硫氧还蛋白-1 在急性坏死性胰腺炎大鼠中的表达及褪黑素对其的影响

目的 观察硫氧还蛋白-1(TRX-1)在急性坏死性胰腺炎(ANP)大鼠胰腺组织的表达和褪黑素干预对其的影响.方法 72只雄性SD大鼠随机分成ANP组、褪黑素组和对照组,每组24只.以腹腔注射6%L-Arginine 25 mL/kg体重3次、每次间隔1 h的方法制备ANP模型.褪黑素组在制模前30min腹腔注射0.25%褪黑素20 ml/kg体重;ANP组和对照组大鼠腹腔注射等容积生理盐水.术后6、12、24 h分批处死大鼠.抽血测定血清淀粉酶含量;取胰腺组织行病理学检查,并评分;检测胰腺组织丙二醛(MDA)、髓过氧化酶(MPO)含量;免疫组化检测胰腺组织TRX-1蛋白表达;RT-PCR检测胰腺组织TRX-1 mRNA的表达.结果 ANP组12 h点血清淀粉酶、胰腺组织MDA和MPO以及TRX-1 mRNA和蛋白表达水平分别为(3 012±1 425)u/L、(4.13±1.85)nmol/mg prot、(7.45±1.26)nmol/mg prot、0.68±0.18、66.8±8.1;褪黑素组分别为(1 835±499)U/L、(3.03±2.12)nmol/mg prot、(5.32±1.06)nmml//mgprot、0.50±0.09、80.29±8.14,两组比较均有显著差异(P<0.05).褪黑素组胰腺TRX-1 mRNA和蛋白表达峰值从ANP组的制模后12 h提前到制模后6 h.结论 ANP大鼠胰腺组织TRX-1 mRNA和蛋白表达增高;褪黑素干预能促进胰腺组织早期表达TRX-1 mRNA和蛋白,减轻胰腺组织的损伤.     

α-硫辛酸对大鼠急性胰腺炎的保护作用及其抗氧化机制

目的 探讨抗氧化剂α-硫辛酸对急性胰腺炎(AP)的治疗作用以及可能的机制.方法 3.5%牛磺胆酸钠逆行胰胆管注射制备AP大鼠模型,数字表法随机分为假手术组、AP组、生理盐水组和α-硫辛酸组,每组30只.α-硫辛酸组于造模后腹腔内注射α-硫辛酸1 mg/kg体重,生理盐水组注射等量生理盐水.分别于术后1、3、6,9、12 h处死大鼠,检测血清淀粉酶、TNF-α、ICAM-1水平,观察胰腺病理改变,测定胰腺组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量.结果 AP组胰腺水肿、粘连、坏死,腹腔内可见血性腹水.术后6 h AP组血清淀粉酶、TNF-a、ICAM-1水平以及胰腺组织MDA含量分别为(2211.0±547.4)U/L、(174.8±7.9)ng/ml、(49.3±8.0)ng/ml和(32.2±5.9)U/mg prot,较假手术组的(160±23)U/L、(6.5±1.1)mg/ml、(13.9±3.4)ms/ml、(16.2±3.2)U/mg prot明显升高(P<0.05);胰腺组织SOD活力为(38.5±9.5)U/mg prot,显著低于假手术组(56.7±6.6)U/mg prot (P<0.05).α-硫辛酸6 h组的血清淀粉酶、TNF-α、ICAM-1水平以及胰腺组织MDA含量分别为(1478±642)U/L、(164.8±6.2)ng/ml、(37.5±3.9)ng/ml和(20.2±8.4)U/mg prot,较AP组显著降低(p<0.05);胰腺组织SOD活力为(66.0±8.6)U/mg prot,较AP组显著升高(P<0.05).结论 AP发病与氧化应激有关,抗氧化剂α-硫辛酸对AP大鼠具有较好的治疗作用,其机制可能与抑制TNF-a、ICAM-1 活性有关.     

