Early systemic anticoagulation reduces hospital readmission in acute necrotizing pancreatitis patients:A retrospective cohort study

Background:Early systemic anticoagulation(SAC)is a common practice in acute necrotizing pancreatitis(ANP),and its impact on in-hospital clinical outcomes had been assessed.However,whether it affects long-term outcomes is unknown.This study aimed to evaluate the effect of SAC on 90-day readmission and other long-term outcomes in ANP patients.Methods:During January 2013 and December 2018,ANP patients admitted within 7 days from the onset of abdominal pain were screened.The primary outcome was 90-day readmission after discharge.Cox proportional-hazards regression model and mediation analysis were used to define the relationship between early SAC and 90-day readmission.Results:A total of 241 ANP patients were enrolled,of whom 143 received early SAC during their hospitalization and 98 did not.Patients who received early SAC experienced a lower incidence of splanchnic venous thrombosis(SVT)[risk ratio(RR)=0.40,95%CI:0.26-0.60,P<0.01]and lower 90-day readmission with an RR of 0.61(95%CI:0.41-0.91,P=0.02)than those who did not.For the quality of life,patients who received early SAC had a significantly higher score in the subscale of vitality(P=0.03)while the other subscales were all comparable between the two groups.Multivariable Cox regression model showed that early SAC was an independent protective factor for 90-day readmission after adjusting for potential confounders with a hazard ratio of 0.57(95%CI:0.34-0.96,P=0.04).Mediation analysis showed that SVT mediated 37.0%of the early SAC-90-day readmission causality.Conclusions:The application of early SAC may reduce the risk of 90-day readmission in the survivors of ANP patients,and reduced SVT incidence might be the primary contributor.

Management of infected acute necrotizing pancreatitis

Necrotizing or severe pancreatitis represents approximately 10%-20%of acute pancreatitis.30%-40%of patients with acute necrotizing pancreatitis(ANP)will develop debris infection through translocation of intestinal microbial flora.Infected ANP constitutes a serious clinical condition and is complicated by severe sepsis with high mortality rates of up to 40%despite progress in current intensive care.The timely detection of sepsis is crucial.The Quick Sequential Organ Failure Assessment score,procalcitonin levels>1.8 ng/mL and increased lactates>2 mmol/L(>18 mg/dL),indicate the need for urgent management.The escalated step-by-step management protocol starts with broad-spectrum antibiotics,percutaneous drainage or endoscopic management,and ends with surgical management if needed.The latter includes necrosectomy(either laparoscopic or traditional open surgery),peritoneal lavage and extensive drainage.This management protocol increases the chance of survival to approximately 60%in patients with otherwise fatal cases.Any treatment choice must be individualized,and the timing is critical.

Acute necrotizing pancreatitis: Surgical indications and technical procedures

Necrosis of pancreatic parenchyma or extrapancreatic tissues is present in 10%-20% of patients with acute pancreatitis, defining the necrotizing presentation frequently associated with high morbidity and mortality rates. During the initial phase of acute necrotizing pancreatitis the most important pillars of medical treatment are fluid resuscitation, early enteral nutrition, endoscopic retrograde colangiopancreatography if associated cholangitis and intensive care unit support. When infection of pancreatic or extrapancreatic necrosis occurs, surgical approach constitutes the most accepted therapeutic option. In this context, we have recently assited to changes in time for surgery(delaying the indication if possible to around 4 wk to deal with "walledoff" necrosis) and type of access for necrosectomy: from a classical open approach(with closure over large-bore drains for continued postoperative lavage or semiopen techniques with scheduled relaparotomies), trends have changed to a "step-up" philosophy with initial percutaneous drainage and posterior minimally invasive or endoscopic access to the retroperitoneal cavity for necrosectomy if no improvement has been previously achieved. These approaches are progressively gaining popularity and morbidity and mortality rates have decreased significantly. Therefore, a staged, multidisciplinary, step-up approach with minimally invasive or endoscopic access for necrosectomy is widely accepted nowadays for management of pancreatic necrosis.

