Long-term aspirin pretreatment in the prevention of cerulein-induced acute pancreatitis in rats

AIM:To investigate the effects of long term pretreatment with low-,medium-and high-dose aspirin(acetylsalicylic acid,ASA) on a model of acute pancreatitis(AP) induced in rats.METHODS:Forty male Wistar rats were used.Three experimental groups,each consisting of eight animals,received low-(5 mg/kg per day),medium-(150 mg/kg per day) and high-dose(350 mg/kg per day) ASA in supplemented pellet chow for 100 d.Eight animals,serving as the AP-control group,and another eight,serving as reference value(RV) group,were fed with standard pellet chow for the same period.After pretreatment,AP was induced in the experimental animals by intraperitoneal administration of cerulein(2 × 50 μg/kg),while the RV group received saline in the same way.Twelve hours after the second injection,the animals were sacrificed.Pancreatic tissue and plasma samples were collected.One part of the collected pancreatic tissues was used for histopathological evaluation,and the remaining portion was homogenized.Cytokine levels [tumor necrosis factor,interleukin(IL)1β,IL-6],hemogram parameters,biochemical parameters(amylase and lipase),nuclear factor-κB,aspirin triggered lipoxins and parameters related to the antioxidant system(malondialdehyde,nitric oxide,hemeoxygenase-1,catalase and superoxide dismutase) were measured.RESULTS:Cerulein administration induced mild pancreatitis,characterized by interstitial edema(total histopathological score of 5.88 ± 0.44vs 0.25 ± 0.16,P < 0.001).Subsequent pancreatic tissue damage resulted in an increase in amylase(2829.71 ± 772.48 vs 984.57 ± 49.22 U/L,P = 0.001) and lipase(110.14 ± 75.84 U/L vs 4.71 ± 0.78 U/L,P < 0.001) in plasma,and leucocytes(6.89 ± 0.48 vs 4.36 ± 0.23,P = 0.001) in peripheral blood.Cytokines,IL-1β(18.81 ± 2.55 pg/μg vs 6.65 ± 0.24 pg/μg,P = 0.002) and IL-6(14.62 ± 1.98 pg/μg vs 9.09 ± 1.36 pg/μg,P = 0.04) in pancreatic tissue also increased.Aspirin pretreatment reduced the increase in the aforementioned parameters to a certain degree and partially improved the histopat     

血清降钙素原水平与细菌感染的相关性分析

目的：探讨血清降钙素原（PCT）检测在感染性疾病中的临床意义，分析血清PCT水平与细菌感染的相关性。方法：研究对象为356例各种感染性疾病患者，其中细菌感染98例，病毒感染258例，采用半定量固相免疫测定法测定患者血清中的PCT，结果分为＜0．5ng/ml;≥0.5ng/ml;≥2.0ng/ml和≥10ng/ml四个等级。组间差异采用卡方检验。结果：若以血清PCT≥0.5ng/ml以上为阳性标准，并结合全身炎性反应综合征（SIRS）参数，血清PCT检测对细菌感染诊断的敏感性为98．7％，特异性为72．0％，阳性预测值为49．4％，阴性预测值为99．5％，阳性拟然比为3．53，阴性拟然比为0．018，诊断符合率为77．80％。血清PCT阳性患者SIRS、MODS和MOF的发生率明显高于血清PCT阴性患者（P＜0．01），5例死亡患者血清PCT均阳性，其中3例≥2ng/ml，2例PCT≥10ng/ml。结论：血清PCT半定量检测可用于细菌感染与病毒感染的鉴别诊断，结合SIRS参数可提高对细菌感染诊断的敏感性和特异性，对抗生素的使用提供可行依据；同时，PCT水平的高低反映了病情的严重程度，可作为评估病情，判断预后的指标；PCT在由SIRS向多器官功能障碍综合征或多器官功能衰竭的发生发展过程中可能发挥着重要作用。     

Therapeutic effect of caffeic acid phenethyl ester on cerulein-induced acute pancreatitis

