个体化健康教育在急性重症胰腺炎并发症防治中的应用

目的:通过对急性胰腺炎病人实施个体化健康教育,帮助其改变不健康的行为,促进健康,预防并发症.方法:对65例病人,因人而异地进行健康评估,实施健康教育和行为干预:(1)常规性教育;(2)疼痛教育;(3)促进健康行为;(4)心理教育.结果:通过实施个体化的健康教育,效果满意.观察指标实验组与对照组比较:其病人满意率提高16%,并发症发生率降低14%,再次住院率下降18%.两组指标经统计学处理,P＜0.05,具有显著性差异.因此实施个体化的健康教育,可有效防治急性重症胰腺炎的并发症,降低其再次住院率,提高病人满意率.

生长抑素治疗急性重症胰腺炎临床观察

目的探讨生长抑素十四肽(施他宁)治疗急性重症胰腺炎的疗效。方法总结1996年至2006年收治的急性重症胰腺炎病例,将保守治疗的病例分为生长抑素十四肽治疗组(治疗组)和非生长抑素十四肽组(对照组),比较两组的疗效,治疗组采取常规治疗加用施他宁持续静脉滴注3～5d,对照组采取常规治疗。结果治疗组临床症状和体征恢复好转时间比对照组提前3～6d,并发症减少,降低病死率,住院天数减少。结论施他宁能在一定程度上控制病情发展,减少并发症发生,降低病死率,对于重症胰腺炎治疗有重要价值,早期应用生长抑素十四肽可以明显改善重症急性胰腺炎的治疗效果。

重症急性胰腺炎并发胰性脑病的护理

目的探讨提高重症胰腺炎合并胰性脑病的救护成功率的方法。方法根据患者具体情况,按照个体化的原则,严密观察病情,合理营养支持,加强基础护理,减少并发症发生。结果本组17例,死亡8例,治愈5例,好转4例。结论重症急性胰腺炎并发胰性脑病,预后差,需严密观察病情,精心护理,加强营养支持,预防并发症,提高生存质量。

重症胰腺炎营养支持方式的选择与韦尼克脑病发生关系的观察体会

韦尼克脑病［1‐2］是因硫胺素（Vit‐B1）缺乏所致的一种中枢神经系统症状综合征，在胰腺炎患者特别是重症患者，因其病程时间长，长期禁饮食，可导致韦尼克脑病的发生。本文通过回顾我科2014年1－7月期间45例住院时间超过30 d的重症急性胰腺炎患者在肠内或肠外营养治疗下与韦尼克脑病发生情况的临床对比观察，可见肠内营养支持下韦尼克脑病的发生率较肠外营养低，为本病治疗过程中营养支持方式的选择提供临床经验。

重症急性胰腺炎预防与阻断急诊专家共识

急性膜腺炎是急诊科常见的严重消化系统疾病之一,近年来急诊科收治的急性肤腺炎患者有增无减。急诊科早期积极有效地处理可以减轻肤腺炎带来的器官功能损害,改善患者预后。目前急性肤腺炎的严重程度分型需要在发病后48h才能确定,这种诊断时间上的“带后性”,无法为急诊科急性肤腺炎分级诊疗提供帮助。该共识通过文献整理、专家讨论,根据患者的基础病情、来急诊时全身和肤腺局部表现等,提出“疑似重症急性肤腺炎(SSAP)”的概念,为急性膜腺炎的早期规范化处理提出了病理生理学依据,为预防与阻断重症急性膜腺炎的发生提供了基础。本共识总结既往研究,从高危患者筛选到细胞因子测定,联合多项重症患者通用评分和肤腺炎专项评分,使急性胶腺炎患者在急诊科得到充分评估,并提出一系列包括液体复苏、器官支持、中医中药等SSAP阻断方案,促进急性肤腺炎患者早期康复。

重症急性胰腺炎术后死亡原因分析

重症急性胰腺炎(SAP)是一个复杂多变的疾病,病情进展快,并发症多,死亡率高.我院自1990～2000年手术收治17例SAP,其中死亡7例.死亡率41.2%(7/17).笔者就其死亡原因予以浅析.

