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| 1 | Pancreatits after endoscopic retrograde cholangio-pancreatography显示文摘Pancreatitis is the most common complication after endoscopic retrograde cholangio-pancreatography (ERCP); the reported incidence of this complication varies from less than 1% to 40%, but a rate of 4%-8% is reported in most prospective studies involving non-selected patients. Differences in criteria for defining pancreatitis, methods of data collection, and patient populations (i.e. number of high-risk patients included in the published series) are factors that are likely to affect the varying rates of post-ERCP pancreatitis. The severity of post-ERCP pancreatitis (PEP) can range from a minor inconvenience with one or two days of added hospitalization with full recovery to a devastating illness with pancreatic necrosis, multiorgan failure, permanent disability, and even death. Although, most episodes of PEP are mild (about 90%), a small percentage of patients (about 10%) develop moderate or severe pancreatitis. In the past, PEP was often viewed as an unpredictable and unavoidable complication, with no realistic strategy for its avoidance. New data have aided in stratifi cation of patients into PEP risk categories and new measures have been introduced to decrease the risk of PEP. As most ERCPs are performed on an outpatient basis, the majority of patients will not develop PEP and can be discharged. Alternatively, early detection of those patients who will go on to develop PEP can guide decisions regarding hospital admission and aggressive management. In the last decade, great efforts have been addressed toward prevention of this complication. Points of emphasis have included technical measures, pharmacological prophylaxis, and patient selection. This review provides a comprehensive, evidence-based assessment of published data on PEP and current suggestions for its avoidance. | Ayman M Abdel Aziz Glen A Lehman | 2007 | World Journal of Gastroenterology2007，13，19： | 19 |