AIM: To evaluate the therapeutic role of caffeic acid phenethyl ester (CAPE) in a rat model of ceruleaninduced acute pancreatitis (AP). METHODS: Seventy male Wistar albino rats were divided into seven groups. Acute edematous pancreatitis was induced by subcutaneous cerulein injection (20 μg/kg) four times at 1-h intervals. CAPE (30 mg/kg) was given by subcutaneous injection at the beginning (CAPE 1 group) and 12 h after the last cerulein injection (CAPE 2 group). Serum amylase, lipase, white blood cell count, and tumor necrosis factor (TNF)-α levels were measured, and pancreatic histopathology was assessed. RESULTS: In the AP group, amylase and lipase levels were found to be elevated and the histopathological evaluation showed massive edema and inflammation of the pancreas, with less fatty necrosis when compared with sham and control groups. Amylase and lipase levels and edema formation decreased significantly in the CAPE therapy groups (P < 0001); especially in the CAPE 2 group, edema was improved nearly completely (P = 0001). Inflammation and fatty necrosis were partially recovered by CAPE treatment. The pathological results and amylase level in the placebo groups were similar to those in the AP group. White blood cell count and TNF-α concentration was nearly the same in the CAPE and placebo groups. CONCLUSION: CAPE may be useful agent in treatment of AP but more experimental and clinical studies are needed to support our observation of beneficial effects of CAPE before clinical usage of this agent.     

Effect of endogenous cholecystokinin on the course of acute pancreatitis in rats

AIM: To examine the effects of pancreatic rest, stimulation and rest/stimulation on the natural course of recovery after acute pancreatitis. METHODS: Acute hemorrhagic pancreatitis(AP) was induced in male rats by intraductal infusion of 40 μl/100 g body weight of 3% sodium taurocholate. All rats took food ad libitum. At 24 h after induction of AP, rats were divided into four groups: control(AP-C), pancreas rest(AP-R), stimulation(AP-S), and rest/stimulation(AP-R/S). Rats in the AP-C, AP-R and AP-S groups received oral administration of 2 ml/kg body weight saline, cholecystokinin(CCK)-1 receptor antagonist, and endogenous CCK release stimulant, respectively, twice daily for 10 d, while those in the AP-R/S group received twice daily CCK-1 receptor antagonist for the first 5 d followed by twice daily CCK release stimulant for 5 d. Rats without any treatment were used as control group(Control). Biochemical andhistological changes in the pancreas, and secretory function were evaluated on day 12 at 24 h after the last treatment. RESULTS: Feeding ad libitum(AP-C) delayed biochemical, histological and functional recovery from AP. In AP-C rats, bombesin-stimulated pancreatic secretory function and HOMA-β-cell score were significantly lower than those in other groups of rats. In AP-R rats, protein per DNA ratio and pancreatic exocrine secretory function were significantly low compared with those in Control rats. In AP-S and AP-R/S rats, the above parameters recovered to the Control levels. Bombesinstimulated pancreatic exocrine response in AP-R/S rats was higher than in AP-S rats and almost returned to control levels. In the pancreas of AP-C rats, destruction of pancreatic acini, marked infiltration of inflammatory cells, and strong expression of α-smooth muscle actin, tumor necrosis factor-α and interleukin-1β were seen. Pancreatic rest reversed these histological alterations, but not atrophy of pancreatic acini and mild infiltration of inflammatory cells. In AP-S and AP-R/S rats, the pancreas showed almost normal architecture. CONCLUSION: The favorable treatment strategy for AP is to keep the pancreas at rest during an early stage followed by pancreatic stimulation by promoting endogenous CCK release.     