Experimental study of therapeutic efficacy of Baicalin in rats with severe acute pancreatitis

AIM： To observe the therapeutic efficacy of Baicalin in rats with severe acute pancreatitis （SAP） and explore its therapeutic mechanisms. METHODS： The SAP rat models were randomly divided into the model control group, Baicalin treatment group, octreotide treatment group and sham operation group. All groups were randomly subdivided into 3 h, 6 h and 12 h groups with 15 rats in each group. The survival, ascites volume and pathological changes of pancreas in all rats were observed at different time points after operation. The plasma amylase content and serum TNF-α, IL-6, malonaldehyde （MDA） and PLA2 contents were also determined. RESULTS： The survival was not obviously different between the treated groups, and was significantly higher in treated groups at 12 h compared to the model control group （P 〈 0.05, 15 vs 10）. The ascites/body weight ratio at 3 h and 6 h was significantly lower in Baicalin treatment group compared to the model control group and octreotide treatment group （P 〈 0.05, 1.00 vs 2.02 and 1.43 and P 〈 0.001, 2.29 （1.21） vs 2.70 （0.80） and 2.08 （2.21）, respectively）. The contents of amylase, TNF-α, IL-6, MDA and PLA2 were significantly lower in the treated groups than in the model control group （P 〈 0.05, 4342 vs 5303, 5058 vs 6272 in amylase, P 〈 0.01, 21.90 vs 36.30, 23.80 vs 39.70, 36 vs 54.35 in MDA and 56.25 vs 76.10 in PIA2, or P 〈 0.001, 65.10 and 47.60 vs 92.15 in TNF-α, 3.03 vs 5.44, 2.88 vs 6.82, 2.83 vs 5.36 in IL-6, respectively）. The pathological scores of pancreas in the treated groups were significantly lower than that in the model control group （P 〈 0.05, 9.00 vs 10.05, 6.00 vs 9.00, 8.00 vs 10.05）, but no marked difference was found between the treated groups. CONCLUSION： The Baicalin injection has significant therapeutic effects on SAP rats, its effects are similar to those of octreotide. The Baicalin injection is also cheap and has a big application range, quite hopefully to be used in clinical treatment of SAP.

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis （SAP） in multiple organ injury is a hotspot in the surgical field. In clinical practice, the main complicated organ dysfunctions are shock, respiratory failure, renal failure, encephalopathy, with the rate of hepatic diseases being closely next to them. The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis, but also develop into hepatic failure and cause patient death, lts complicated pathogenic mechanism is an obstacle in clinical treatment. Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR （oxygen free radical）, endotoxin, etc. may play important roles in its progression.

Analysis of the delayed approach to the management of infected pancreatic necrosis

AIM: To analyze outcomes of delayed single-stage necrosectomy after early conservative management of patients with infected pancreatic necrosis (IPN) associated with severe acute pancreatitis (SAP). METHODS: Between January 1998 and December 2009, data from patients with SAP who developed IPN and were managed by pancreatic necrosectomy were analyzed. RESULTS: Fifty-nine of 61 pancreatic necrosectomies were performed by open surgery and 2 laparoscopically. In 55 patients, single-stage necrosectomy could be performed (90.2%). Patients underwent surgery at a median of 29 d (range 13-46 d) after diagnosis of acute pancreatitis. Sepsis and multiple organ failure accounted for the 9.8% mortality rate. Pancreatic fistulae (50.8%) predominantly accounted for the morbidity. The median hospital stay was 23 d, and the median interval for return to regular activities was 110 d.CONCLUSION: This series supports the concept of delayed single-stage open pancreatic necrosectomy for IPN. Advances in critical care, antibiotics and interventional radiology have played complementary role in improving the outcomes.

Comparison of early enteral nutrition in severe acute pancreatitis with prebiotic fiber supplementation versus standard enteral solution:A prospective randomized double-blind study

