摘要:目的:探讨重症急性胰腺炎(SAP)继发感染的临床特点。方法:将我院20039~20053收治的SAP140例,按是否感染,分成感染组和对照组,对比分析其临床资料。结果:感染组病死率高于对照组(P=0023);感染组入院初期,Ranson评分、CT评分、APACHE Ⅱ评分、血糖、ARDS和肠麻痹发生率、感染前手术率及呼吸机辅助呼吸率高于对照组(Plt;005);以G感染胰腺、胰周围及肺部为主;肺部感染时间为107±25d,胰腺或胰周为176±29d。结论:急性期全身反应轻重及胰腺坏死程度是SAP继发感染的基础;临床有创治疗措施是促进因素。
Objective To explore the protective effect of rapamycin on brain tissues injury in severe acute pancreatitis (SAP) and its possible mechanism in experimental rats. Methods Ninety SPF males SD rats were randomly divided into 3 groups by random envelope opening method: sham operation group (SO group), SAP group, and rapamycin group (RAPA group), then the rats of each group were divided into 24 h, 36 h, and 48 h 3 subgroups by random number table method. Rats in each group underwent laparotomy, the model was prepared by retrograde injection of solutions into biliopancreatic duct, rat of the SO group was injected with 0.9% normal saline (2 mL/kg), rats of the SAP group and the RAPA group were injected with 5% sodium taurocholate solution (2 mL/kg), but rat of the RAPA group was injected with rapamycin (1 mg/kg) at 30 min before narcosis. All survival rats in each subgroup were killed at 24 h, 36 h, and 48 h respectively, then the pancreas and brain tissues of rats were collected, pancreas and brain tissues were stained by hematoxylin-eosin staining, brain tissues were stained by Luxol fast blue additionally, pathological changes of brain tissues were scored under light microscope. The protective effect of rapamycin on brain tissues injury was determined by comparing the differences in the degree of brain tissues among 3 groups. The phosphorylated mammaliantarget of rapamycin (p-mTOR) and phosphorylated ribosomal 40S small subunitS6 protein kinase (p-S6K1) expression levels in brain tissues were detected by Western blot. In addition, the correlations between the expression levels of p-mTOR and p-S6K1 in brain tissues and the degree of brain tissues injury were analyzed to further explore the possible mechanism of rapamycin’s protective effect on brain tissues injury in SAP. Results① At the point of 24 h, 36 h, and 48 h, the order of the relative expression levels of p-mTOR and p-S6K1 in brain tissues of three groups were all as follows: the SO group < the RAPA group < the SAP group (P<0.05). ② At the point of 24 h, 36 h, and 48 h, the order of brain histological score in three groups were all as follows: the SO group < the RAPA group < the SAP group (P<0.05). ③ The relative expression levels of p-mTOR and p-S6K1 in brain tissues were positively correlated with pathological scores of brain tissues (r=0.99, P<0.01; r=0.97, P<0.01). ConclusionRapamycin plays a protective role in pancreatic brain tissues injure by down-regulating the expression levels of p-mTOR and p-S6K1 in mTOR signaling pathway.
Objective To examine the effects of carbon dioxide (CO2) pneumoperitoneum on local pancreas pathological changes, serum levels of amylase, IL-1, IL-6, and the positive rate of dissolubility adhesion molecule (CD11a/CD18 and CD11b/CD18) expression in rats with severe acute pancreatitis (SAP). Methods Fifty healthy male SpragueDawley (SD) rats were randomly divided into 3 groups: CO2 pneumoperitoneum group (n=20): SAP was induced by injecting 5% sodium taurocholate through retrogradely common biliopancreatic ducts via duodenal papilla， and then CO2 pneumoperitoneum was established at a pressure of 12 mm Hg (1 mm Hg=0.133 kPa) for 30 min; SAP group (n=20): The rats were treated as same as CO2 pneumoperitoneum group, except CO2 pneumoperitoneum； Simple operation group (n=10): Laparotomy was performed and nothing was done to duodenum and pancreas except for moving them softly. The blood samples were collected for examining serum levels of amylase, IL-1, IL-6, and the positive rates of CD11a/CD18 and CD11b/CD18 expression, and histopathologic examination of pancreas was performed. Results Compared with simple operation group, the pancreatic pathologic histology score, serum levels of amylase, IL-1, IL-6, and the positive rates of CD11a/CD18 and CD11b/CD18 expression were significantly higher in CO2 pneumoperitoneum group and SAP group (P=0.000). The levels of IL-1 and IL-6 were significantly lower in CO2 pneumoperitoneum group as compared to SAP group (P=0.000). There was no significant difference between CO2 pneumoperitoneum group and SAP group in pancreatic pathologic histology score (P=0.294), the level of serum amylase (P=0.073), the positive rates of CD11a/CD18 (P=0.155) and CD11b/CD18 expression (P=0.201). Conclusion CO2 pneumoperitoneum has inhibitory effect on the levels of IL-1 and IL-6, rather than the positive rates of CD11a/CD18 and CD11b/CD18 expression in SD rats with SAP.