Fatty acids of erythrocyte membrane in acute pancreatitis patients

AIM:To evaluate changes in the fatty acid composition of erythrocyte membrane phospholipids during severe and mild acute pancreatitis(AP)of alcoholic and nonalcoholic etiology.METHODS:All consecutive patients with a diagnosis of AP and onset of the disease within the last 72 h admitted to the Hospital of Lithuanian University of Health Sciences between June and December 2007 were included.According to the Acute Physiology and ChronicHealth Evaluation(APACHEⅡ)scale,the patients were subdivided into the mild(APACHEⅡscore<7,n=22)and severe(APACHEⅡscore≥7,n=17)AP groups.Healthy individuals(n=26)were enrolled as controls.Blood samples were collected from patients on admission to the hospital.Fatty acids(FAs)were extracted from erythrocyte phospholipids and expressed as percentages of the total FAs present in the chromatogram.The concentrations of superoxide dismutase and glutathione peroxidase were measured in erythrocytes.RESULTS:We found an increase in the percentages of saturated and monounsaturated FAs,a decrease in the percentages of total polyunsaturated FAs(PUFAs)and n-3 PUFAs in erythrocyte membrane phospholipids of AP patients compared with healthy controls.Palmitic(C16:0),palmitoleic(C16:1n7cis),arachidonic(C20:4n6),docosahexaenoic(DHA,C22:6n3),and docosapentaenoic(DPA,C22:5n3)acids were the major contributing factors.A decrease in the peroxidation and unsaturation indexes in AP patients as well as the severe and mild AP groups as compared with controls was observed.The concentrations of antioxidant enzymes in the mild AP group were lower than in the control group.In severe AP of nonalcoholic etiology,the percentages of arachidic(C20:0)and arachidonic(C20:4n6)acids were decreased as compared with the control group.The patients with mild AP of nonalcoholic etiology had the increased percentages of total saturated FAs and gama linoleic acid(C18:3n6)and the decreased percentages of elaidic(C18:1n9t),eicosapentaenoic acid(EPA,C20:5n3),DPA(C22:5n3),DHA(C22:6n3)as well as total and n-3 PUFAs in erythro     

Immune-modulating therapy in acute pancreatitis: Fact or fiction

Acute pancreatitis (AP) is one of the most common diseases of the gastrointestinal tract, bearing significant morbidity and mortality worldwide. Current treatment of AP remains unspecific and supportive and is mainly targeted to aggressively prevent systemic complications and organ failure by intensive care. As acute pancreatitis shares an indistinguishable profile of inflammation with sepsis, therapeutic approaches have turned towards modulating the systemic inflammatory response. Targets, among others, have included pro- and anti-inflammatory modulators, cytokines, chemokines, immune cells, adhesive molecules and platelets. Even though, initial results in experimental models have been encouraging, clinical implementation of immune-regulating therapies in acute pancreatitis has had a slow progress. Main reasons include difficulty in clinical translation of experimental data, poor understanding of inflammatory response time-course, flaws in experimental designs, need for multimodal approaches and commercial drawbacks. Whether immune-modulation in acute pancreatitis remains a fact or just fiction remains to be seen in the future.     

Heat shock proteins and autophagy in rats with cerulein-induced acute pancreatitis

Background/Aims

Heat shock proteins (HSPs) protect rats from cerulein-induced acute pancreatitis (AP) by preventing the subcellular redistribution of cathepsin B and the activation of trypsinogen. Autophagy plays a critical role in the secretion of digestive enzymes and triggering of cerulein-induced AP via the colocalization of trypsinogen and lysosomes. Therefore, using a rat cerulein-induced AP model, we investigated whether HSPs prevent AP by regulating autophagy.

Methods

Twelve hours after fed standard laboratory chow and water, the experimental groups (cerulein, water-immersion [WI]-cerulein and heat-shock [HS]-cerulein) and the control groups (control, WI, and HS) received one intraperitoneal injection of cerulein (50 µg/kg) or saline, respectively. All of the rats were sacrificed at 6 hours after injection. The severity of the AP was assessed based on the serum amylase level and the histological and electron microscopy findings. Western blotting was also performed for HSP60/70 and LC3B-II.

Results

WI and HS induced HSP60 and HSP70, respectively. The induced HSP60/70 effectively prevented the development of cerulein-induced AP. Autophagy developed in the rats with cerulein-induced AP and was documented by the expression of LC3-II and electron microscopy findings. The WI-stressed rats and HS-treated rats did not develop cerulein-induced autophagy.

Conclusions

HSPs exert protective effects against cerulein-induced AP in rats by inhibiting autophagy.     

Hydrocortisone Treatment of Early SIRS in Acute Experimental Pancreatitis

This work studied the effects of hydrocortisone treatment in experimental acute pancreatitis on cytokines, phospholipase A₂, and breakdown products of arachidonic acid and survival. Edematous and necrotizing pancreatitis were induced in Wistar rats by cerulein hyperstimulation and retrograde intraductal infusion of sodium taurocholate, respectively. Hydrocortisone (10 mg/kg) was administered intravenously 10 minutes after induction of acute pancreatitis. Serum was assayed for phospholipase A₂; interleukin (IL) 1, IL-6, IL-10, thromboxane B₂; Prostaglandin E₂; and leukotriene B₄ at five different time points. A significant release of inflammatory mediators was seen only in the severe model. Hydrocortisone powerfully suppressed arachidonic acid breakdown products and only mildly attenuated the systemic increase of phospholipase A₂ and pro- and antiinflammatory cytokines. The mortality rate after 72 hr in the severe model was 86%. Hydrocortisone treatment reduced mortality to 13% (P = 0.001; Fisher's exact test). Hydrocortisone seems to be effective in the treatment of the early systemic inflammatory response syndrome associated with severe acute pancreatitis.     