α-硫辛酸对链脲菌素诱发的大鼠胰岛β细胞损伤的保护作用

目的 研究α-硫辛酸(ALA)对链脲菌素(STZ)诱导的糖尿病大鼠胰岛β细胞损伤的保护作用.方法 30只SD大鼠按数字随机法分为正常对照组(NC组)、STZ组和ALA+STZ组(ALA组),各10只.后2组以STZ(70 mg/kg体重)一次性腹腔内注射诱发糖尿病,ALA组在注射前8 d开始给予ALA(50 mg·kg-1·d-1,强饲)直至实验结束(4周).STZ注射后每3天监测血糖、体重一次.测定胰腺匀浆中丙二醛(MDA)含量及还原型谷胱甘肽(GSH)水平,免疫组化方法检测胰岛β细胞内胰岛素水平.结果 STZ使大鼠血糖明显升高,STZ和ALA组制模成功率分别为90%(9/10)和70%(7/10),相差显著(P<0.05).实验结束时NC组、STZ组和ALA组平均体重分别为(368±3)g、(301±2)g和(341±26)g,3组间相差显著(P<0.05).STZ组胰腺组织内MDA水平为(1.22±0.14)nmol/mg prot,NC组为(0.57±0.04)nmol/mg prot,相差显著(P<0.05);STZ组胰腺组织内GSH含量为(16.54±1.10)mg/g prot,NC组为(25.46±0.62)mg/g prot(P<0.05);STZ组胰岛细胞呈退行性变.ALA组血糖较STZ组明显降低(P<0.05),胰腺组织匀浆MDA含量为(0.72±0.23)nmol/mg prot,较STZ组明显降低(P<0.05),GSH含量为(35.33 4±2.66)ms/s prot,较STZ组明显升高(P<0.05),胰岛的胰岛素分泌增强,较STZ组显著(P<0.05),胰岛β细胞损伤减轻.结论 ALA可通过减轻氧化应激来保护胰岛β细胞结构和功能的完整性.     

依达拉奉对大鼠急性坏死性胰腺炎的保护作用

目的:探讨自由基清除剂依达拉奉对大鼠急性坏死性胰腺炎的保护作用及其机制.方法:90只♂SD大鼠随机分为假手术组(SHAM组)、坏死性胰腺炎组(ANP组)、依达拉奉治疗组(EDA组),每组30只.SHAM组为开腹后只翻动十二指肠及胰腺后关腹;ANP组胰胆管内逆行输注1.5%脱氧胆酸钠制备急性坏死性胰腺炎模型;EDA组为ANP造模后立即尾静脉注射依达拉奉(6mg/kg).分别于术后6、12、24h处死大鼠(每个时点10只),观察胰腺病理形态改变并评分;检测血清淀粉酶、TNF-α、ET-1、sICAM-1含量;检测胰腺组织中丙二醛(MDA)含量及总超氧化物歧化酶(T-SOD)活力.结果:与ANP组比较,EDA治疗组在胰腺病理改变、血清TNF-α水平(6h:109.6ng/L±49.0ng/Lvs190.2ng/L±46.6ng/L,12h:405.4ng/L±116.3ng/Lvs559.7ng/L±203.9ng/L,24h:415.4ng/L±164.6ng/Lvs648.7ng/L±222.1ng/L,均P<0.05)、血清ET-1水平(6h:45.6ng/L±13.5ng/Lvs66.0ng/L±16.0ng/L,12h:83.5ng/L±15.4ng/Lvs96.8ng/L±23.0ng/L,24h:85.1ng/L±25.8ng/Lvs103.9ng/L±28.9ng/L),血清sICAM-1水平(6h:0.58ng/L±0.13ng/Lvs0.78ng/L±0.14ng/L,12h:0.78ng/L±0.10ng/Lvs0.94ng/L±0.12ng/L,24h:0.96ng/L±0.16ng/Lvs1.24ng/L±0.30ng/L,均P<0.05)、胰腺组织MDA含量(6h:4.22nmol/mgprot±0.40nmol/mgprotvs8.79nmol/mgprot±0.80nmol/mgprot,12h:5.90nmol/mgprot±0.51nmol/mgprotvs12.30nmol/mgprot±1.02nmol/mgprot,24h:9.10nmol/mgprot±0.84nmol/mgprotvs17.88nmol/mgprot±1.43nmol/mgprot)均有不同程度减轻(均P<0.05),T-SOD活力增强(6h:88.6U/mgprot±7.1U/mgprotvs68.8U/mgprot±10.5U/mgprot,12h:77.6U/mgprot±6.8U/mgprotvs46.0U/mgprot±8.9U/mgprot,24h:45.5U/mgprot±5.3U/mgprotvs27.8U/mgprot±4.3U/mgprot,均P<0.05);血清淀粉酶变化无显著差异.与SHAM组比较,ANP组胰腺组织病理评分、血清淀粉酶、TNF-α、ET-1、sICAM-1明显升高,胰腺组织MDA含量升高,T-SOD活力下降,差异均有统计学意义.结论:依达拉奉可以清除坏死性胰腺炎体内过量生成的氧自由基并减少炎性因子的表达,减轻胰腺组织损伤.     

