胰胆管合流异常与胆道肿瘤

胰胆管合流异常(anomalous Dancreaticobiliary ductal union，APBDU)于1969年由Babbitt等^[1]首次报道，随着内镜逆行性胆管胰管造影术(endoscopic retrograde cholangiopancreatography，ERCP)和磁共振胰胆管成像(magnetic resonance cholangiography，MRCP)等影像学检查的广泛应用，APBDU检出率有增多趋势。APBDU与     

胰胆管合流异常和胆道疾病

胰胆管合流异常和胆道疾病上海第二医科大学附属仁济医院（２００００１）季福，施维锦由于内镜逆行胰胆管造影（ＥＲＣＰ）和经皮经肝胆管穿刺造影（ＰＴＣ）在临床上的广泛应用，发现胰胆管合流异常（ＡＪＰＢＤ）的病例增多。自从１９６９年Ｂａｂｉｔｔ首先提出ＡＪＰ...     

胰胆管合流异常与胆道疾病的关系

我院自1980-1994年间经影像学检查证实胰胍管合流异常28例．其中合并胆总管囊状扩张15例，柱状扩张7例，胆囊癌变4例，胆总管癌变1例。本文就胰胆管合流异常的慨念，分型及与胆道疾患发病之间的关系，病理和病因方面进行了讨论，井对胰胆管台流异常并发胆道疾患时的特殊处理原则进行探讨。     

原发胆道结石与胰胆管合流异常关系的临床初步研究

原发胆道结石多为胆红素钙结石,其病因未明,一般认为与胆道感染,胆流淤滞,胆汁成份改变有关.近来对胰胆管合流异常的研究发现,长期胰液胆道返流可刺激胆管壁和改变胆汁成分,导致胆管扩张或结石形成[1].原发性胆道结石病例都有不同程度的胆管扩张和胆汁病理性外观变化,其胆道内是否有胰液返流尚不清楚.本文旨在探讨原发性胆道结石病人胆道内有关胰液返流的临床证据及其与胰胆管合流异常的关系.     

胰胆管合流异常致胆总管扩张症的诊断治疗

目的探讨胰胆管合流异常致胆总管扩张症的诊断和治疗措施,减少胆道肿瘤的发生率。方法回顾分析13例,从发病原因、临床症状及手术方法进行探讨。结果反复发作胆管炎是主要临床表现,ERCP检查发现胰胆管合流部压力高,胆汁中淀粉酶>10 000 U/L可确诊,治疗应彻底切除扩张之胆总管,胆肠吻合术。结论胰胆管合流异常致胆总管扩张症是潜在恶变发生率较高的疾病,本组病理证实为38.4%,临床诊断和治疗应高度重视。     

胰胆管合流异常的病理特征与诊治进展

胰胆管合流异常 (pancreaticobiliary maljunction,PBM)是胰管和胆总管异常汇合的一种先天性畸形 [1 ]。从 1916年 Kizu-mi首先提出 PBM这一概念 ,至 1978年日本学者因此成立“胰胆管合流异常研究会”,PBM已日渐引起国内外广泛关注 ,对PBM基础及临床的研究正逐步深入。1　PBM的病理特征约 75 %的正常人胆总管与主胰管在十二指肠粘膜下汇合成共通管 ,并随着年龄逐渐增长。共通管周围及近端具有 Oddi氏括约肌 ,其中胆总管括约肌部分恒定存在 ,在神经与体液双重因素的调节下可控制胆汁的正常排出 ,亦可防止胰液逆流入胆管。据 1991年日…     

胰胆管合流异常与胆胰肿瘤发生的研究进展

近年来，随着磁共振胰胆管成像( magnetic resonance cholangiography,MRCP) 和内镜逆行性胆管胰管造影术( endoscopic retrograde cholangiopancreatography, ERCP)等影像学检查的广泛应用，胰胆管合流异常(pancreaticobiliary realjunction，PBM)病例的检出率有较大幅度提高，PBM与胆胰部疾病的相关性也越来越引起重视。胰胆管合流异常的概念首先由Kozumi和Kodama于1916年提出，他们是从先天性胆管囊肿的病例中发现胰胆管汇合的异常。直到1969年，Babbitt等从病因学方面报道了PBM与先天性胆总管囊肿的相关性后，PBM才开始作为一个独立的疾病诊断，无论其是否合并有胆管囊肿。随后的研究也表明，PBM不仅与先天性胆总管囊肿有关，还与胆道结石、胆囊炎、急慢性胰腺炎等多种疾病的发生相关。最近许多研究者发现PBM与胆胰部恶性肿瘤的发生有着密切的关系[2，3]，这为研究胆胰肿瘤发生的机制提供了新的思路，现综述如下。     