Ligustrazine alleviates gastric mucosal injury in a rat model of acute necrotizing pancreatitis

BACKGROUND: Acute necrotizing pancreatitis (ANP) leads to a systemic inflammatory response characterized by widespread leukocyte activation and, as a consequence, distant organ injury. The aim of this study was to explore the relationship between gastric microcirculatory impairment and inflammatory mediators released in rats and to evaluate the therapeutic effect of ligustrazine extracted from Rhizoma ligusticum wallichii on gastric mucosa injury in a rat model of ANP. METHODS: Ninety-six Sprague-Dawley rats were randomly divided into three groups: normal control (group Q; ANP without treatment (group P); and ANP treated with ligustrazine (group T). The ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane (4 ml/kg). Group C was given isovolumetric injection of 9 g/L physiological saline by the same route. Group T was injected with ligustrazine (10 ml/kg) via the portal vein. The radioactive biomicrosphere technique was used to measure the blood flow 2 and 12 hours after the induction of ANP. Samples of the pancreas and stomach were taken to assess pathological changes by a validated histology score; meanwhile, the levels of serum interleukin-1 beta (IL-1 beta) were determined. Gastric tissues were also used to measure the level of myeloperoxidase (MPO), which is expressed intracellularly in the azurophilic granules of neutrophils. RESULTS: Blood flow in group P was significantly lower than that in group C (P < 0.01). Pathological changes were significantly aggravated in group P. The gastric MPO activity in group P was significantly higher than that in group C (P < 0.01). The level of serum IL-1 beta in group P increased more significantly than that in group C (P < 0.01). Blood flow of the stomach in group T was significantly higher than that in group P after 2 hours (P < 0.01). The pathological changes were significantly alleviated in group T. The MPO activity of group T was significantly lower than that of group P (P < 0.01). Although serum IL-1 beta level of group T, was higher than of group C (P < 0.01), it was lower than that of group P (P < 0.01). There was a negative correlation between gastric blood flow and MPO activity (r=-0.983, P < 0.01), and between gastric blood flow and pathological score (r=-0.917, P < 0.05). CONCLUSIONS: Decreased gastric blood flow and increased inflammatory mediators can be seen early in ANP, and both are important factors for gastric and mucosal injury. Ligustrazine can ameliorate microcirculatory disorder and alleviate the damage to the pancreas and stomach.

Effect of nitric oxide on toll-like receptor 2 and 4 gene expression in rats with acute lung injury complicated by acute hemorrhage necrotizing pancreatitis

BACKGROUND: Toll-like receptor (TLR) 2/4 might play important roles in mediating proinflammatory cytokine synthesis and release. And nitric oxide (NO) has been used to treat acute respiratory distress syndrome (ARDS). This study aimed to investigate the changes in TLR2/4 gene expression in the lungs of rats with acute lung injury (ALI) complicated by acute hemorrhage necrotizing pancreatitis (AHNP) and the effect of NO on the TLR2/4 gene expression. METHODS: One hundred and ten SD male rats were randomly divided into sham-operated group ( n = 10) , AHNP group (n = 30) , chloroquine-treated group ( n = 30) , and L-Arg-treated group (n =40). The lungs were dissected for lung histological scoring, and bronchoalveolar lavages were harvested for lung injury indexing. TLR2/4 mRNA expression in the lungs was measured by RT-PCR. RESULTS: TLR2/4mRNA was detected in the lungs with low values in the sham-operated group (0.016±0. 210E-2, 0.112 ±0.750E-2) , but it was markedly increased at 3 hours in the AHNP group (0.787±0.751E-2, 1.512 ±1.794E-2) , peaking at 12 hours (1.113 ±6.141E-2, 2.957±2.620E-2; P <0.05 or P <0.01). When lung injuries were aggravated, TNF-α concentrations in the lungs were increased, but NO concentrations were decreased ( P < 0.05 or P < 0.01 ) . When TLR2/4mRNA was inhibited by CQ (3h: 0.313 ± 5.491E-2, 0.005 ±1.419E-3 ; 6h: 0.488 ±7.442E-2, 0.010 ± 1.518E-3; 12h: 0.883 ± 8.911E-2, 0.024 ± 2.760E-3; P< 0.05 or P <0.01) , lung injuries were relieved. NO concentrations in the lungs were increased but TNF-α concentrations were decreased (P <0. 05 or P <0.01). When the rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the lungs could be effectively inhibited (50mg-T: 0.656 ±3. 977E-2, 1. 501 ±6.111E-2; 100mg-T: 0.260± 0.891E-2, 0.732 ±5.135E-2; 200mg-T: 0.126 ±0.914E-2, 0.414 ± 1.678E-2; 400mg-T: 0.091 ±0.399E-2, 0.287 ± 0.176E-2; P <0.05 or P <0. 01) and lung injuries were relieved. At the same time, NO concentrations in the lungs were markedly increased, but TNF-α concentrations were decreased (P <0.05 or P <0.01). CONCLUSIONS: The expression of TLR2/4mRNA is increased in the lungs in rats with AHNP and lung injuries are aggravated. TLR2/4mRNA gene expression of the lungs of rats with AHNP could be markedly inhibited by NO, leading to the relief of lung injuries.