| 2 | 生长抑素及ENBD对预防ERCP术后胰腺炎的临床对照显示文摘目的:探讨预防性应用生长抑素及术后放置鼻胆引流管对经内镜胰胆管造影术(endoscopic retrograde cholangiopancreatography,ERCP)后胰腺炎及高淀粉酶血症的作用及安全性.方法:按照既定标准入院接受ERCP诊治的患者110例,随机分为3组,分别给予生长抑素组、ENBD及安慰剂.观察术后胰腺炎、高淀粉酶血症的发生情况、预后及经济学评价.结果:3组患者中术后胰腺炎总发生率为17.2%(n=19),高淀粉酶血症为4.54%(n=5),对照组胰腺炎、高淀粉酶血症发生率明显高于其余2组(P<0.05);血清淀粉酶变化,生长抑素组(467IU/L±63IU/L)、ENBD组(501IU/L±405IU/L)术后6h较对照组(1323IU/L±46IU/L)低,差距有统计学意义(P<0.05);但术后24h血清淀粉酶水平无显著性差异(P>0.05);生长抑素组及ENBD组胰腺炎患者腹部症状体征消失时间、血象下降时间、平均住院时间均较对照组明显缩短,差距有统计学意义(P<0.05);对比2种预防ERCP术后胰腺炎的方法,生长抑素费用明显低于ENBD,可大大降低医疗费用的支出,差距有统计学意义(P<0.05).结论:生长抑素、鼻胆引流管均可有效预防ERCP术后胰腺炎及高淀粉酶血症的发生,生长抑素更为经济. | 郭汉斌 李浩然 李绍祥 马丽 龚丽娟 曹建彪 | 2012 | 世界华人消化杂志2012，20，25： | 14 |
| 3 | 内镜逆行胰胆管造影术后胰腺炎的发病机制及药物预防研究显示文摘内镜逆行胰胆管造影术(ERCP)是广泛用于肝、胆、胰疾病的诊治手段。ERCP后胰腺炎(PEP)是ERCP后最常见的并发症,文献报道发生率为1%~40%,在多数前瞻性随机研究中其发生率在4%~8%不等。有少数PEP患者可发展为重症急性胰腺炎(SAP),甚至可危及生命。近年来,许多学者致力于ERCP后胰腺炎的发病机制和药物预防研究,本文对这方面的进展作一综述。 | 孙勇 贾红 | 2009 | 国际内科学杂志2009，36，8： | 7 |
| 4 | 乌司他丁、奥曲肽对治疗性ERCP术后高淀粉酶血症和胰腺炎预防的临床观察显示文摘目的探讨乌司他丁、奥曲肽预防治疗性ERCP术后高淀粉酶血症和胰腺炎的临床疗效。方法将拟行治疗性ERCP患者随机分为3组。对照组ERCP术后仅采用禁食、抗炎、补液、营养支持等常规治疗,术后1h给予NS500ml滴注2h滴完;奥曲肽组(治疗1组)在对照组用药基础上,ERCP术前1h给予奥曲肽0.1mg皮下注射1次,术后1h给予奥曲肽0.1mg+NS500ml持续匀滴2h,静脉滴注停止后6h、12h再分别给予奥曲肽0.1mg皮下注射各1次;乌司他丁联合奥曲肽组(治疗2组)在对照组用药基础上,ERCP术前1h给予奥曲肽0.1mg皮下注射1次,术后1h给予乌司他丁10wu+NS500ml均匀滴注2h滴完,静脉滴注停止后6h、12h再分别给予奥曲肽0.1mg皮下注射各1次。结果奥曲肽组、联合组与对照组比较,在高淀粉酶血症及ERCP术后胰腺炎发生率差异均有统计学意义(P<0.05),奥曲肽组与联合组比较,差异无统计学意义(P>0.05)。结论乌司他丁联合奥曲肽及单用奥曲肽对治疗性ERCP术后高淀粉酶血症、胰腺炎均有预防作用。 | 郭变 石自刚 | 2011 | 中国医疗前沿2011，6，1： | 5 |
| 5 | 急性胰腺炎与自噬显示文摘急性胰腺炎(AP)是长期困扰人类的一类复杂的疾病,随着生活水平的提高,发病率有逐年增高的趋势,其中10%-20%的AP可发展为重症急性胰腺炎(SAP)。 | 李红昌 徐可 陈亚峰 奉典旭 | 2016 | 中华胰腺病杂志2016，16，6： | 5 |
| 6 | Molecular architecture of mouse and human pancreatic zymogen granules: protein components and their copy numbers显示文摘A molecular model of pancreatic zymogen granule (ZG) is critical for understanding its functions. We haveextensively characterized the composition and membrane topology of rat ZG proteins. In this study, wereport the development of targeted proteomics approaches to quantify representative mouse and humanZG proteins using LC-SRM and heavy isotope-labeled synthetic peptides. The absolute quantities of mouseRab3D and VAMP8 were determined as 1242 ± 218 and 2039±151 (mean ± SEM) copies per ZG. Thesize distribution and the averaged diameter of ZGs 750 ±23 nm (mean ± SEM) were determined byatomic force microscopy. The absolute quantification of Rab3 D was then validated using semi-quantitativeWestern blotting with purified GST-Rab3D proteins as an internal standard. To extend our proteomicsanalysis to human pancreas, ZGs were purified using human acini obtained from pancreatic islet