胰胆管合流异常三例

胰胆管汇合异常是指胆总管与主胰管在十二指肠壁外汇合的一种少见的解剖异常 ,可引起许多胆胰系统疾病。我院 2 8例术后胆道造影患者中 ,有 8例出现主胰管显影 ,其中 3例清晰显示胆总管与主胰管在十二指肠壁外汇合 ,现对其作一报道。病历摘要例 1:男 ,5 7岁。无痛性黄疸 10ｄ以“肝门部胆管癌”住院。术中见 :肿瘤位于肝门部 ,直径 4ｃｍ ,固定。以胆道探子扩张右肝管 ,置入 6ｃｍ长镍钛记忆合金胆道支架 ,胆总管内置 1根引流管 ,肿瘤表面以钛夹标志。术后 10ｄ经胆管引流管行胆道造影 ,见胆总管直径 0 .8ｃｍ ,肝内胆管直径 1.0ｃｍ ,主胰…     

胰胆管合流异常胆道损伤抗氧化治疗的实验研究

目的 研究胰胆管合流异常(PBM)胆道损伤的抗氧化治疗的效果.方法 选取13只健康杂种猫,建立PBM动物模型后随机分为2组:7只不进行抗氧化治疗(非抗氧化治疗组),6只行抗氧化治疗(抗氧化治疗组);以动物建模术前情况作为对照.建模术后饲养6个月观察胆囊组织的病理学改变,检测过氧化产物丙二醛(maleic dialdehyde,MDA)的变化情况、PCNA的表达情况以及胆汁淀粉酶水平.结果 13只动物建模后均存活6个月.非抗氧化治疗组较正常对照组胆管增粗,胆囊壁增厚,胆囊内胆汁稠厚;抗氧化治疗组和非抗氧化治疗组相比上述改变无明显不同.光镜下见正常对照组的胆囊黏膜呈指状,黏膜数目少,无增生;非抗氧化治疗组的胆囊黏膜增生及炎性细胞浸润,部分纤维组织增生.电镜下见正常对照组的胆囊黏膜上皮细胞排列紧密、规则;非抗氧化治疗组胆囊黏膜上皮细胞的内质网扩张成囊状,细胞间隙增宽,细胞核变形;抗氧化治疗组的上述改变较非抗氧化治疗组好转.胆汁淀粉酶正常对照组为(203.02±65.04)U,非抗氧化治疗组为(9 368.09±2 204.42)U,抗氧化治疗组为(8 746.25±2 077.95)U,后2组高于正常对照组(P=0.003),但后2组间比较差异无统计学意义(P=0.642).PCNA表达阳性细胞所占百分比正常对照组为(7.29±2.71)％,非抗氧化治疗组为(54.71±10.90)％,抗氧化治疗组为(48.17±l3.06)％,3组间相比差异有统计学意义(F=48.11,P=-0.001),其中非抗氧化治疗组高于抗氧化治疗组(P=0.001).MDA正常对照组为(1.095±0.653) nmol/mg prot,非抗氧化治疗组为(2.745±1.533)nmol/mg prot,抗氧化治疗组为(1.302±0.771) nmol/mg prot,3组间相比差异有统计学意义(F=5.17,P=0.017),其中非抗氧化治疗组高于抗氧化治疗组(P=0.017).结论 抗氧化治疗对PBM有效.     

Extracystic biliary carcinoma associated with anomalous pancreaticobiliary junction and cysts

Anomalous pancreaticobiliary junction with cystic dilatation of the biliary tract is usually associated with carcinoma arising from the cyst wall. We report an extracystic location of biliary carcinoma in the presence of anomalous pancreaticobiliary junction and cysts in a patient with obstruction of the origin of the left hepatic duct who underwent hepatobiliary resection. Cholangiocarcinoma was found to have arisen in a noncystic left hepatic duct, in conjunction with cystic dilatation involving both the cystic and common bile ducts. The present case supports a relationship between anomalous pancreaticobiliary junction and biliary carcinogenesis that may affect the extracystic biliary tree.     