AIM: To compare the benefi cial effects of early enteral nutrition (EN) with prebiotic fiber supplementation in patients with severe acute pancreatitis (AP).METHODS: Thirty consecutive patients with severe AP, who required stoppage of oral feeding for 48 h, were randomly assigned to nasojejunal EN with or without prebiotics. APACHE Ⅱ score, Balthazar’s CT score and CRP were assessed daily during the study period.RESULTS: The median duration of hospital stay was shorter in the study group [10 ± 4 (8-14) d vs 15 ± 6 (7-26) d] (P < 0.05). The median value of days in intensive care unit was also similar in both groups [6 ± 2 (5-8) d vs 6 ± 2 (5-7) d]. The median duration of EN was 8 ± 4 (6-12) d vs 10 ± 4 (6-13) d in the study and control groups, respectively (P > 0.05). Deaths occurred in 6 patients (20%), 2 in the study group and 4 in the control group. The mean duration of APACHE Ⅱ normalization (APACHE Ⅱ score < 8) was shorter in the study group than in the control group (4 ± 2 d vs 6.5 ± 3 d, P < 0.05). The mean duration of CRP normalization was also shorter in the study group than in the control group (7 ± 2 d vs 10 ± 3 d, P < 0.05).CONCLUSION: Nasojejunal EN with prebiotic fiber supplementation in severe AP improves hospital stay, duration nutrition therapy, acute phase response and overall complications compared to standard EN therapy.

Timing of mortality in severe acute pancreatitis:Experience from 643 patients

AIM: To determine the timing of mortality after onset of severe acute pancreatitis (SAP) and the course of the disease in a large series of patients. METHODS: From July 1996 to June 2005, all patients diagnosed with acute pancreatitis at Chang Gung Memorial Hospital, Taipei, Taiwan were retrospectively studied. Three thousand two hundred and fifty episodes of acute pancreatitis were recorded in 2248 patients (1431 males and 817 females; median age, 55.6 years; range, 18-97 years). Mortality was divided into two groups: early death (≤ 14 d after admission), and late death (> 14 d after admission). The clinical features of patients in these two groups were compared. RESULTS: Although the overall mortality rate of acute pancreatitis was 3.8% (123/3250), mortality rate of SAP was as high as 16.3% (105/643). Of those 105 SAP mortalities, 44 (41.9%) deaths occurred within the first 14 d after admission and 61 (58.1%) occurred after14 d. Incidence of early death did not significantly differ from that of late death. The co-morbidities did not contribute to the timing of death. Early deaths mainly resulted from multiple organ failure. Late deaths were mainly caused by secondary complication of infected necrosis. Intra- abdominal bleeding significantly caused higher mortality in late death. CONCLUSION: Approximately half (42%) of SAP deaths occur within 14 d and most were due to multiple organ failure. The late deaths of SAP were mostly due to infected necrosis.

Effect of BN52021 on NFκ-Bp65 expression in pancreatic tissues of rats with severe acute pancreatitis

AIM： To investigate dynamic changes and significance of expression of NF-κBp65 in pancreatic tissues of rats with severe acute pancreatitis （SAP）, as well as BN52021 effects. METHODS： Wistar male rats were randomly divided into negative control group （NC group, n = 60）, SAP-model group （SAP group, n = 60）, and BN52021-treated group （BN group, n = 60）, and each of the above groups was respectively divided into 6 subgroups at different time points after operation （1 h, 2 h, 3 h, 6 h, 12 h, and 24 h） （n = 10）. By RT-PCR and Western blot, NF-κBp65 mRNA and its protein expression in pancreatic tissues of rats were detected respectively. RESULTS： The expression of NF-κBp65 mRNA dynamically changed in both SAP groups and BN groups. The mRNA level was higher in SAP groups than NC groups at 2 h, 3 h, 12 h, and 24 h after operation （P 〈 0.05）, higher in BN groups than NC groups at all time points （P 〈 0.05）, and higher in BN groups than SAP group at 1 h （P 〈 0.05）. The NF-κBp65 protein level was higher in SAP groups than NC groups at 1 h, 3 h, and 6 h （P 〈 0.01）, and 2 h, 12 h, and 24 h （P 〈 0.05）, higher in BN groups than NC groups at all time points （P 〈 0.05）, and lower in BN groups than SAP groups at 1 h, 3 h, and 6 h （P 〈 0.05）. CONCLUSION： The expression of NF-κBp65 in pancreatic tissues is dynamically changed and the changes play an important role in pathogenesis of SAR BN52021 exerts therapeutic effects through reducing the expression level of NF-κBp65 protein in the early stage of SAR

Recovery from respiratory failure after decompression laparotomy for severe acute pancreatitis

We present three cases of patients (at the age of 56 years, 49 years and 74 years respectively) with severe acute pancreatitis (SAP), complicated by intra-abdominal compartment syndrome (ACS) and respiratory insufficiency with limitations of mechanical ventilation. The respiratory situation of the patients was significantly improved after decompression laparotomy (DL) and lung protective ventilation was re-achieved. ACS was discussed followed by a short review of the literature. Our cases show that DL may help patients with SAP to recover from severe respiratory failure.