胰胆管合流异常对肝脏损伤作用的实验研究

胰胆管合流异常(APBDU)是胰管和胆管在十二指肠壁外汇合,形成共同通道过长,十二指肠乳头部括约肌的作用不能影响整个合流部位,胆汁、胰液互流而引起的胆道、肝脏和胰腺疾病.自APBDU这-概念提出以来,人们进行了大量研究[1],但其发生的病因学机制尚未完全阐明,其与急性胰腺炎、胆道癌,胆管扩张等疾病的因果关系,也仍是进一步深入研究的课题.关于APBDU时胆道和胰腺损伤的报道有很多,我们建立APBDU的实验动物模型来研究肝脏的损伤.     

胰胆管合流异常影像学诊断和外科治疗原则探讨

目的分析胰胆管合流异常的影像学诊断特点,探讨如何选择合理的手术治疗.方法回顾性分析64例胰胆管合流异常症患者的影像学特点和治疗结果.结果64例患者的胰胆管共同通道平均长度是(19.0±0.6)mm.胰管型患者28例(占43.8%),胆管型32例(占50%),共同通道型4例(占6.2%).对胆肠囊状扩张患者行囊肿切除术,加胆肠吻合术;胆道结石患者行胆囊切除术;对晚期肿瘤行保守治疗,其余肿瘤患者行根治术.结论胰胆管合流异常同许多胆道、胰腺疾病的发生有密切关系.在临床工作中早发现该症患者,给予合理的手术治疗可避免严重合并症的发生.     

内镜诊治儿童胰胆管合流异常合并胰腺分裂伴罕见解剖变异一例

胰胆管合流异常(pancreaticobiliary maljunction,PBM)是指胰胆管汇合部位位于十二指肠壁外或汇合部形态和解剖发生先天性异常的一种情况。而胰腺分裂(pancreas divisum,PD)是胰腺最常见的先天性解剖异常,由胚胎发育时期腹侧胰管与背侧胰管融合失败所致。本文报道1例3岁患儿在ERCP下证实同时存在3种胆胰管解剖异常,除PBM合并PD外,在背侧胰管与胆总管末端之间还存在罕见的交通支,内镜下成功治疗。     