Acute necrotizing pancreatitis as fi rst manifestation of primary hyperparathyroidism

We report the case of a female patient with severe acute necrotizing pancreatitis associated with hypercalcemia as first manifestation of primary hyperparathyroidism caused by a benign parathyroid adenoma.Initially the acute pancreatitis was treated conservatively.The patient subsequently underwent surgical resection of the parathyroid adenoma and surgical clearance of a large infected pancreatic pseudocyst.Although the association of parathyroid adenoma-induced hypercalcemia and acute pancreatitis is a known medical entity,it is very uncommon.The pathophysiology of hypercalcemia-induced acute pancreatitis is therefore not well known,although some mechanisms have been proposed.It is important to treat the provoking factor.Therefore,the cause of hypercalcemia should be identif ied early.Surgical resection of the parathyroid adenoma is the ultimate therapy.

Chloroquine Relieves Acute Lung Injury in Rats with Acute Hemorrhagic Necrotizing Pancreatitis

Summary： This study preliminarily investigated the mechanism by which chloroquine （CQ） relieves acute lung injury （ALI） complicated in acute hemorrhagic necrotizing pancreatitis （AHNP）. Sixty male Wistar rats were randomized into sham-operated group （group A, n=10）, AHNP group （group B, n=10）, L-arginine-treated group （group C, n=10）, L-N-nitro-L-arginine methyl ester （NAME）-treated group （group D, n=10）, CQ-treated group （group E, n=10） and CQ＋L-NAME-treated group （group F, n=10）. TLR4 expression was measured by using real time-PCR and Western blotting respectively. The results showed that, in the group B, the expression of TLR4 and the levels of TNF-α and IL-6 in the lungs were significantly increased, and the nitric oxide （NO） concentration was reduced, as compared with those in the group A （P〈0.05 or P〈0.01）. Lung injury was aggravated with the increased expression of TLR4. When the inhibitor and stimulator of TLR4, namely L-Arg and L-NAME, were added respectively, lung injury was correspondingly relieved or aggravated （P〈0.05 or P〈0.01）. In the group E, TLR4 expres- sion was substantially lower and NO concentration higher than those in the group B （P〈0.05 or P〈0.01）. However, in the group F, NO concentration was markedly decreased, and the inhibitory effect of CQ on TLR4 expression and the relief of lung injury were weakened when compared with those in the group E （P〈0.05 or P〈0.01）. It was concluded that TLR4 may play an important role in the pathogenesis and development of ALl complicated in AHNP. CQ could relieve ALl by decreasing the TLR4 expression and increasing the NO release.

A minimally invasive multiple percutaneous drainage technique for acute necrotizing pancreatitis