A simple taurocholate-induced model of severe acute pancreatitis in rats

AIM: To investigate gut barrier damage and intestinal bacteria translocation in severe acute pancreatitis (SAP), a simple rat model of SAP was induced and studied.METHODS: Pancreatitis was induced by uniformly distributed injection of 3.8% Na taurocholate (1 mL/kg) beneath the pancreatic capsule. Rats in the control group were injected with normal saline in the identical location. RESULTS: Serum amylase, plasma endotoxin, intestinal permeability, and pancreatitis pathology scores were all markedly higher in the pancreatitis group than in the control group (P < 0.01). The bacterial infection rate was signif icantly higher in the SAP group than in the control group (P < 0.01), observed in parallel by both bacterial culture and real-time polymerase chain reaction. Acute damage of the pancreas was observed histologically in SAP rats, showing interstitial edema, leukocyte infiltration, acinar cell necrosis and hemorrhage. The microstructure of the intestinal mucosa of SAP ratsappeared to be destroyed with loose, shortened microvilli and rupture of the intercellular junction, as shown by electron microscopy. CONCLUSION: Significant gut barrier damage and intestinal bacterial translocation were def initely observed with few potential study confounders in this SAP rat model, suggesting that it may be an appropriate animal model for study of gut barrier damage and bacterial translocation in SAP.

Pioglitazone attenuates the severity of sodium taurocholate-induced severe acute pancreatitis

AIM： To determine the effect of pioglitazone, a specific peroxisome proliferator-activated receptor-γ, （PPARγ） ligand, on development of severe acute pancreatitis （SAP） and expression of nuclear factor-kappa B （NF-κB） and intercellular adhesion molecule-1 （ICAM-1） in the pancreas. METHODS： Male Sprague-Dawley （SD） rats （160-200 g） were randomly allocated into three groups （n = 18 in each group）： severe acute pancreatitis group, pioglitazone group, sham group. SAP was induced by retrograde infusion of 1 mL/kg body weight 5% sodium taurocholate （STC） into the biliopancreatic duct of male SD rats. Pioglitazone was injected intraperitoneally two hours piror to STC infusion. Blood and ascites were obtained for detecting amylase and ascitic capacity. Pancreatic wet/dry weight ratio, expression of NF-κB and ICAM-1 in pancreatic tissues were detected by immunohistochemical staining. Pancreatic tissue samples were stained with hematoxylin and eosin （HE） for routine optic microscopy. RESULTS： Sham group displayed normal pancreatic structure. SAP group showed diffuse hemorrhage, necrosis and severe edema in focal areas of pancreas. There was obvious adipo-saponification in abdominal cavity. Characteristics such as pancreatic hemorrhage, necrosis, severe edema and adipo-saponification were found in pioglitazone group, but the levels of those injuries were lower in pioglitazone group than those in SAP group. The wet/dry pancreatic weight ratio, ascetic capacity, serum and ascitic activities of anylase in the SAP group were significantly higher than those in the sham group and pioglitazone group respectively （6969.50 ± 1368.99 vs 2104.67 ± 377.16, 3.99 ± 1.22 vs 2.48 ± 0.74, P 〈 0.01 or P 〈 0.05）. According to Kusske criteria, the pancreatic histologic score showed that interstitial edema, inflammatory infiltration, parenchyma necrosis and parenchyma hommorrhage in SAP group significantly differed from those in the sham group and pioglitazone group （7.17 ± 1.83 vs 0.50 ± 0.55, 7.67 ± 0.82 vs 6.83 ± 0.75, P 〈 0.01, P 〈 0.05. The expression of NF-κB and ICAM-1 in sham group was lower than that in SAP group and pioglitazone group （0.50 ± 0.55 vs 33 ± 1.21, P 〈 0.01）. There was a significant difference in the expression of NF-κB and ICAM-1 between SAP group and pioglitazone group （7.50 ±1.05 vs 11.33 ± 1.75, 0.80 ± 0.53 vs 1.36 ± 0.54, P 〈 0.01 or P 〈 0.05） at 12 h after the induction of pancreatitis. CONCLUSION： Pioglitazone attenuates the severity of SAP. The beneficial effect of pioglitazone is multifactorial due to its anti-inflammatory activities, most likely through the inhibition of ICAM-1 expression and NF-κB activation. Specific ligands of PPARy may represent the novel and effective means of clinical therapy for SAP.