脂质过氧化损伤对高脂血症大鼠重症急性胰腺炎的作用及机制

目的:观察高脂血症对大鼠急性胰腺炎病情的影响,探讨脂质过氧化损伤在伴高脂血症重症急性胰腺炎(SAP)中的作用及其机制.方法:SD大鼠脂肪乳剂灌胃2 wk建立高脂血症模型,逆行胰胆管注射3.5%牛磺胆酸钠诱发SAP模型.将大鼠50只随机分为4组:正常组(n=10);高脂血症对照组(HL组,n=10);SAP组(n=15);伴高脂血症SAP(HAP,n=15).检测血清淀粉酶(AMS)、甘油三酯(TG)及胆固醇(CH)水平,并检测血清及胰腺组织的丙二醛(MDA)、超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)、一氧化氮(NO),观察胰腺组织病理改变.结果:HAP组胰腺组织病理改变较SAP组严重:HAP组血清及胰腺组织MDA、XOD水平显著高于SAP组(血清:30.76±2.67 nmol/mLvs 23.14±3.42 nmol/mL,55.72±10.49 U/L vs 45.78±8.98 U/L,均P<0.01:胰腺组织:4.33±0.48 nmol/mgprot vs 2.87±0.45 nmol/mgprot,5.57±0.63 U/gprot vs 4.33±0.79 U/gprot,均P<0.01):其血清及胰腺组织SOD、NO水平显著低于SAP组(血清:85.46±13.56 U/mLvs 97.16±13.77 U/mL,31.72±10.50μmol/Lvs 52.97±6.01μmol/L,均P<0.05;胰腺组织:22.65±3.85 U/mgprot vs 27.88±4.43 U/mgprot,均P<0.01;1.09±0.21 μmol/gprot vs 1.48±0.40μmol/gprot,均P<0.05).结论:高脂血症可加SAP的胰腺病理改变;脂质过氧化损伤可能在高脂血症加重SAP的机制中发挥重要作用.     

胰管内注射乌司他丁对实验犬ERCP术后胰腺损伤的预防

目的:评价胰管内注射乌司他丁对内镜逆行胆胰管造影术(encoscopic retrograde cholangio-pancreatography,ERCP)术后胰腺损伤的预防作用.方法:将实验犬随机分为3组,分别为乌司他丁组(A组)、生理盐水组(B组)、对照组(C组),每组8只.在麻醉状态下行ERCP检查,内镜通过幽门,在十二指肠降段找到十二指肠乳头开口后,A、B两组导丝插入胆管,并向胆管内注入三代显10.0 mL胆管显影后,将导丝选择性插入胰管,A组注入向胰管内缓慢注入乌司他丁10万单位(2.0 mL)(溶于0.9%氯化钠8.0 mL)、B组向胰管内缓慢注入0.9%氯化钠10.0 mL.5 min后,A、B两组均在1 min内注入三代显10.0 mL,使胰管显影;C组将导丝插入胆管,并向胆管内注入三代显10.0 mL,胰管不插管.3组实验犬术后定时采静脉血,生化仪测量血淀粉酶含量,ELISA方法测定3组各时段IL-6、IL-8及胰蛋白酶原激活肽的含量.于ERCP术后第6天处死所有动物,取胰腺标本进行组织学检查.比较各组组织病理学指标的变化情况,综合判断ERCP术后胰腺损伤的发生情况.结果:(1)E R C P术后2 h A组血清淀粉酶、I L-6、I L-8及T A P值分别为3 9 1.0 U/L±67.2 U/L,51.91 ng/L±4.87 ng/L,4.070μg/L±0.089μg/L,3.234 nmol/L±0.185 nmol/L,B组分别为1 077.0 U/L±246.1 U/L,78.11 ng/L±11.25 ng/L,4.520μg/L±0.195μg/L,4.001 nmol/L±0.237 nmol/L,IL-6及IL-8随时间延长而逐渐降低,TAP及血清淀粉酶在24 h达峰值,后逐渐降低,与C组相比均有升高,B组各值均高于A组;(2)胰腺病理学检测结果:A组损害较B组无明显差异.结论:胰管内注射乌司他丁可以使ERCP术后胰腺损伤的发病情况减轻.     