BACKGROUND: In approximately 20% of patients, necrotizing pancreatitis is complicated with severe acute pancreatitis, with high morbidity and mortality rates. Minimally invasive step-up approach is both safe and effective, but sometimes requires multiple access sites.METHODS: A 62-year-old woman was admitted with diabetic ketoacidosis, and initial computed tomography(CT) revealed no evidence of acute pancreatitis. She was clinically improved with insulin therapy, fl uid administration, and electrolyte replacement. However, on the 14 th day of admission, she developed a high-grade fever, and CT demonstrated evidence of acute necrotizing pancreatitis with a large collection of peripancreatic fl uid. Percutaneous transgastric drainage was performed and a 14 French gauge(Fr) pigtail catheter was placed 1 week later, which drained copious pus. Because of persistent high-grade fever and poor clinical improvement, multiple 8 and 10 Fr pigtail catheters were placed via the initial drainage route, allowing the safe and effective drainage of the extensive necrotic tissue that was occupying the bilateral anterior pararenal space.RESULTS: After drainage, the patient recovered well and the last catheter was removed on day 123 of admission.CONCLUSIONS: Multiple percutaneous drainage requires both careful judgment and specialist skills. The perforation of the colon and small bowel as well as the injury of the kidney and major vessels can occur. The current technique appears to be safe and minimally invasive compared with other drainage methods in patients with extended, infected necrotic pancreatic pseudocysts.

Effects of chondroitin sulfate on alteration of actin cytoskeleton in rats with acute necrotizing pancreatitis

BACKGROUND: In experimental acute pancreatitis, a large amount of reactive oxygen species are produced, and in turn cytoskeletal changes may be induced in pancreatic tissue. These changes contribute to an imbalance of digestive enzyme segregation, transport, exocytosis and activation, resulting in cell injury. In this study, we assessed the effects of chondroitin sulfate (CS) on attenuation of oxidative damage and protection of F-actin in rats with acute necrotizing pancreatitis (ANP). METHODS: Ninety male Wistar rats were divided randomly into three groups. Group A was infused with 5% sodium taurocholate; group B was treated with CS; and group C served as control. Rats from the three groups were killed at 1, 3 or 8 hours. The levels were measured of malonyl dialdehyde (MDA), total superoxide dismutase (SOD), glutathione synthetase (GSH), serum amylase (SAM) and adenosine triphosphate (ATP). F-actin immunostained with rhodamine-phalloidin was analyzed using a confocal laser scanning system and the content of F-actin protein was determined. RESULTS: The levels of SAM increased in groups A and B, whereas the levels of GSH, SOD and ATP in group A decreased markedly during pancreatitis, and MDA increased significantly. The levels of GSH, SOD and ATP in group B were higher than those in group A, but the level of MDA was lower than in group A. At the same time, ANP resulted in early disruption of the cytoskeleton with dramatic changes and a loss of F-actin. Administration of CS moderated the damage to the actin cytoskeleton. CONCLUSIONS: Retrograde infusion of sodium taurocholate via the pancreatic duct may produce pancreatic necrosis and a marked increase in serum amylase activity, induce a severe depletion of ATP level, prime lipid peroxidation, and damage F-actin. Treatment with CS can ameliorate pancreatic cell conditions, limit cell membrane peroxidation, protect F-actin, and attenuate pancreatitis.

Early versus delayed intervention in necrotizing acute pancreatitis complicated by persistent organ failure

Background:Current guidelines for the treatment of patients with necrotizing acute pancreatitis(NAP)recommend that invasive intervention for pancreatic necrosis should be deferred to 4 or more weeks from disease onset to allow necrotic collections becoming“walled-off”.However,for patients showing signs of clinical deterioration,especially those with persistent organ failure(POF),it is controversial whether this delayed approach should always be adopted.In this study,we aimed to assess the impact of differently timed intervention on clinical outcomes in a group of NAP patients complicated by POF.Methods:All NAP patients admitted to our hospital from January 2013 to December 2017 were screened for potential inclusion.They were divided into two groups based on the timing of initial interven-tion(within 4 weeks and beyond 4 weeks).All the data were extracted from a prospectively collected database.Results:Overall,131 patients were included for analysis.Among them,100(76.3%)patients were in-tervened within 4 weeks and 31(23.7%)underwent delayed interventions.As for organ failure prior to intervention,the incidences of respiratory failure,renal failure and cardiovascular failure were not signifi-cantly different between the two groups(P>0.05).The mortality was not significantly different between the two groups(35.0%vs.32.3%,P=0.83).The incidences of new-onset multiple organ failure(8.0%vs.6.5%,P=1.00),gastrointestinal fistula(29.0%vs.12.9%,P=0.10)and bleeding(35.0%vs.35.5%,P=1.00),and length of ICU(30.0 vs.22.0 days,P=0.61)and hospital stay(42.5 vs.40.0 days,P=0.96)were com-parable between the two groups.Conclusion:Intervention within 4 weeks did not worsen the clinical outcomes in NAP patients compli-cated by POF.