Self-expandable metallic stents for malignant biliary obstruction with an anomalous pancreaticobiliary junction

Background Anomalous pancreaticobiliary junction (APBJ) is associated with pancreaticobiliary cancer. Limited data are available on endoscopic biliary drainage for unresectable malignant biliary obstruction with APBJ. This study evaluated the efficacy and safety of self-expandable metallic stents (EMSs) for the management of malignant biliary obstruction with APBJ. Methods Between 1993 and 2005, 324 patients with unresectable malignant biliary obstruction underwent insertion of an EMS. Six of these patients with concomitant APBJ constituted the subjects of this study. Early (≤30 days after EMS insertion) and late (>30 days after EMS insertion) stent-related complications and stent patency were evaluated in these six patients. Results The cause of biliary obstruction was gallbladder cancer in four patients and pancreatic cancer in two patients. Uncovered EMSs were inserted across the common channel without performance of a biliary sphincterotomy. The diameter of the uncovered EMS used was based on the diameter of the common channel. For all six patients, endoscopic biliary drainage was successful, and their jaundice subsided steadily. None of the six patients experienced early complications, including acute pancreatitis. The mean stent-related complication-free period was 163 days. Stent occlusion caused by tumor ingrowth occurred in two patients. Acute cholangitis and cholecystitis were observed in one patient each. Conclusions Uncovered EMSs are effective for palliation of unresectable malignant biliary obstruction in patients who have APBJ without increasing the risk of stent-related early complications.     

胰胆管合流异常并发急性胰腺炎的诊治策略及文献复习

目的 探讨胰胆管合流异常并发急性胰腺炎的诊治策略.方法 回顾性分析22例胰胆管合流异常病人的临床资料.结果 22例中急性胰腺炎发生7例,占31.8%(7/22),其中C-P型5例(71.4%,5/7),P-C型2例(28.6%,2/7).7例均行ERCP+EST+ENBD,2例伴胆总管结石者行网篮取石,2例伴胆囊结石的病人在急性胰腺炎稳定后行胆囊切除术.所有病人均成功治愈,随访一年,未有胰腺炎复发.结论 胰胆管合流异常常并发急性胰腺炎的发生,C-P型及合并胆石症者更常见;ERCP+EST+ENBD+胆囊切除术是防治此类胰腺炎的有效方法.     

Clinical experience of biliary tract carcinoma associated with anomalous union of the pancreaticobiliary ductal system

Between 1978 and 1988, 15 patients with gallbladder cancer and 2 patients with bile duct cancer were seen among 49 patients with anomalous union of the pancreaticobiliary ductal system. Radiographic findings revealed two types of this anomalous condition: one in which the pancreatic duct entered the common bile duct(type 1) and one in which the common bile duct entered the pancreatic duct (type 2). In gallbladder cancer, the common bile duct presented no dilatation, or in some patients, mild dilatation, and type-1 anomalous union was frequently found among these patients. In contrast, the two patients with bile duct cancer had cystic dilatation of the common bile duct and type-2 anomalous union. The bile amylase level, which was determined in seven patients, was extremely high in all the patients. Histopathologically, the tumors in most patients showed papillary to papillo-tubular proliferation in the mucosal layer while atypical epithelial hyperplasia was noted in the vicinity of the tumor area. These findings suggest that this congenital anomaly in both ducts results in a loss of the normal sphincteric mechanism of the doudenal papilla, and that chronic relapsing cholecystitis or cholangitis, caused by the reflux of pancreatic juice into the biliary tract, can induced progressive changes to atypical epithelial hyperplasia which may develop into carcinoma.     

Type classification of anomalous pancreaticobiliary junction by ERCP

The role of endoscopic retrograde cholangiopancreatography (ERCP) in the preoperative assessment of anomalous pancreaticobiliary junction was retrospectively evaluated in 74 consecutive patients (19 males and 55 females; aged 0–80 years). Sixty-three patients had congenital biliary dilatation and 11 did not. Type classification of congenital biliary dilatation was possible by ERCP alone in 45 patients (71%). The main causes of classification failure were previous bilio-enteric anastomosis and restriction of postural changes during ERCP due to general anesthesia in pediatric patients. Classification of anomalous junction was possible in 69 patients (93%). Technical difficulty in ERCP caused classification failure in 5 patients. Neoplastic lesions were found in 12 patients (16%) and all but 1 were correctly diagnosed by ERCP. We conclude that ERCP plays an important role in the preoperative diagnosis and type classification of anomalous pancreaticobiliary junction and congenital biliary dilatation.     

