivity and specificity of the urinary amylase assay and the ratio of urinary amylase to urinary creatinine were 88.9 (cutoff value, 2000 U per liter), 94.4 (cutoff value, 120 U per mmol Cr), 84.6 and 89.7 percent, respectively. The sensitivity and specificity of the urinary trypsinogen-2 test strip were 94.4 and 92.3 percent. The sensitivity of the ultrasonography were 88.9 percent. Conclusion Urinary trypsinogen-2 dipstick test is a good index for the diagnosis of AP. The ratio of urinary amylase to urinary creatinine is also a useful index and may be better than urinary amylase for the diagnosis of AP.
Objective To evaluate the activity of the pancreatic tissue phospholipase A2 (PLA2) in acute pancreatitis (AP) and the therapeutic effects of verapamil in rats. MethodsThe model of rat AP induced by a closed duodenal loop technique was established to observe the changes of PLA2 activity in AP group and treated group. The pancreatic histology was examined by light and electron microscopy. Results At 16 and 24 hours after induction of AP in rats, significant inhibition of the pancreatic tissue PLA2 activity was shown in the treated group as compared with AP group, with 32.34±3.87u, 35.26±4.52u and 44.83±5.31u, 47.77±5.86u respectively. The treated animals also showed a decrease in the severity of pancreatic hemorrhage, necrosis and damage to the cellular ultrastructures. Conclusion There exists high activity of PLA2 in rats AP. Calcium channel blocker, verapamil might take therapeutic effects on AP by inhibiting activity of PLA2.
Objective To investigate therapeutic effects of continous regional arterial infusion with verapamil on preventing the progression of acute pancreatitis. Methods Forty-five patients with mild acute pancreatitis were randomly divided into three groups: conventional treatment group, intravenous treatment group and arterial infusion group. After admission, conventional treatments were performed in conventional treatment group. Reasonable fluid and verapamil were intravenously injected to the patients in intravenous treatment group, and fluid treatments and continous regional arterial infusion with verapamil were performed in arterial infusion group for 1－2 weeks. The levels of serum TNF-α, IL-1β, ICAM-1 and P-selectin were determined on the 1st, 4th and 7th day after treatment, respectively. Results On the 4th and 7th day after treatment, the levels of serum TNF-α and P-selectin significantly decreased in arterial infusion group compared with the other two groups （P＜0.05）, while the level of serum IL-1β significantly decreased in arterial infusion group and intravenous treatment group compared with the conventional treatment group （P＜0.05）. The level of serum ICAM-1 significantly decreased in arterial infusion group compared with the conventional treatment group （P＜0.05）.Conclusion Continous regional arterial infusion with verapamil could reduce the production of inflammatory cytokines and inhibit the up-regulation of adhesion molecules ICAM-1 and P-selectin, and prevent the progression of acute pancreatitis ultimately.
ObjectiveTo explore the regulation of nuclear factorκB (NFκB) on tumor necrosis factorα (TNFα) expression in the liver and its role in liver injury in rats with acute pancreatitis.MethodsSeventytwo Wistar rats were randomly divided into three groups: acute pancreatitis group (AP), acute pancreatitis treated with pyrrolidine dithiocarbamate (PDTC) group (APP) and sham operation group (SO). The hepatic NFκB activities were determined with electrophoretic mobility shift assays. The expressions of hepatic TNFα mRNA were detected with RTPCR. The levels of serum alanine aminotransferase (ALT) were also measured.ResultsThe NFκB activities were significantly higher in AP and APP groups than those in SO group 3-6 hours after operation. The expressions of TNFα mRNA were ber in AP and APP groups than those in SO group 3-24 hours after operation. The levels of serum ALT were also significantly higher in these two groups than those in SO group 3-24 hours after operation. However, compared with AP group, the activities of NFκB, the expressions of TNFα mRNA and the levels of ALT significantly decreased in APP group.ConclusionThe activation of hepatic NFκB is associated with the liver injury by regulating TNFα mRNA expression in acute pancreatitis.
Objective To summarize the role of inflammatory cytokines in the pathogenesis of acute pancreatitis (AP) and gut barrier dysfunction in recent years. Methods Literatures on cytokines and experimental pancreatitis as well as clinical pancreatitis were collected and reviewed. Results Tumor necrosis factor-α and other inflammatory cytokines were elevated significantly during pancreatitis in many tissues, especially in pancreas and alimentary tract, in a fashion independent of the animal model used. Anti-cytokine therapy could decrease the concentration of the cytokines in experimental animal. Conclusion Inflammatory cytokines are believed to be primarily responsible for the pathogenesis of acute pancreatitis and its associated distant organ dysfunction. Further study of the nature of these cytokines may provide a new approach to treating this disease.
Objective To investigate the CT manifestation and clinical significance of the gastrointestinal tract involvement in acute pancreatitis (AP). Methods Two hundreds CT scans in 131 patients with acute pancreatitis between Jan. 1, 2009 and Jun. 30, 2009 were included into the study. Two radiologists analyzed the images retrospectively, paying attention to the CT features of the gastrointestinal tract involvement, such as the style, distribution, and so on. The correlation between gastrointestinal tract involvement and CT severity index, clinical severity grading, and turnover of acute pancreatitis were studied using a SPSS 14.0 for windows statistics software. Results The CT images in 109 (83.2%) patients showed gastrointestinal tract involvement, which distributing mainly stomach, duodenum, jejunum, and transverse colon, and showing mainly the gastrointestinal tract wall thickening and distension. The gastrointestinal tract involvement had positive correlation with CT severity index, clinical severity grading, and turnover of acute pancreatitis (r=0.689， P=0.000; r=0.584， P=0.000; r=0.346， P=0.000). Conclusions The gastrointestinal tract involvement is common complication in acute pancreatitis and concerns with severity and prognosis of the disease. As other extrapancreatic organs involvement, the gastrointestinal tract involvement has important value for severity assessment, prognosis evaluation, and therapeutic effect monitoring of acute pancreatitis.
To evaluate the effects of different pressure and duration of autologous bile perfusion into dog’s pancreatic duct on the severity of induced acute pancreatitis. Thirty mongrel dogs were divided into five groups, with each group consisting of six dogs. Histological changes of pancreas were observed. Results: Histological changes of pancreas were correlated with the pressure and duration of autologous bile perfusion into pancreatic duct. It was easier to produce acute hemorrhagic necrotizing pancreatitis in the groups with a higher pressure and a longer duration of perfusion than in the groups with a lower pressure and a shorter duration. The results indicated that there was a significant effect of higher pressure and longer duration bile perfusion into pancreatic duct on the severity of induced acute pancreatitis.