Rapid detection of sepsis complicating acute necrotizing pancreatitis using polymerase chain reaction

INTRODUCTIONAcute narcotizing pancreatitis usually takes a severe clinical course and is associated with multiple organ dysfunction .With the further understanding of pathophysiological events of acute pancreatisis and the therapeutic measuses taken by the clinicians ,the patients can pass through the critical carry stages ,and then the septic complication caused by rtanslocated bacteria, mostly gram-negative microbes from the intestines ensues[1].

A one-stage model of experimental acute necrotizing pancreatitis in rats

AIM:To establish a one-stage model of experimental acute necrotizing pancreatitis(ANP)in rats characterized by the simplicity of performance and a high degree of repeatability.METHODS:ANP modeling in rats was performed based on modification of the ligation model as follows:synthetic material ligature using an atraumatic needle was performed to capture pancreatic gland ducts and marginal duodenum vessels.Ligature tips were exteriorized to the abdominal wall,and the ligature was skinned over to avoid catching intestine loops.Pancreatic macroscopic appearance and histological changes were observed.Blood biochemical and hemostatic indicators were also determined.RESULTS:Laboratory analysis of rats with experimental ANP showed a pattern of disturbances similar to that observed during pancreatic necrosis in humans as soon as the first day.General blood analysis revealed enhanced leukocytosis and alterations in leukogram characteristics,indicating acute inflammation.Serum levels of amylase,aspartate aminotransferase and creatinine significantly increased(P<0.05).Hemostatic indicators showed alterations indicating formation of disseminated intravascular coagulation,and signs of endotoxicosis were observed.These typical pancreatic necrosis patterns of disturbances were validated by the results of histological investigation.CONCLUSION:Histological changes and laboratory indicators confirm the development of a suitable model of ANP.

Surgical management of acute pancreatitis: Historical perspectives, challenges, and current management approaches

Acute pancreatitis(AP)is a serious condition presenting catastrophic consequences.In severe AP,the mortality rate is high,and some patients initially diagnosed with mild-to-moderate AP can progress to a life-threatening severe state.Treatment of AP has evolved over the years.Drainage was the first surgical procedure performed for AP;however,later,surgical approaches were replaced by more conservative approaches due to the availability of advanced medical care and improved understanding of the course of AP.Currently,surgery is used to manage several complications of AP,such as pseudocysts,pancreatic fistulas,and biliary tract obstruction.Patients who are unresponsive to conservative treatment or have complications are typically considered for surgical intervention.This review focuses on the surgical approaches(endoscopic,percutaneous,and open)that have been established in recent studies to treat this acute condition and summarizes the common management guidelines for AP,discussing the relevant indications,significance,and complications.It is evident that despite their reduced involvement,surgeons lead the multidisciplinary care of patients with AP;however,given the gaps in existing knowledge,more research is required to standardize surgical protocols for AP.

Pathophysiology of severe gallstone pancreatitis:A new paradigm

Severe gallstone pancreatitis(GSP)refractory to maximum conservative therapy has wide clinical variations,and its pathophysiology remains controversial.This Editorial aimed to investigate the pathophysiology of severe disease based on Opie’s theories of obstruction,the common channel,and duodenal reflux and describe its types.Severe GSP might be a hybrid disease with pathology polarized between acute cholangitis with mild pancreatitis(biliary type)and necrotizing pancreatitis uncomplicated with biliary tract disease(pancreatic type),in which hepatobiliary and pancreatic lesion severity is inversely related to the presence or absence of impacted ampullary stones.Severe GSP is caused by stones that are persistently impacted at the ampulla with biliopancreatic obstruction(biliary type),and probably,stones that are either temporarily lodged at the duodenal orifice or passed into the duodenum,thereby permitting reflux of bile or possible duodenal contents into the pancreas(pancreas type).When the status of the stones and the presence or absence of impacted ampullary stones with biliopancreatic obstruction are determined,the clinical course and outcome can be predicted.Gallstones represent the main cause of acute pancreatitis globally,and clinicians are expected to encounter GSP more often.Awareness of the etiology and pathogenesis of severe disease is mandatory.

