Problems of pancreatitis

Pancreatitis is not one disease but several and perhaps many. Diagnosis is imperfect in all forms and the usual lack of histologic material has hampered attempts to understand the pathogenesis and possible interrelationships of the different forms of pancreatic inflammation. Acute pancreatitis does not as a rule evolve into chronic pancreatitis, even after multiple recurrences. Recurrent acute attacks can be ended by identifying and treating the factor causing the disease, including recently recognized entities such as accessory papilla stenosis associated with pancreas divisum. Attempts to improve the treatment of severe acute pancreatitis are focussing upon preventing injury to pancreatic cell structures, enhancing endogenous mechanisms for capture and disposal of activated enzymes, and upon early detection and debridement of damaged pancreatic and peripancreatic tissues. Pancreatic duct stricture or obstruction as a consequence of scarring from necrotizing pancreatitis may produce recurrent symptoms, now designated as obstructive pancreatitis. Obstructive pancreatitis has its own unique histologic characteristics and is appropriately treated by resection of the blocked segment of pancreas when the point of obstruction is distal to the papilla. Chronic pancreatitis differs from acute or obstructive pancreatitis in that it is difficult or impossible to halt its progression. The role of intraductal protein precipitates, whether of enzymes or perhaps of other unique pancreatic secretory proteins, in the pathogenesis of the disease is being evaluated. The goal of surgical treatment is not to cure, but to reduce pain, overcome associated obstruction of the bile duct or duodenum, and to treat pancreatic duct disruptions including pseudocysts and internal pancreatic fistulas. Because continuing deterioration of pancreatic function is to be expected in chronic pancreatitis, maximum conservation of pancreatic tissue by avoiding resectional procedures is advisable.     

Classification and pathogenesis of pancreatitis

Full functional and morphologic restitution of the pancreas is possible after an attack of acute pancreatitis if the initiating agent or process is removed, whereas chronic pancreatitis is associated with irreversible changes. Most attacks of acute pancreatitis are related to biliary tract stone disease, and it is likely that the offending stone causes obstruction of the pancreatic duct with ductal hypertension. Some recent experimental observations suggest that acute pancreatitis may involve intra-acinar cell activation of digestive enzymes by lysosomal hydrolases. Most patients with chronic pancreatitis develop their disease after many years of ethanol abuse, but the events underlying the pathogenesis of chronic pancreatitis are not known.     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.     

慢性胰腺炎的个体化外科干预

慢性胰腺炎发病机制复杂,病情进展多变,导致外科干预时机及手术方式的选择存在一定困难。慢性胰腺炎的治疗应依据个体化原则去除病灶,尽量保存正常胰腺实质,延缓胰腺内、外分泌功能损害的进程,改善患者生命质量,降低胰腺癌发生的风险。慢性胰腺炎患者早期可考虑保守和内镜治疗,胰管梗阻、狭窄合并结石、胰腺实质广泛钙化等慢性胰腺炎患者则需手术治疗。Frey术适合以胰管扩张和胰管结石为主的慢性胰腺炎患者,Beger术适合以胰头部炎性肿块或胰头部钙化为主的慢性胰腺炎患者。     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.     

慢性胰腺炎的手术适应证和术式选择

目的提高慢性胰腺炎的外科治疗效果. 方法回顾性总结分析55例慢性胰腺炎外科治疗资料.发病因素:嗜酒5年以上、胆系结石、急性胰腺炎病史分别占38.2%,29.1%和20.0%.主要临床表现:慢性腹痛、梗阻性黄疸、体重减轻、消化不良、糖尿病分别为98.2%,38.2%,34.5%,20.0%和10.9%.全组均因慢性腹痛或伴有胰管和(/或)胆管梗阻、结石、胰腺钙化、肿块、假性囊肿等行外科治疗,共采用了10种术式. 结果无手术死亡和严重并发症.术后效果良好43例(78.2%),症状减轻好转10例(18.2%),无效2例(3.6%). 结论慢性胰腺炎长期慢性腹痛并胰胆管梗阻、结石、肿块、假性囊肿适于外科治疗,应根据病变类型和特点选择不同的术式.胰管梗阻扩张、结石或假性囊肿宜行胰管或囊肿空肠吻合,胰头肿块并胆、胰管梗阻可行胰头十二指肠切除或胆胰管空肠吻合术.     