胰胆管合流异常并发急性胰腺炎的诊治策略及文献复习

目的 探讨胰胆管合流异常并发急性胰腺炎的诊治策略.方法 回顾性分析22例胰胆管合流异常病人的临床资料.结果 22例中急性胰腺炎发生7例,占31.8%(7/22),其中C-P型5例(71.4%,5/7),P-C型2例(28.6%,2/7).7例均行ERCP+EST+ENBD,2例伴胆总管结石者行网篮取石,2例伴胆囊结石的病人在急性胰腺炎稳定后行胆囊切除术.所有病人均成功治愈,随访一年,未有胰腺炎复发.结论 胰胆管合流异常常并发急性胰腺炎的发生,C-P型及合并胆石症者更常见;ERCP+EST+ENBD+胆囊切除术是防治此类胰腺炎的有效方法.     

Carcinoma in adenoma of the gallbladder in a patient with anomalous pancreaticobiliary ductal junction

We present a case of carcinoma in adenoma of the gallbladder with anomalous pancreaticobiliary ductal junction (APBDJ) in a 60-year-old Japanese woman. The patient had no abdominal symptoms. Serum levels of carcinoembryonic antigen, carbohydrate antigen 19-9, elastase 1, and α-fetoprotein were all within normal limits. Ultrasonography demonstrated two irregular hyperechoic lesions of the gallbladder. Computed tomography showed two soft-tissue density masses in the gallbladder. Endoscopic retrograde cholangiopancreatography showed APBDJ and two protruding lesions in the gallbladder. Angiography displayed a hypervascular lesion fed by the cystic artery. The patient underwent total cholecystectomy; the diagnosis of the intraoperative frozen section was well differentiated adenocarcinoma with possible mucosal invasion. Amylase level in the gallbladder bile was 90600 IU/l. Macroscopically, there were two polyps in the gallbladder. The larger one, 3.5 cm in diameter, was adenocarcinoma in adenoma, and the smaller one, an inflammatory polyp. We briefly discuss the relationship among adenoma, adenocarcinoma of the gallbladder, and APBDJ.     

正常胰胆管合流病人胆汁淀粉酶升高的病因分析及内镜治疗

目的:探讨正常胰胆管合流胆汁淀粉酶升高的原因及内镜治疗效果.方法:回顾性分析2016年1月至2019年12月96例正常胰胆管合流行腹腔镜胆囊切除术病人.切除胆囊前抽取并测定胆囊胆汁淀粉酶(gallbladder bile amylase,GBA).部分病人行十二指肠镜检查、内镜逆行胰胆管造影术(endoscopic r...     

胰胆管合流异常胰腺损伤的抗氧化治疗实验研究

目的：研究胰胆管合流异常（APBDU）胰腺损伤的抗氧化治疗。方法：采用13只健康杂种猫建立APBDU动物模型,随机分为A组（7只,不作抗氧化治疗）、B组（6只,抗氧化治疗）;并将13只的术前情况作为对照。饲养6个月,观察其胰腺的病理,胰腺过氧化产物丙二醛（MDA）变化。结果：13只猫均成活6个月;术前胰腺均呈粉红色。6个月后,A组胰腺颜色加重,充血、水肿,其中3只可见扩张的胰管;B组胰腺颜色稍加重,但无胰管扩张及腺体水肿。光镜下,A组有3只猫的胰腺可见炎性细胞浸润,4只见间质血管增生、白细胞附壁;而B组中未见炎性细胞浸润,仅2只间质血管内白细胞增多。电镜下,A组粗面内质网扩张;线粒体数量增多,体积增大,崩解;高尔基复合体发达,数量增多。而B组的胰酶分泌减少,较A组好转。对照组的MDA值为（1.234±0.716）μmol/gprot（微摩尔/克蛋白）,而A组为（2.900±1.888）μmol/gprot,B组为（0.927±0.880）μmol/gprot。ANOVA检验,P=0.0215,F=4.80,有统计学意义。结论：抗氧化治疗对APBDU有效。