Pharmacologic therapy for acute pancreatitis

While conservative management such as fluid,bowel rest,and antibiotics is the mainstay of current acute pancreatitis management,there is a lot of promise in pharmacologic therapies that target various aspects of the pathogenesis of pancreatitis.Extensive review of preclinical studies,which include assessment of therapies such as anti-secretory agents,protease inhibitors,anti-inflammatory agents,and anti-oxidants are discussed.Many of these studies have shown therapeutic benefit and improved survival in experimental models.Based on available preclinical studies,we discuss potential novel targeted pharmacologic approaches that may offer promise in the treatment of acute pancreatitis.To date a variety of clinical studies have assessed the translational potential of animal model effective experimental therapies and have shown either failure or mixed results in human studies.Despite these discouraging clinical studies,there is a great clinical need and there exist several preclinical effective therapies that await investigation in patients.Better understanding of acute pancreatitis pathophysiology and lessons learnedfrom past clinical studies are likely to offer a great foundation upon which to expand future therapies in acute pancreatitis.     

Two cases of acute respiratory distress syndrome resulting from adult-onset Still's disease

 Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder of unknown origin. Acute respiratory distress syndrome (ARDS) is a rare complication of AOSD, with only nine cases having been reported in the literature. Here, we describe two cases of AOSD complicated with ARDS that were successfully treated with immunosuppressive therapy, including corticosteroids. Although ARDS is a life-threatening complication in AOSD, early commencement of high-dose corticosteroids and mechanical ventilation improve the prognosis. Received: February 1, 2002 / Accepted: June 5, 2002 Correspondence to:N. Miyasaka     

Leptin treatment ameliorates acute lung injury in rats with cerulein-induced acute pancreatitis

AIM:To determine the effect of exogenous leptin on acute lung injury (ALI) in cerulein-induced acute pancreatitis (AP). METHODS:Forty-eight rats were randomly divided into 3 groups. AP was induced by intraperitoneal (i.p.) injection of cerulein (50 μg/kg) four times,at 1 h intervals. The rats received a single i.p. injection of 10 μg/kg leptin (leptin group) or 2 mL saline (AP group) after cerulein injections. In the sham group,animals were given a single i.p. injection of 2 mL saline. Experimental samples were collected for biochemical and histological evaluations at 24 h and 48 h after the induction of AP or saline administration. Blood samples were obtained for the determination of amylase,lipase,tumor necrosis factor (TNF)-a,interleukin (IL)-1β,macrophage inflammatory peptide (MIP)-2 and soluble intercellular adhesion molecule (sICAM)-1 levels,while pancreatic and lung tissues were removed for myeloperoxidase (MPO) activity,nitric oxide (NOx) level,CD40 expression and histological evaluation. RESULTS:Cerulein injection caused severe AP,confirmed by an increase in serum amylase and lipase levels,histopathological findings of severe AP,and pancreatic MPO activity,compared to the values obtained in the sham group. In the leptin group,serum levels of MIP-2,sICMA-1,TNF-a,and IL-1b,pancreatic MPO activity,CD40 expression in pancreas and lung tissues,and NOx level in the lung tissue were lower compared to those in the AP group. Histologically,pancreatic and lungdamage was less severe following leptin administration. CONCLUSION:Exogenous leptin attenuates inflammatory changes,and reduces pro-inflammatory cytokines,nitric oxide levels,and CD40 expression in ceruleininduced AP and may be protective in AP associated ALI.     