THE CHANGES OF PANCREATIC ACINAR CELL FUNCTION IN ACUTE NECROTIZING PANCREATITIS OF RATS

ObjectiFe To evaluate the changes of pancreatic acinar cell functions in the rats with acutenecrotizing pancreatitis (ANP). methods Seventy SD rats were randomized into two groups: experimental group(n=35) and control group (n=35). To prepare the experimental model, the retrograde injection of 5% sodiumtaurocholate into the pancreatic duct was used for inducing ANP. Radioactive tracing by L -3H-phenylalanineand autoradiography were performed for scoring the differences of changes of amino acid uptake, enzyme-proteinsynthesis and output from acinar cells in rats between both groups. Results No changes were observed in aminoacid uptake and enzyme -protein synthesis in rats with dotted and haemorrhagic necrotizing foci as compared withcontrol group. However, accumulated zymogen granules in the interstitial of acinar cells were seen in theexperimental group. Conclusion It indicates that in experimental ANP rats, the functions of acinar cells in bothamino acid uptake and protein synthesis were essentially normal, but the pathway of enzyme output was affectedinto ectopic secretion through the bottom or lateral cellular membrane of pancreatic acinar cell.

Changes of gastric and intestinal blood flow, serum phospholipase A_2 and interleukin-1β in rats with acute necrotizing pancreatitis

AIM: To explore the relationship between gastric and intestinal microcirculatory impairment and inflammatory mediators released in rats with acute necrotizing pancreatitis (ANP).METHODS: A total of 64 rats were randomized into control group and ANP group. ANP model was induced by injection of 5% sodium taurocholate under the pancreatic membrane.Radioactive biomicrosphere technique was used to measure the gastric and intestinal tissue blood flow at 2 and 12 h after the induction of ANP, meanwhile serum phospholipase A2 (PLA2) activities and interleukin-1β levels were determined. Pathologic changes in pancreas, gastric and intestinal mucosae were studied. RESULTS: The gastric blood flow in ANP group (0.62±0.06 (P＜0.01) at 2 and 12 h after induction of ANP. The intestinal blood flow in ANP group (0.80±0.07 and (P＜0.01). Serum PLA2 activities (94.29±9.96 and 103.71± 14.40) U/L and IL-1β levels (0.78±0.13 and 0.83±0.20) μg/L in ANP group were higher than those in control group (65.27±10.52 and 66.63±9.81) U/L, (0.32±0.06 and 0.33±0.07) μg/L (P＜0.01). At 2 and 12 h after introduction of the model, typical pathologic changes were found in ANP. Compared with control group, the gastric and intestinal mucosal pathologic changes were aggravated significantly (P＜0.01) at 12 h after induction of ANP. Gastric and intestinal mucosal necrosis, multiple ulcer and hemorrhage occurred.CONCLUSION: Decrease of gastric and intestinal blood flow and increase of inflammatory mediators occur simultaneously early in ANP, both of them are important pathogenic factors for gastric and intestinal mucosal injury in ANP.

Preventive effect of tetramethylpyrazine on intestinal mucosal injury in rats with acute necrotizing pancreatitis