Value of adipokines in predicting the severity of acute pancreatitis:Comprehensive review

AIM:To analyze the prognostic value of adipokines in predicting the course,complications and fatal outcome of acute pancreatitis(AP).METHODS:We performed the search of PubMed database and the systemic analysis of the literature for both experimental and human studies on prognostic value of adipokines in AP for period 2002-2012.Only the papers that described the use of adipokines for prediction of severity and/or complications of AP were selected for further analysis.Each article had to contain information about the levels of measured adipokines,diagnosis and verification of AP,to specify presence of pancreatic necrosis,organ dysfunction and/or mortality rates.From the very beginning,study was carried out adhering to the PRISMA checklist and flowchart for systemic reviews.To assess quality of all included human studies,the Quality Assessment of Diagnostic Accuracy Studies tool was used.Because of the high heterogeneity between the studies,it was decided to refrain from the statistical processing or meta-analysis of the available data.RESULTS:Nine human and three experimental studies were included into review.In experimental studies significant differences between leptin concentrations at 24 and 48 h in control,acute edematous and acute necrotizing pancreatitis groups were found(P = 0.027 and P < 0.001).In human studies significant differences between leptin and resitin concentrations in control and acute pancreatitis groups were found.1-3 d serum adiponectin threshold of 4.5 μg/mL correctly classified the severity of 81% of patients with AP.This threshold yielded a sensitivity of 70%,specificity 85%,positive predictive value 64%,negative predictive value88%(area under curve 0.75).Resistin and visfatin concentrations differ significantly between mild and severe acute pancreatitis groups,they correlate with severity of disease,need for interventions and outcome.Both adipokines are good markers for parapancreatic necrosis and the cut-off values of 11.9 ng/mL and 1.8 ng/mL respectively predict the high ranges of radiological scores.However,the review revealed that all nine human studies with adipokines are very different in terms of methodology and objectives,so it is difficult to generalize their results.It seems that concentrations of the leptin and resistin increases significantly in patients with acute pancreatitis compared with controls.Serum levels of adiponectin,visfatin and especially resitin(positive correlation with Acute Physiology and Chronic Health Evaluation Ⅱ,Ranson and C-reactive protein) are significantly different in mild acute pancreatitis and severe acute pancreatitis patients,so,they can serve as a markers for the disease severity prediction.Resistin and visfatin can also be used for pancreatic and parapancreatic necrosis prediction,interventions needs and possible,outcome.CONCLUSION:High levels of adipokines could allow for prediction of a severe disease course and outcome even in small pancreatic lesions on computed tomography scans.

Melatonin attenuates acute pancreatitis-associated lung injury in rats by modulating interleukin 22

