【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.
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.
ObjectiveTo study the function of selectin in the pathogenesis and advancement of acute pancreatitis(AP), so as to guide further investigation and clinical treatment. MethodsCorrelative articles in recent years were reviewed. ResultsSelectins act as an indicator of the activation of endothelium. Their expression changes markedly during AP and is closely related to cytokines, oxygen free radicals and complements. Conclusion Selectin is a component which is engaged in the pathology of AP, the level of selectin is useful in guiding clinical observation and treatment.
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.
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 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.
Seventeen cases of pancreatic encephalopathy (PE) with acute pancreatitis were studied retrospectively. It was found that on the basis of brain damage caused by pancreatic enzyme, many factor might play a role in the development of PE. It suggests that PE should not be accepted as an operative indication separately in severe acute pancreatitis. Chinese medicine can benefit the patient in the treatment of this disease. Operation is the only choice while patient get worsened even after appropriate and enough nonoperative therapy, as well as while pancreatic necrosis become infected or pancreatic abcess formed. Mortality of PE in this series is 52.9%, slightly less than the level (66.7%-100%) reported by other authors.
ObjectiveTo find out the diagnostic power and correlation between platelet-related parameters and inflammatory indicators in acute pancreatitis patients with different severity.MethodsA total of 88 patients with acute pancreatitis diagnosed in West China Hospital of Sichuan University from January 2019 to August 2019 were enrolled in the retrospective study, including 58 mild acute pancreatitis patients and 30 severe acute pancreatitis patients. The patients’ platelet-related parameters and inflammatory indicators were collected. The platelet parameters and inflammatory indicators in different severity acute pancreatitis groups were compared and the diagnostic power and correlation were analyzed.ResultsThe platelet count and plateletcrit of the severe group were lower than those of the mild group, the difference was statistically significant (Z=–5.502, –3.673; P<0.001). The immature platelet fraction, platelet distribution width, mean platelet volume and platelet-large cell ratio levels of the severe group were higher than those of the mild group (Z=–4.217, –2.998, –3.754, –3.816; P<0.05). Platelet-related parameters platelet count, immature platelet fraction, platelet distribution width, mean platelet volume, platelet-large cell ratio, plateletcrit and inflammatory indicators procalcitonin, interleukin-6 showed good diagnostic power with areas under under receiver operating characteristic curves greater than 0.75 in differentiating the severity of acute pancreatitis. Correlation analysis showed that immature platelet fraction was positively correlated with procalcitonin and interleukin-6 levels in patients with acute pancreatitis (rs=0.457, 0.385; P<0.05).ConclusionsImmature platelet fraction is correlated with the severity of acute pancreatitis, and positively correlated with the levels of inflammatory indicators procalcitonin and interleukin-6.
ObjectiveTo study the techniques of mimicking multifactors induced acute pancreatitis in rat by slow-release pump. MethodsSeventy-five healthy SD rats were randomly divided into slowrelease pump group (SRP group), traditional group (TAP group), and sham operation group (SO group). Four percent sodium taurocholate was injected through pancreatobiliary duct of rats directly and retrogradely in TAP group and by slow-release pump in SRP, which mimicked AP pathogenesis from selfdigestion, obstruction, cytokine activation, and many other mechanisms. Detection of serum amylase and pancreatic myeloperoxidase (MPO) leves, observation of pancreatic histological changes and scoring of pancreatitis severity in three groups were performed at 1, 6, 12, and 24 h after successful model induction, respectively. ResultsSerum amylase and pancreatic MPO levels, and the pathological grading score of rats were significantly higher in SRP and TAP groups than in SO group at different time point (Plt;0.05 or Plt;0.01), while they were lower in SRP group than in TAP group with a slowly rising tendency, and there were significant differences at 6 and 12 h time point, respectively (Plt;0.05 or Plt;0.01). Conclusions Slow-release pump technique can induce AP through increasing the pressure of pancreatic duct, tissue edema and sustained releasing inflammation factors by mimicking the pathophysiological process of pancreatitis. Slow-release pump can be kept in place to monitor and control the pressure of pancreatic duct. Slow-release pump method is relatively moderate and easy to manage with a lower mortality.
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.