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.
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.
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.
ObjectiveTo compare the predictive value of Balthazar computed tomography severity index (CTSI), Modified computed tomography severity index (MCTSI) and extrapancreatic inflammation on CT (EPIC) in patients diagnosed as acute pancreatitis with organ dysfunction based on the revised Atlanta classification. MethodsThe clinical data of patients diagnosed as acute pancreatitis from December 2013 to January 2014 were analyzed retrospectively. Four imaging score systems (CTSI, MCTSI, EPIC, and local complications) and two clinical score systems were assessed with ROC and AUC. Results①There were no statistical significances in the age, gender, time after onset of symptoms to CT scanning in 54 patients (P > 0.05).②CTSI, MCTSI, EPIC, and local complications were good independent predictors of organ dysfunction in the early phase (P < 0.05), while BISAP and NJSS were not (P > 0.05). ConclusionCT scoring systems can accurately evaluate organ dysfunction of acute pancreatitis in the early phase.
【Abstract】Objective To summarize the effects of vasoactive mediators on local microvasculature in acute pancreatitis（AP）. Methods Literatures concerning metabolism, receptors, action mechanisms of vasoactive mediators and their effects in AP were reviewed. Results Bradykinin, endothelin, platelet activating factor and nitric oxide were important mediators in the development of microcirculatory disturbance in AP, however the results of experiments were inconsistent. Conclusion The roles which vasoactive mediators play in microcirculatory disturbance of AP are affected by many factors, and await further study.
Fifty three patients with acute necrotizing pancreatitis were performed operation, treated surgically, including incision of the pancreatic capsule to release the pancreatic presure, removal of necrotic tissue, and placement of drainage tube around pancreas. Twenty two patients (41.5%) developed postoperative peripancreatic abscess. The average hospitalized days (83.3±25.1 days) of the patients with peripancreatic abscess was longer than those without (22.7±14.7 days) peripancreatic abscess (Ｐ＜0.01). Six cases of 28 (21.4%) patients who had localized or scattered pancreatic necrosis developed peripancreatic abscess, 16 cases of 25 (64.0%) patients who had subtotal or total pancreatic necrosis developed peripancreatic abscess which showed significant difference between two groups (Ｐ＜0.01). Among 21 patients in whom 2 to 4 doublelumened tubes for negative presure drainage were placed,5 cases (23.8%) had peripancreatic abscess but 32 patients with only one tube placed, 17 patients (53.1%) had peripancreatic abscess, the difference between two groups were significant (Ｐ＜0.05). At least 6 patients whose drainage tubes worked badly produced postoperative peripancreatic abscess. These results indicate that the peripancreatic abscess is closely related with the severity of the disease, surgical treatment, and proper postoperative care of the drainage tubes.
【Abstract】Objective To investigate the protective effect of improving the pancreatic ischemia and calcium channel blockers on preventing the progression of acute pancreatitis. Methods Twenty-four patients with mild acute pancreatitis were randomly divided into two groups： control group and treated group. Within the first 72 hours from the onset of AP, routine conservative managements were performed in control group, improving the pancreatic ischemia and preventing Ca2+ overload were performed in treated group for two weeks. The hemorrheological parameters were measured at 1,4,7,14 days after adimission, simultanously, serum TNFα, IL-1β, C-reactive protein and plasma TXB2, 6-keto-PGF1α levels were determined with ELISA methods. Results The hemorrheological changes were improved in treated group, serum TNFα, IL-1β, C-reactive protein and plasma TXB2, 6-keto-PGF1α levels were significantly decreased each time point in treated group as compared with control group. Conclusion Improving the pancreatic ischemia and calcium channel blockers have protective effect through reducing the generation of cytokines and inflammatory mediators on preventing the progression of acute pancreatitis.