AIM： To investigate whether therapeutic treatment with melatonin could protect rats against acute pan- creatitis and its associated lung injury. METHODS： Seventy-two male Sprague-Dawley rats were randomly divided into three groups： the sham op- eration （SO）, severe acute pancreatitis （SAP）, and mel- atonin treatment （MT） groups. Acute pancreatitis was induced by infusion of 1 mL/kg of sodium taurocholate （4% solution） into the biliopancreatic duct. Melatonin （50 mg/kg） was administered 30 min before pancre- atitis was induced, and the severity of pancreatic and pulmonary injuries was evaluated 1, 4 and 8 h after induction. Serum samples were collected to measure amylase activities, and lung tissues were removed to measure levels of mRNAs encoding interleukin 22 （IL-22） and T helper cell 22 （Th22）, as well as levels of IL-22.ing IL-22 and Th22 were significantly higher （P 〈 0.001） in the MT group than in the SAP group （0.526 ± 0.143 vs 0.156 ± 0.027, respectively, here and throughout, after 1 h; 0.489 ± 0.150 vs 0.113 ± 0.014 after 4 h; 0.524 ± 0.168 vs 0.069 ± 0.013 after 8 h, 0.378 ± 0.134 vs 0.122 ± 0.015 after 1 h; 0.205 ± 0.041 vs 0.076 ± 0.019 after 4 h; 0.302 ± 0.108 vs 0.045 ± 0.013 after 8 h, respectively） and significantly lower （P 〈 0.001） in the SAP group than in the SO group （0.156 ± 0.027 vs 1.000 ± 0.010 after 1 h; 0.113 ± 0.014 vs 1.041 ± 0.235 after 4 h; 0.069 ± 0.013 vs 1.110 ± 0.213 after 8 h, 0.122 ± 0.015 vs 1.000 ± 0.188 after 1 h; 0.076 ± 0.019 vs 0.899 ± 0.125 after 4 h; 0.045 ± 0.013 vs 0.991 ± 0.222 after 8 h, respectively）. The mean pathologi- cal scores for pancreatic tissues in the MT group were significantly higher （P 〈 0.01） than those for samples in the SO group （1.088 ± 0.187 vs 0.488 ± 0.183 after 1 h, 2.450 ± 0.212 vs 0.469 ± 0.242 after 4 h; 4.994 ± 0.184 vs 0.513 ± 0.210 after 8 h）, but were significantly lower （P 〈 0.01） than those for samples in the SAP group at each time point （1.088 ± 0.187 vs 1.969 ± 0.290 after 1 h; 2.450 ± 0.212 vs 3.344 ± 0.386 after 4 h; 4.994 ± 0.184 vs 6.981 ± 0.301 after 8 h）. The severity of SAP increased significantly （P 〈 0.01） over time in the SAP group （1.088 ± 0.187 vs 2.450 ± 0.212 between 1 h and 4 h after inducing pancreatitis; and 2.450 ± 0.212 vs 4.994 ± 0.184 between 4 and 8 h after inducing pan- creatitis）. CONCLUSION： Melatonin protects rats against acute pancreatitis-associated lung injury, probably through the upregulation of IL-22 and Th22, which increases the innate immunity of tissue cells and enhances their regeneration.

Association of polymorphisms of IL and CD14 genes with acute severe pancreatitis and septic shock

AIM. To investigate IL-1β＋3 594 in the 5^th intron, IL-10-1 082 and CD14-159 polymorphisms in patients with acute pancreatitis （AP） and septic shock.METHODS： The study induded 215 patients （109 with acute severe pancreatitis （SAP）, 106 with acute mild pancreatitis （MAP）） and 116 healthy volunteers. Genomic DNA was prepared from peripheral blood leukocytes. Genotypes and allele frequencies were determined in patients and healthy controls using restriction fragment length polymorphism analysis of PCR products.RESULTS： The frequencies of IL-β＋3 594T, IL-10-1082G and CD14-159T allele were similar in patients with mild or severe pancreatitis and in controls. Within SAP patients, no significant differences were found in the allele distribution examined when etiology was studied again. Patients with septic shock showed a significantly higher prevalence of IL-10-1082G allele than those without shock （X^2 = 5.921,P= 0.015）.CONCLUSION： IL-10-1082G plays an important role in the susceptibility of SAP patients to septic shock. Genetic factors are not important in determination of disease severity or susceptibility to AP.

Association between acute pancreatitis and peptic ulcer disease

AIM:To evaluate the relationship between peptic ulcer disease(PUD) and acute pancreatitis.METHODS:A cohort of 78 patients with acute pancreatitis were included in this study.The presence of PUD and the Helicobacter pylori(H.pylori) status were assessed by an endoscopic method.The severity of acute pancreatitis was assessed using Ranson's score,the Acute Physiology and Chronic Health Evaluation(APACHE) □ score,computed tomography severity indexand the clinical data during hospitalization,all of which were compared between the patients with and without PUD.The risk factors for PUD were also evaluated.RESULTS:Among 78 patients,41 patients(52.6%) with acute pancreatitis suffered from PUD,but only 13(31.7%) patients with PUD were infected by H.pylori.On univariate analysis,male gender,an etiology of alcohol-induced pancreatitis,a history of smoking or alcohol consumption,elevated triglyceride and C-reactive protein levels,and high APACHE □ score were signif icantly associated with PUD.However,on multivariate logistic regressionanalysis,the APACHE □ score(odds ratio:7.69;95% conf idence interval:1.78-33.33;P < 0.01) was found to be the only independent risk factor for PUD.CONCLUSION:Patients with acute pancreatitis are liable to suffer from PUD.PUD is associated with severeacute pancreatitis according to the APACHE □ score,and treatment for PUD should be considered for patients with severe acute pancreatitis.