AIM: To evaluate the role of microcirculatory disorder (MCD) and the therapeutic effectiveness of tetramethyl- pyrazine (TMP) on intestinal mucosa injury in rats with acute necrotizing pancreatitis (ANP). METHODS: A total of 192 Sprague-Dawley rats were randomly divided into three groups: normal control group (C group), ANP group not treated with TMP (P group), ANP group treated with TMP (T group). An ANP model was induced by injection of 50 g/L sodium tau- rocholate under the pancreatic membrane (4 mL/kg). C group received isovolumetric injection of 9 g/L physi- ological saline solution using the same method. T group received injection of TMP (10 mL/kg) via portal vein. Ra- dioactive biomicrosphere technique was used to measure the blood flow at 0.5, 2, 6 and 12 h after the induction of ANP. Samples of pancreas, distal ileum were collected to observe pathological changes using a validated histol- ogy score. Intestinal tissues were also used for examina- tion of myeloperoxidase (MPO) expressed intracellularly in azurophilic granules of neutrophils. RESULTS: The blood flow was significantly lower in P group than in C group (P < 0.01). The pathological changes were aggravated significantly in P group. The longer the time, the severer the pathological changes. The intestinal MPO activities were significantly higher in P group than in C group (P < 0.01). The blood flow of intestine was significantly higher in T group than in P group after 2 h (P < 0.01). The pathological changes were alleviated significantly in T group. MPO activities were significantly lower in T group than in P group (P < 0.01 or P < 0.05). There was a negative correlation be- tween intestinal blood flow and MPO activity (r = -0.981, P < 0.01) as well as between intestinal blood flow and pathologic scores (r = -0.922, P < 0.05).CONCLUSION: MCD is an important factor for intestinal injury in ANP. TMP can ameliorate the condition of MCD and the damage to pancreas and intestine.

Outcome of patients with acute, necrotizing pancreatitis requiring drainage-does drainage size matter?

AIM:To assess the outcome of patients with acute necrotizing pancreatitis treated by percutaneous drainage with special focus on the influence of drainage size and number. METHODS:We performed a retrospective analysis of 80 patients with acute pancreatitis requiring percutaneous drainage therapy for infected necroses. Endpoints were mortality and length of hospital stay. The influence of drainage characteristics such as the median drainage size, the largest drainage size per patient and the total drainage plane per patient on patient outcome was evaluated. RESULTS:Total hospital survival was 66%. Thirty-four patients out of all 80 patients (43%) survived acute necrotizing pancreatitis with percutaneous drainage therapy only. Eighteen patients out of all 80 patients needed additional percutaneous necrosectomy (23%). Ten out of these patients required surgical necrosectomy in addition, 6 patients received open necrosectomy without prior percutaneous necrosectomy. Elective surgery was performed in 3 patients receiving cholecystectomy and one patient receiving resection of the parathyroid gland. The number of drainages ranged from one to fourteen per patient. The drainage diameter ranged from 8 French catheters to 24 French catheters. The median drainage size as well as the largest drainage size used per patient and the total drainage area used per patient did not show statistically significant influence on mortality. CONCLUSION:Percutaneous drainage therapy is an effective tool for treatment of necrotizing pancreatitis.Large bore drainages did not prove to be more effective in controlling the septic focus.

Dynamic changes of IL-2/IL-10, sFas and expression of Fas in intestinal mucosa in rats with acute necrotizing pancreatitis