硫化氢对MDA及GSH在大鼠肝星状细胞氧应激中表达的影响

目的:探讨硫化氢对MDA与GSH在大鼠肝星状细胞氧应激中表达的影响.方法:将HSCT6分为8组:空白组(B组,HSC-T6)、对照组(C组,B组+500 μmol/L Fe-NTA)、NaHS组(N1:C组+20 μmol/L NaHS;N2:C组+100 μmol/L NaHS;N3:C组+200μmol/L NaHS)、格列苯脲组(G1:C组+20μmol/LGLBN;G2:C组+200 μmol/L GLBN;G3:C组+700 μmol/L GLBN).用MDA试剂盒测试血清MDA含量;用GSH试剂盒测定上清中GSH含量.结果:24 h后MDA含量对照组和空白组有明显差异(P<0.05),而GSH含量12与24 h均有明显差异(均P<0.05).给予NaHS后,MDA含量24 h N2和N3组与对照组均有明显差异(4.48±0.07 nmol/mg prot,3.58±0.02 nmol/mg protvs 5.05±0.07 nmol/mg prot,均P<0.05),12与24 h GSH含量N2和N3组与对照组有明显差异(35.57±2.02 mg/g prot,36.92±2.30 mg/g protvs 33.64±2.95 mg/g prot;36.49±2.08 mg/gprot,37.59±2.03 mg/g prot vs 31.06±3.08 mg/g prot,均P<0.05).给予GLBN处理后,各项指标结果与给予NaHS处理后结果相对应,各组与相对应组比较均有明显差异(均P<0.05).结论:氧应激下硫化氢对HSC细胞具有保护作用,可抑制肝纤维化的发生发展.     

Association of anomalous pancreaticobiliary ductal junction with gallbladder carcinoma in Chinese patients: an ERCP study

BACKGROUND: Anomalous pancreaticobiliary ductal junction, a rare congenital anomaly, is associated with various biliary and pancreatic diseases. The aim of this study was to determine the frequency of anomalous pancreaticobiliary ductal junction in Chinese patients with gallbladder cancer. METHODS: One thousand eight hundred seventy-six patients underwent ERCP between April 2000 and September 2001 with biliary and pancreatic duct opacification in 1082. Among the latter patients, those with proven gallbladder carcinoma were identified. Anomalous pancreaticobiliary ductal junction was defined as a common channel greater than 15 mm in length or a contractile segment totally distal to the union of the biliary and pancreatic ducts. When the common bile duct appeared to join the main pancreatic duct, the anomalous pancreaticobiliary ductal junction was denoted as B-P subtype; if the main pancreatic duct appeared to join the common bile duct, it was denoted P-B subtype. RESULTS: Fifty-four patients had gallbladder carcinoma, 7 of whom (3 men, 4 women) had anomalous pancreaticobiliary ductal junction (P-B subtype 6, B-P subtype 1). The mean (SD) length of the common channel was 21.0 mm (11.2 mm) with a range of 12 to 45 mm. One patient had early cystic dilation of bile duct. Three other patients had anomalous pancreaticobiliary ductal junction; 1 had an associated choledochal cyst and 2 a normal biliary tree. The overall frequency of anomalous pancreaticobiliary ductal junction was 0.9% (10/1082 cases). The frequency of anomalous pancreaticobiliary ductal junction was significantly higher in patients with gallbladder carcinoma (p < 0.001; OR, 50.7; 95% CI [12.7, 202.3]). CONCLUSIONS: Anomalous pancreaticobiliary ductal junction is strongly associated with gallbladder cancer among Chinese patients.     

Association of gallbladder carcinoma and anomalous pancreaticobiliary ductal union

A total of 96 patients with gallbladder carcinoma in whom direct cholangiography clearly opacified the pancreaticobiliary ductal union and the common channel, and 65 patients with an anomalous union of these two duct systems at a distance greater than 15 mm from the papilla of Vater (normally less than 4.6 +/- 2.2 mm, mean +/- SD) were studied. It was found that this anomalous ductal union occurred in 16.7% of the patients with gallbladder carcinoma in comparison with an incidence of 2.8% among 641 consecutive patients with various hepatobiliary and pancreatic diseases studied by endoscopic retrograde cholangiopancreatography who did not have gallbladder carcinoma. It was also found that gallbladder carcinoma occurred in 24.6% of the 65 cases of anomalous ductal union in comparison with a 1.9% incidence of this cancer among 635 consecutive patients similarly studied and found to have normal ductal union (p less than 0.001). Thus, a close etiologic association was suggested between this anomaly in the terminal segment of the biliary tract and gallbladder carcinoma. Of the 65 patients with anomalous ductal union, 50 had the so-called congenital cystic dilatation of the common bile duct and 15 did not. Five of the 50 (10%) and 11 of the 15 (73.3%) had gallbladder carcinoma (p less than 0.01), and this carcinoma seems to be related to anomalous ductal union rather than to cystic dilatation of the common bile duct. As a tumorigenic factor in this anomaly, regurgitation of pancreatic juice has been stressed.     