Prevalence,predictors and impact of bacterial infection in acute on chronic liver failure patients

BackgroundAcute on chronic liver failure (ACLF) is associated with high short term mortality. We aimed to evaluate the prevalence, predictors and impact of bacterial infection in ACLF.MethodsConsecutive hospitalized patients with cirrhosis and acute decompensation (AD), from January 2011–March 2017, were included. Predictors of survival and infection were assessed.Results572 patients with cirrhosis and AD were classified into 3 groups — no infection (group 1, n = 190, 33.2%), infection at admission/within 48 h (group 2, n = 298, 52.1%) and infection after 48 h (group 3, n = 84, 14.7%). Higher frequency of organ failures – kidney, brain, circulation and respiratory failure – were seen in groups 2 and 3 as compared with group 1 (P < 0.001 for all). Most common site of infection was lungs, followed by spontaneous bacterial peritonitis and urinary tract infection. The frequency of infection increased with higher ACLF grades. Among ACLF patients, on Cox-proportional multivariate analysis, presence of infection was associated with significantly higher mortality [group 2 (HR 2.93; 95%CI, 1.97–4.38, P < 0.001) and group 3 (HR 1.84; 95%CI, 1.16–2.91, P = 0.009)], as compared with group 1. On multivariate logistic regression analysis, advanced hepatic encephalopathy and elevated total leucocyte count were independently associated with development of infection.ConclusionsInfections are common in ACLF, and associated with poor outcome.     

Management of infection in acute pancreatitis

The clinical course of acute pancreatitis varies from a mild, transitory illness to a severe, rapidly fatal disease. In about 80% to 90% of cases pancreatitis presents as a mild, self‐limiting disease with low morbidity and mortality. Unlike mild pancreatitis, necrotizing pancreatitis develops in about 15% of patients, with infection of pancreatic and peripancreatic necrosis representing the single most important risk factor for a fatal outcome. Infection of pancreatic necrosis in the natural course develops in the second and third week after onset of the disease and is reported in 40% to 70% of patients with necrotizing pancreatitis. Just recently, prevention of infection by prophylactic antibiotic treatment and assessment of the infection status of pancreatic necrosis by fine‐needle aspiration have been established in the management of severe pancreatitis. Because medical treatment alone will result in a mortality rate of almost 100% in patients with signs of local and systemic septic complications, patients with infected necrosis must undergo surgical intervention, which consists of an organ‐preserving necrosectomy combined with a postoperative closed lavage concept that maximizes further evacuation of infected debris and exudate. However, intensive care treatment, including prophylactic antibiotics, reduces the infection rate and delays the need for surgery in most patients until the third or fourth week after the onset of symptoms. At that time, debridement of necrosis is technically easier to perform, due to better demarcation between viable and necrotic tissue compared with necrosectomy earlier in the disease. In contrast, surgery is rarely needed in the presence of sterile pancreatic necrosis. In those patients the conservative approach is supported by the present data.     

急性胰腺炎小鼠对脂多糖耐受性及其机制的研究

目的　观察急性胰腺炎(AP)小鼠对脂多糖(LPS)的耐受性并探讨其可能机制。方法　210只C57BL/6J小鼠分为生理盐水(NS)+LPS组(n=105)和AP+LPS组(n=105),两组均以不同LPS剂量分为7个亚组。AP模型制备采用间隔1 h腹腔内注射雨蛙肽(50μg/kg),共7次,于第1次雨蛙肽注射后6 h腹腔内注射LPS;NS+LPS组以NS代替雨蛙肽。每个亚组随机分出10 只观察7 d死亡率,其余5只于第1 次雨蛙肽注射后12 h处死,留取血清及肝、肺、肾、胰腺等组织,检测血清淀粉酶(AMS)、乳酸脱氢酶(LDH)水平及各脏器病理学改变。应用含12 489条小鼠全长基因的寡核苷酸芯片分别检测NS+LPS(15 mg/kg)亚组和AP+ LPS(15 mg/kg)亚组小鼠血白细胞基因表达谱并重复3次,筛选两组间的表达差异基因。结果　NS+LPS组和AP+LPS组死亡率均随LPS剂量增加逐步升高,AP+LPS组死亡率均显著低于同等LPS剂量的NS+LPS组(P<0.05)。AP+LPS组LDH水平明显低于相同LPS剂量的NS+LPS组(P<0.05),而AMS水平显著高于相同LPS剂量的NS+LPS组(P<0.05)。AP+LPS组肝、肺、肾组织损伤较相同LPS剂量的NS+LPS组明显减轻。基因芯片筛选结果显示,AP+LPS(15 mg/kg)亚组与NS +LPS(15 mg/kg)亚组相比炎症反应基因、细胞内信号传导基因、转录调节基因表达下调。结论　AP可增强小鼠对LPS耐受性,其可     