trans-plantation center. One hundred and eighty human ZG proteins were identified for the first time includingboth the membrane and the content proteins. Furthermore, the copy number per ZG of human Rab3 D andVAMP8 were determined to be 1182 ± 45 and 485 ± 15 (mean ± SEM). The comprehensive proteomicanalyses of mouse and human pancreatic ZGs have the potential to identify species-specific ZG proteins.The determination of protein copy numbers on pancreatic ZGs represents a significant advance towardsbuilding a quantitative molecular model of a prototypical secretory vesicle using targeted proteomicsapproaches. The identification of human ZG proteins lays a foundation for subsequent studies of altered ZGcompositions and secretion in pancreatic diseases. | Jin-sook Lee Joseph A. Caruso Garrett Hubbs Patricia Schnepp Jlames Woods Jingye Fang Chunying Li Kezhong ghang Paul M. Stemmer Bhanu P. Jena Xuequn Chen | 2018 | Biophysics Reports2018，4，2： | 2 |
| 7 | 急性胰腺炎中自噬的变化及意义的研究进展显示文摘急性胰腺炎发生时可出现胰腺腺泡细胞的大量死亡,其死亡形式主要包括凋亡和坏死。近年来,很多学者研究发现还有一种细胞死亡方式——自噬。经多数研究表明,急性胰腺炎中,自噬现象较正常情况下明显增加,且加重腺泡细胞的坏死程度。但关于自噬与腺泡细胞死亡的关系仍未明确。本文结合近年来相关研究及报道就自噬现象对急性胰腺炎中可能的作用机制做一综述。 | 马美妮 何池义 | 2016 | 辽宁医学院学报2016，37，1： | 1 |
| 8 | 八肽胆囊收缩素致急性胰腺炎体外模型的建立及其研究显示文摘目的用CCK-8建立体外急性胰腺炎模型,并在模型中观察胰腺腺泡细胞淀粉酶、胰蛋白酶活性及F—actin的分布变化。方法用胶原酶分离的胰腺腺泡细胞体外培养,设不同浓度的CCK-8组(10^-12~10-8mol/L)和对照组,CCK-8刺激30min后,用淀粉酶、胰蛋白酶试剂盒检测腺泡细胞淀粉酶、胰蛋白酶活性,用激光共聚焦显微镜观察细胞内F—actin分布的变化。结果CK-8诱导的淀粉酶分泌率呈双峰曲线,低浓度CCK-8组(10-12~10^-8 mol/L),淀粉酶分泌率呈剂量依赖,高浓度CCK-8组(10-9 mol/L、10^-8 mol/L),淀粉酶分泌被抑制;10-10mol/LCCK-8时,细胞内胰蛋白酶活性明显升高(P〈0.05),10-9mol/L后升高更为急剧;CCK-8刺激浓度达10-9mol/L后,细胞内F—actin出现重新分布,近细胞顶部区域/细胞基底部侧面的比值与对照组比较,出现显著改变(P〈0.05)。结论成功建立了体外AP模型,CCK-8刺激可使胰腺腺泡细胞内F—actin分布从顶部向胞浆部、基底部变化,抑制了细胞消化酶分泌,并与腺泡细胞内胰蛋白酶的过早激活相关。 | 黄刚 汤为学 陶小红 | 2009 | 中国急救医学2009，29，12： | 1 |
| 9 | 急性胰腺炎腺泡细胞的死亡方式显示文摘普遍认为胰酶的激活与释放在急性胰腺炎的发生发展中发挥关键作用,引发一系列后续病理改变(图1):周围腺泡细胞自身消化;胰腺组织肿胀,加重胰腺组织缺血缺氧;胞内容物释放引起组织内的炎症反应,随着炎症因子的链式反应造成炎症风暴的产生,可导致多器官损害[1]。胰酶的自身消化、胰腺组织缺血缺氧以及全身的炎症反应会进一步损伤腺泡细胞,释放与激活更多胰酶。 | 楚江涛 薛东波 | 2012 | 中国现代普通外科进展2012，15，4： | 1 |
| 10 | 自噬在急性胰腺炎中作用的研究进展显示文摘急性胰腺炎是由多种病因引起酶原激活,从而导致胰腺组织自我消化,进而水肿、出血甚至坏死的急性炎症性疾病。自噬,又被称为Ⅱ型程序型死亡,是机体细胞清除多余或损伤的细胞器以及为细胞代谢提供必需能量和营养物质的一种重要方式。自噬在胰腺炎的发生发展过程中扮演重要角色。本文就自噬来源、自噬与酶原激活的关系及自噬在胰腺炎发生发展过程中的作用作一综述。 | 尹金祥 李文星 | 2015 | 中华临床医师杂志(电子版)2015，9，20： | 0 |
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