ObjectiveTo systematically review the efficacy and safety of early abdominal paracentesis drainage (APD) in patients with severe acute pancreatitis (SAP). MethodsThe PubMed, Cochrane Library, Web of Science, CNKI, WanFang Data, and VIP databases were searched to collect randomized controlled trials and cohort studies on the management of SAP via early APD from inception to December 10, 2022. Two reviewers independently screened the literature, extracted data, and assessed the risk of bias of the included studies. Meta-analysis was then performed using RevMan 5.4 software and Stata 17.0 software. ResultsEighteen studies were included, with a total sample size of 2 685 patients. The meta-analysis showed that early APD could decrease mortality (OR=0.49, 95%CI 0.35 to 0.69, P<0.01) and the incidences of multiple organ failure (OR=0.56, 95%CI 0.45 to 0.71, P<0.01), ARDS (OR=0.54, 95%CI 0.41 to 0.71, P<0.01), and infectious complications (OR=0.72, 95%CI 0.57 to 0.92, P<0.01) and also reduce the need for further interventions and the total cost incurred during hospitalization, reduce the length of hospital stay, and reduce the number of days spent in the intensive care unit. However, there were no significant differences in the incidence of pneumonia, bacteremia, and sepsis between the two groups. ConclusionThe treatment of SAP via early APD, which has high clinical value, could decrease the incidence of multiple organ failure, improve the prognosis of patients, and reduce the associated mortality rate. Moreover, APD does not increase the risk of infection-related complications. Due to the limited quantity and quality of the included studies, more high-quality studies are needed to verify the above conclusion.
ObjectiveTo summary the advances of application of JAK/STAT signal transduction pathways in severe acute pancreatitis (SAP). MethodsBy using the method of literature review, the relevant literatures on JAK/STAT signal transduction pathway and its role in various organs damage of SAP were reviewed. ResultsIn the early of SAP, due to the pancreatic acinar cells were damaged, lead to the pancreatic enzyme release, then caused the local inflammatory mediators such as cytokines release, activated the JAK/STAT signal transduction pathways, and through the cascade effect with other signaling pathways further lead to the greater amounts of the release of inflammatory mediators, and that caused the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). ConclusionsThe JAK/STAT signal transduction pathway may be the key factor of cytokine waterfall cascade reaction process in SAP. Inhibition of this pathway may be a new measure to control the "inflammatory reaction waterfall" in treatment SAP.
Objective To investigate the mechanism of gastrointestinal motility disorder of severe acute pancreatitis （SAP） in rats. Methods SD rats were randomly divided into 2 groups：sham operation （SO） group （n=16） and SAP group （n=16）. The gastric antrum interdigestive myoelectric complex （IMC） of rat was recorded by using bipolar silver electrode recording， the concentration of serum motilin （MTL） and vasoactive intestinal peptide （VIP） were detected by enzyme-linked immunosorbent assay （ELISA） method， and determined the pancreatic pathology score. Results Compared with SO group， the concentration of serum MTL obvious decreased and the concentration of VIP obvious rised in SAP group （P＜0.01）. Compared with SO group， the time of IMC cycle， andⅠand Ⅱ phase were extended， and time of Ⅲ phase was shortened， also the amplitude and frequency of peak electric of Ⅲ phase were declined in SAP group （P＜0.01）. And the concentration of MTL in SAP group showed positive correlation with the time of Ⅲ phase of IMC （r=0.967， P＜0.01）， the concentration of VIP in SAP group showed negative correlation with the time of Ⅲ phase of IMC （r=-0.592， P＜0.05）. The pancreatic organization pathological score in SAP group was higher than that in SO group （P＜0.01）. Conclusion There is gastrointestinal motility disorder in SAP rats， furthermore， it may induce gastrointestinal motility disorder through effecting the gastrointestinal smooth muscle electrical activity.
ObjectiveTo observe the effects and mechanism of MCP-1 in ileum and pancreatic tissues in rats with severe acute pancreatitis(SAP). MethodsTwenty-fourth healthy SD rats were randomly divided into two groups:control group(n=12) and SAP model group(n=12). SAP was induced in model group by retrograde injection of 3% sodium taucrocholate into the biliopancreatic duct of rats. The control group underwent laparotomy with the manipulation of the intestinal canal. The rats were killed at 12 h and 24 h respectively after operation, blood and tissue samples were collected to detect the indexes as follows:①Expressions of MCP-1 mRNA of pancreatic and ileum tissues were detected by RT-PCR; ②blood plasma MCP-1 and IL-10 levels were detected by ELISA; ③blood plasma AMY and DAO levels were detected by colorimetry; ④the pathological changes of pancreas and ileum tissues were observed. ResultsCompared with the control group, the levels of MCP-1, IL-10, AMY, and DAO in plasma, pancreas, and ileum tissues were significantly increased in SAP model group(P < 0.01), the expressions of MCP-1 mRNA in pancreas and ileum tissues were up-regulated simultaneously(P < 0.01), and pathological scoring increased obviously(P < 0.01). ConclusionThe levels of MCP-1 in plasma, pancreas and ileum tissues are significantly increased in rats with SAP, MCP-1 aggravate the injury of pancreas and ileum tissues.
Objective To summarize the recent progress in pathogenetic, diagnostic and therapeutic researches on the intestinal barrier dysfunction (IBD) of severe acute pancreatitis (SAP). MethodsThe advancement of IBD in SAP, which was published recently at home and abroad, was collected and reviewed. Results The pathogenesis of IBD in patients with SAP was complex. Ischemia-reperfusion injury, endotoxin, inflammatory mediators and gastrointestinal hormone played an important role in the process of IBD. There were many ways to detect IBD, and the ratio of lactulose and mannitol, plasma diamine oxidase were relatively ideal markers. Medical therapies, such as treatment of SAP and maintaining the perfusion of intestines, were essential to cure IBD. On this basis, the propulsives, nutritional support and traditional Chinese drugs should be administered reasonably. Conclusions IBD is a sophisticated process of pathophysiology. In recent years, abundant of animal experiments and clinical researches have provided new clue for prevention and cure of IBD, but further researches are still needed on the mechanism of the cells and molecules implicated.