慢加急性乙型肝炎肝衰竭患者并发细菌感染及其预测模型效能评价

目的 调查慢加急性乙型肝炎肝衰竭(HBV-ACLF)患者并发细菌感染发生情况及常见临床指标预测感染的效能。方法 2015年1月～2022年2月我院诊治的HBV-ACLF患者214例,自医院HIS系统调查细菌感染资料,应用多因素Logistic回归分析影响感染发生的因素。结果 在本组214例HBV-ACLF患者中,并发细菌感染145例(67.7%),其中1个部位感染113例,2个部位感染28例,3个部位感染4例;自发性细菌性腹膜炎127例(85.2%),肺部感染41例(27.5%),急性胆囊炎25例(16.8%),尿路感染4例(2.7%)和肛周感染2例(1.3%);感染组年龄、全身炎症反应综合征(SIRS)评分、外周血WBC计数、血小板计数、血清C反应蛋白(CRP)、降钙素原(PCT)、凝血酶原活动度(PTA)、血清总胆红素(TBIL)、白蛋白(ALB)、肝性脑病(HE)和腹水发生率与未并发感染组比,差异显著(P<0.05);将单因素分析结果中对感染有影响的指标进一步行多因素Logistic回归分析,结果显示年龄、SIRS评分、WBC、PCT和腹水是影响HBV-ACLF患者并发细菌...     

Effect of early administration of exogenous basic fibroblast growth factor on acute edematous pancreatitis in rats

AIM: To observe the therapeutic effect of early administration of exogenous Basic fibroblast growth factor (bFGF) on acute edematous pancreatitis (AEP) in rats. METHODS: Thirty male Sprague-Dawley rats were randomly divided into three (n = 10): normal control group (groupⅠ), AEP group (groupⅡ) and AEP with bFGF treatment group (groupⅢ). AEP was induced by subcutaneous injection of cerulein (5.5μg/kg and 7.5μg/kg) at 1 h interval into rats of groupsⅡandⅢ. Three hours after induction of AEP, 100μg/kg bFGF was administrated intraperitoneally for 1h to groupⅢrats. For test of DNA synthesis in acinar cells, 5-bromo-2'-deoxyuridine (BrdU) labeling solution was intraperitoneally injected into the rats of groupsⅡandⅢ24 h after bFGF treatment. The changes in serum amylase, lipase, pancreatic tissue wet/dry ratio were detected. RESULTS: In bFGF treatment group, there was a significant decrease in the volume of serum amylase, lipase and the pancreatic wet/dry weight ratio(1383.0±94.6 U/L, 194.0±43.6 U/L, 4.32±0.32) compared to AEP group (3464±223.7 U/L, 456±68.7 U/L, 6.89±0.47) (P < 0.01), and no significant difference was found between bFGF treatment and control group (1289±94.0 U/L, 171±23.4 U/L, 4.12±0.26, P > 0.05). The inflammatory changes such as interstitial edema, polymorphonuclear neutrophils (PMNs) and vacuolization were significantly ameliorated compared to AEP group (P < 0.01). A small number of BrdU-labeled nuclei were observed in acinar cells of AEP rats (1.8±0.3 nuclei/microscopic field, n = 10) while diffuse BrdU-labeled nuclei were found in bFGF-treated rats (18.9±1.4 nuclei/microscopic field, n = 10) {P < 0.01). Immunohistochemical study showed increased DNA synthesis in pancreatic acinar cells. CONCLUSION: Early administration of exogenous bFGF has significant therapeutic effect on cerulein-induced acute edematous pancreatitis in rats. Its mechanism is related to the amelioration of inflammation and facilitation of pancreatic regeneration.     