慢性胰腺炎的猫模型制作及磁共振影像表现

目的 制备猫慢性胰腺炎(CP)模型,观察其MRI与MRCP的影像学表现.方法 32只猫按数字表法随机分为对照组及制模后3、5、7周组.采用胰管不全结扎法制备CP模型,术后3、5、7周行MRI平扫及MRCP检查,观察胰腺形态,测量胰管直径及感兴趣区(ROI)的T1信号强度值(Tls),计算同层胰腺及肝脏Tls比值.结果 制模的24只猫中存活19只,其中15只形成CP,病理证实轻、中、重度CP分别为7、5、3只,制模成功率为62.5％.在MRI上,猫的正常胰腺显示清晰,T1加权像信号强度高于肝脏,T2加权像信号强度低于肝脏;在MRCP图像上,4只正常猫显示主胰管,胰管最大径(0.79±0.18)mm,并可见胰管及胆总管共同开口于十二指肠降部.正常胰腺及轻、中、重度CP感兴趣区的rTls值分别为1.03±0.06、0.95±0.08、0.90±0.10、0.80±0.11,各CP组与正常对照组间差异均有统计学意义(t=2.18,P＜0.05;t =2.89,P＜0.05;t =4.63,P＜0.01);胰管最大径分别为(0.79±0.18)、(0.95±0.24)、(1.26±0.31)、(2.67±0.71)mm,中、重度CP组与正常对照组间差异均有统计学意义(P＜0.05或＜0.01).结论 胰管不全结扎可制备猫的CP模型.猫的胰腺解剖形态、CP的MRI及MRCP表现与人类相似.     

Liver,biliary and pancreatic injuries in pancreaticobiliary maljunction model in cats

BACKGROUND: Pancreaticobiliary maljunction is a high risk factor of pancreatitis and biliary tract cancer. How this maljunction affects the liver remains obscure. This study aimed to examine the effects of pancreaticobiliary maljunction on the liver, pancreas and gallbladder in a cat model.METHODS: A model of choledocho-pancreatic side-to-side ductal anastomosis was created in ten cats. Before the procedure,a small piece of tissue from the liver, pancreas and gallbladder was collected as a control. The common channel formation was checked by cholecystography. The livers, pancreases and gallbladders of these cats were harvested for histological examination. The expression of proliferating cell nuclear antigen in the gallbladder was examined with immunohistochemistry. RESULTS: Seven of the 10 cats survived for 6 months after surgery. The color of the liver was darker in the PBM model than the control specimen, with nodules on the surface. Histological examination showed ballooning changes and inflammatory infiltrations and the histopathological score increased significantly(P0.05). Also, mitochondria swelling and lipid droplet in cytoplasm were observed under an electron microscope. The pancreas also appeared darker in the PBM model than the control specimen and dilated pancreatic ducts were found in three cats. Histopathological examination revealed vascular proliferation and inflammatory infiltration with numerous neutrophils. Gallbladder epithelial cells were featured by expanded endoplasmic reticulum, increased intercellular space and cellular nucleus deformation. The positive cells ofproliferating cell nuclear antigen were increased significantly(P0.05). CONCLUSION: The present study demonstrated that pancreaticobiliary maljunction can lead to the injuries of the liver, pancreas and gallbladder.     