AIM:To investigate dynamic changes of serum IL-2, IL-10, IL-2/IL-10 and sFas in rats with acute necrotizing pancreatitis. To explore the expression of Fas in intestinal mucosa of rats with acute necrotizing pancreatitis (ANP). METHODS:A total of 64 Sprague-Dawley (SD) rats were randomly divided into two groups:normal control group (C group), ANP group (P group). An ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane. Normal control group received isovolumetric injection of 9 g/L physiological saline solution using the same method. The blood samples of the rats in each group were obtained via superior mesenteric vein to measure levels of IL-2, IL-10, sFas and calculate the value of IL-2/IL-10. The levels of IL-2, IL-10 and sFas were determined by ELISA. The severity of intestinal mucosal injury was evaluated by pathologic score. The expression of Fas in intestinal mucosal tissue was determined by immunohistochemistry staining. RESULTS:Levels of serum IL-2 were significantly higher in P group than those of C group (2.79 ± 0.51 vs 3.53 ± 0.62, 2.93 ± 0.89 vs 4.35 ± 1.11, 4.81 ± 1.23 vs 6.94 ± 1.55 and 3.41 ± 0.72 vs 4.80 ± 1.10, respectively, P < 0.01, for all) and its reached peak at 6 h. Levels of serum IL-10 were significantly higher in P group than those of C group at 6 h and 12 h (54.61 ± 15.81 vs 47.34 ± 14.62, 141.15 ± 40.21 vs 156.12 ± 43.10, 89.18 ± 32.52 vs 494.98 ± 11.23 and 77.15 ± 22.60 vs 93.28 ± 25.81, respectively, P < 0.01, for all). The values of IL-2/IL-10 were higher significantly in P group than those of C group at 0.5 h and 2 h (0.05 ± 0.01 vs 0.07 ± 0.02 and 0.02 ± 0.01 vs 0.03 ± 0.01, respectively, P < 0.01, for all), and it were significantly lower than those of C group at 6 h (0.05 ± 0.02 vs 0.01 ± 0.01, P < 0.01) and returned to the control level at 12 h (0.04 ± 0.01 vs 0.05 ± 0.02, P > 0.05). In sFas assay, there was no significant difference between P group and C group (3.16 ± 0.75 vs 3.31 ± 0.80, 4.05 ± 1.08 vs 4.32 ± 1.11, 5.93 ± 1.52 vs 5.41 ± 1.47 and 4.62 ± 1.23 vs 4.44 ± 1.16, respectively, P > 0.05, for all). Comparison of P group and C group, the pathological changes were aggravated significantly in P group. Immunohistochemistry staining show the expression of Fas was absent in normal intestinal tissues, however, it gradually increased after induction of pancreatitis in intestinal tissue, then reached their peaks at 12 h.CONCLUSION:Fas were involved in the pathogenesis of pancreatitis associated intestinal injury. The mechanisms of Fas may be associated to Fas mediated T helper cell apoptosis.

Role of nitric oxide in Toll-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats

瞄准：调查氮的氧化物的角色(没有) 在像使用费的受体 2 (TLR2 ) 在尖锐出血性的引起坏死胰腺炎(AHNP ) 的肝的 /4mRNA 表示老鼠。方法：110 只 SD 雄的老鼠随机被划分成假冒操作组(n=10 ) ， AHNP 组(n=30 ) ，氯奎(CQ ) 对待组(n=30 ) 和 L-Arg-treated 组(n=40 ) 。在 AHNP 老鼠的肝的 TLR2/4mRNA 表示被 RT-PCR 测量。结果：TLR2/4mRNA 的表示能在假冒操作组(0.155E-5+/-0.230E-6 和 0.115E-2+/-0.545E-4 ) 在 AHNP 老鼠的肝被检测，但是显著地在在 12 h 达到顶点的 AHNP 组(0.197E-2+/-0.114E-3 和 0.175+/-0.349E-2 ) 在 3 h 被增加(0.294E-2+/-0.998E-4 和 2.673+/-2.795E-2， P【0.01 ) 。肝的损害被加重，在肝的 TNF-alpha 集中被增加，没有集中被减少(P【0.05 或 P【0.01 ) 。当 TLR2/4mRNA 表示被 CQ 禁止时(3 h：1.037E-4+/-3.299E-6 和 0.026+/-3.462E-3；6 h：1.884E-4+/-4.679E-6 和 0.108+/-6.115E-3；12 h：2.443E-4+/-7.714E-6 和 0.348+/-6.807E-3；P【0.01 ) ，肝的损害被减轻，在肝的集中都没被增加， TNF-alpha 集中被减少(P【0.05 或 P【0.01 ) 。当有 AHNP 的老鼠与 L-Arg 被对待时，在肝的 TLR2/4mRNA 表示能有效地被禁止(50 mg-T：0.232E-2+/-0.532E-4 和 0.230+/-6.883E-3；100 mg-T：0.210E-2+/-1.691E-4 和 0.187+/-0.849E-2；200 mg-T：0.163E-2+/-0.404E-4 和 0.107+/-0.195E-2；400 mg-T：0.100E-2+/-0.317E-4 和 0.084+/-0.552E-2；P【0.01 ) 并且肝的损害被减轻。同时，在肝的集中都显著地没被增加， TNF-alpha 集中被减少(P【0.05 或 P【0.01 ) 。结论：TLR2/4mRNA 的表示被增加，肝的损害在 AHNP 老鼠的肝被加重。在 AHNP 老鼠的肝的 TLR2/4mRNA 基因表示能显著地被禁止由没有，导致肝的损害的消除。