全身炎症反应综合征对急性胰腺炎预后的影响

目的：探讨全身炎症反应综合征（ＳＩＲＳ）对急性胰腺炎预后的影响。方法２３例非手术治疗的急性胰腺炎患者，按是否伴有ＳＩＲＳ，分为ＳＩＲＳ组（１５例）和非ＳＩＲＳ组（８例），对其合并脏器功能障碍、病程及死亡率进行前瞻性观察。结果：ＳＩＲＳ组和非ＳＩＲＳ组器官功能障碍发生率分别为７３．３％和１２．５％（Ｐ＜０．０５）；ＳＩＲＳ组的死亡率为２０％，而非ＳＩＲＳ组无一例死亡；ＳＩＲＳ组平均住院日也显著高于非ＳＩＲＳ组（Ｐ＜０．０５）。结论：ＳＩＲＳ对急性胰腺炎的预后呈显著负性影响，并使病程延长，住院费用增加。     

Management of acute pancreatitis in Japan: analysis of nationwide epidemiological survey

Acute pancreatitis(AP) is an acute inflammatory disease of the exocrine pancreas. In Japan, nationwide epidemiological surveys have been conducted every 4 to 5 years by the Research Committee of Intractable Pancreatic Diseases, under the support of the Ministry of Health, Labour, and Welfare of Japan. We reviewed the results of the nationwide surveys focusing on the severity assessment and changes in the therapeutic strategy for walled-off necrosis. The severity assessment system currently used in Japan consists of 9 prognostic factors and the imaging grade on contrastenhanced computed tomography. By univariate analysis, all of the 9 prognostic factors were associated with AP-related death. A multivariate analysis identified 4 out of the 9 prognostic factors(base excess or shock, renal failure, systemic inflammatory response syndrome criteria, and age) that were associated with AP-related death. Receiver-operating characteristics curve analysis showed that the area under the curve was 0.82 for these 4 prognostic factors and 0.84 for the 9 prognostic factors, suggesting the comparable utility of these 4 factors in the severity assessment. We also examined the temporal changes in treatment strategy for walled-off necrosis in Japan according to the 2003, 2007, and 2011 surveys. Step-up approaches and lessinvasive endoscopic therapies were uncommon in 2003 and 2007, but became popular in 2011. Mortality has been decreasing in patients who require intervention for walled-off necrosis. In conclusion, the nationwide survey revealed the comparable utility of 4 prognostic factors in the severity assessment and the increased use of less-invasive, step-up approaches with improved clinical outcomes in the management of walled-off necrosis.     

Relationship between the exocrine and endocrine pancreas after acute pancreatitis

AIM:To determine the prevalence and time course of pancreatic exocrine insufficiency in individuals with newly diagnosed prediabetes or diabetes mellitus after acute pancreatitis.METHODS:Relevant literature cited in three major biomedical journal databases(EMBASE,MEDLINE,and Scopus)was reviewed independently by two authors.There were no language constraints but the search was limited to human studies.Studies included were cohort studies of adult patients who were discharged after an attack of acute pancreatitis.Patients were excluded if they were under 18 years of age or had a previous diagnosis of prediabetes or diabetes mellitus,pancreatic exocrine insufficiency,or chronic pancreatitis.The main outcome measure was the prevalence of concomitant pancreatic exocrine insufficiency in patients who were diagnosed with prediabetes and diabetes mellitus after an attack of acute pancreatitis.Subgroup analysis was conducted for patients who were diagnosed with prediabetes only and those who were diagnosed withdiabetes mellitus only.Subgroup analysis looking at the time course of concomitant pancreatic exocrine and endocrine insufficiency was also conducted.Pooled prevalence and corresponding 95%confidence intervals were calculated for all outcome measures and P-values<0.05 were deemed statistically significant.RESULTS:Eight clinical studies comprising of 234patients met all eligibility criteria.The pooled prevalence of newly diagnosed prediabetes or diabetes in individuals after acute pancreatitis was 43%(95%CI:30%-56%).The pooled prevalence of pancreatic exocrine insufficiency in individuals after acute pancreatitis was 29%(95%CI:19%-39%).The prevalence of concomitant pancreatic exocrine insufficiency in individuals with newly diagnosed prediabetes or diabetes was 40%(95%CI:25%-55%).The prevalence of concomitant pancreatic exocrine insufficiency among individuals with prediabetes alone and diabetes mellitus alone was 41%(95%CI:12%-75%)and 39%(95%CI:28%-51%),respectively.Further analysis showed that the prevalence of concomitant pancreatic exocrine insufficiency in individuals with prediabetes or diabetes decreases over time after an attack of acute pancreatitis.CONCLUSION:Pancreatic exocrine insufficiency occurs in 40%of individuals with newly diagnosed prediabetes or diabetes mellitus after acute pancreatitis.Further studies are needed to investigate the pathogenesis of diabetes in this setting.