Acute pancreatitis associated with anomalous union of the pancreaticobiliary ductal system.

Between 1978 and 1989, 13 of 48 patients with anomalous union of the pancreaticobiliary ductal system (AUPBD) were diagnosed as having acute pancreatitis. We have studied the clinical, radiologic, and surgical features of these 13 patients. A transient rise in the intraductal pressure of the pancreatic duct during an episode of abdominal pain is responsible for pancreatitis in patients with AUPBD. This rise in the intraductal pressure must be due to bile reflux into the pancreatic duct when an abnormally long common channel is blocked by cholelithiasis, protein plug, or dysfunction of the sphincter of Oddi. The pancreatitis resolves when the common channel obstruction is removed, and bile and pancreatic juice flow easily into the duodenum. We believe that this phenomenon is responsible for acute relapsing pancreatitis. It is our belief that the pancreas appears almost normal during symptom-free intervals.     

Bile duct schwannoma developed in the remnant choledochal cyst—a case associated with total agenesis of the dorsal pancreas

A 59-year-old Japanese woman was referred to our hospital due to upper abdominal pain. At the age of 44, she was diagnosed with a congenital choledochal cyst, Todani's type Ic. She then underwent bypass operation with end-to-side choledochojejunostomy with Roux-en-Y technique as well as cholecystectomy. Magnetic resonance cholangiopancreatography revealed an 'oval' shaped cystic lesion with a maximal diameter of 25 mm, which had been 'spindle' shaped with a maximal diameter of 18 mm, 15 years ago. It also showed an anomalous pancreaticobiliary ductal union. In addition, a complete absence of the dorsal primordia of pancreas was revealed by magnetic resonance image and computed tomography scan. The patient underwent the surgical exploration for the resection of the 'oval' shaped cystic lesion. Haematoxylin and eosin staining of the thin section of the resected cyst showed a compact spindle cell pattern which was compatible with schwannoma, Antoni type A, which was confirmed by immunocytochemical technique. We present a very interesting case showing choledochal cyst, anomalous pancreaticobiliary ductal union, total agenesis of the dorsal pancreas and late-development of bile duct schwannoma in the remnant choledochal cyst.     

Metachronous double cancer of the gallbladder and pancreas associated with pancreaticobiliary maljunction

A 50-year-old Japanese woman complained of abdominal and back pain. Ten years previously she had undergone cholecystectomy, choledochectomy, and Roux-en-Y choledochojejunostomy for gallbladder cancer associated with pancreaticobiliary maljunction without bile duct dilatation. On the present admission, ultrasonography (US) and computed tomography (CT) demonstrated a large mass, 60 mm in size, in the pancreatic tail. Endoscopic retrograde cholangiopancreatography (ERCP) showed obstruction of the main pancreatic duct in the tail of the pancreas and revealed that the pancreatic duct was joined to the bile duct 25 mm above the papilla of Vater. The patient underwent distal pancreatectomy, splenectomy, left adrenalectomy, and partial gastrectomy. Histological examination revealed moderately differentiated ductal adenocarcinoma that had invaded to the proper muscle of the stomach. Double cancer of the gallbladder and pancreas in a patient with pancreaticobiliary maljunction is rare. Although the etiology of cancer of the pancreas associated with pancreaticobiliary maljunction is unclear, we should pay close attention to the pancreas as well as the biliary tract during the long-term follow-up of patients with pancreaticobiliary maljunction after they have undergone a choledochojejunostomy.     

A case of pancreatic cyst containing gall sludge.

A case of acquired retention cyst of the pancreas containing gall sludge was reported. Gallstones or gall sludge recognized in pancreatic cysts has not been reported. Histological examination suggested that the gall sludge in the pancreatic cyst was caused by the reflux of bile into the pancreatic duct through the papilla of Vater. However, endoscopic retrograde cholangiopancreatography showed no anomalous junction of the pancreatico-biliary ductal system. Crystallization of the components of bile can occur in the pancreas even in a case without anomalous junction of the pancreatico-biliary ductal system.