The role of biliary obstruction in the pathogenesis of acute pancreatitis in the opossum

Pancreatitis was induced in the opossum by occluding the common bile duct above or below the entrance of the pancreatic duct. The common channel theory was tested by evaluating the effect of preligation of the pancreatic duct to prevent the reflux of bile after ligation of the distal common duct. The severity of the disease was determined by histologic grading of the degree of pancreatic tissue necrosis. Serum amylase, lipase, and calcium were determined. Concomitant obstruction of the biliary and pancreatic ducts produced severe necrotizing pancreatitis whether or not bile reflux was present. Pancreatic ductal obstruction alone was associated with acinar atrophy and mild interstitial pancreatitis. Biliary obstruction alone above the entrance of the pancreatic duct resulted in marked hyperemia of the gland but without histologic evidence of pancreatic inflammation. A positive bacterial culture of the pancreas was obtained in only four of 36 opossums in a distribution to suggest random contamination. There was an inverse correlation between calcium levels and the degree of tissue necrosis. This study demonstrates that biliary obstruction rather than bile reflux into the pancreas is a requisite for the pathogenesis of severe biliary pancreatitis in this model.     

Clinical evidence of pathogenesis in chronic pancreatitis

Chronic pancreatitis is a continuing inflammatory disease characterized by irreversible morphological change and, typically, by pain and permanent impairment of function. The pathogenesis of pancreatitis, either acute or chronic, is still controversial. There have been no widely accepted concepts to provide a reasonable explanation linking the known etiological factors and the pathophysiological aspects of the disease. Alcohol is undoubtedly the major etiological factor in most countries, and the relative importance of alcohol as a cause of chronic pancreatitis ranges from 40% to 90% in various countries. As fewer than 10% of alcoholics develop chronic pancreatitis, other nutritional or genetic influences are likely to be involved in the pathogenesis of alcoholic pancreatitis. Accessory pancreas incidentally found in patients with chronic alcoholic pancreatitis does not always have the pathological findings seen in the main pancreas. Integrity of the pancreatic duct seems to be another important factor for chronic alcoholic pancreatitis. Gene mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), cationic trypsinogen, and pancreatic secretory trypsin inhibitor have been investigated in idiopathic chronic pancreatitis. Molecular and cell biology research during the past few years has elucidated pathophysiological factors that are involved in the pathogenesis of chronic pancreatitis, but cannot demonstrate a common pathway between etiological factors and the pathogenesis or development of the disease. Received: March 20, 2002 / Accepted: April 15, 2002 Offprint requests to: T. Hayakawa     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.

Abstract：

Objective To explore the diagnostic methods and reasonable surgical interventions for the chronic obstructive pancreatitis due to the inflammatory lesions at the opening of the pancreatic duct Methods From January 2002 to November 2010 the data of 28 patients who were diagnosed as the chronic obstructive pancreatitis (COP) was retrospectively reviewed. Out of the 28 patients, it was analyzed that the clinical manifestations, diagnostic methods, surgical finding and surgical interventions of the 13 patients who were diagnosed as COP due to the inflammatory lesions at the opening of the pancreatic duct in the exploratory operation accompanying recurrent acute abdominal pain with increased serum amylase and lipase,dilation of entire pancreatic duct on imaging before surgery. The conditions included pain recrudescence,quality of life, pancreatic changes on imaging and the serum amylase and lipase after surgery were recorded.Results All the 13 patients had clinical manifestations of COP. However, 12 patients had different manifestations on imaging from those chronic pancreatitis imaging due to tumors at the duodenal papilla,ampulla or inner pancreatic duct. Via exploratory operation and magnetic resonance cholangiopancreatography (MRCP) , there were short pancreaticobiliary common channel or pancreas divisum existing in most patients. There was no acute abdominal pain with the increased serum amylase and lipase in the 12 patients who receiving the transduodenal mastoid, ampulla and pancreatic ductal opening incision and plasty, the paramastoideus incision and plasty in the visit Conclusions The imaging character of COP due to the inflammatory lesions at the opening of the pancreatic duct is the dilation of the pancreatic duct without the chronic obstruction in the bile duct The patients with short pancreaticobiliary common channel or pancreas divisum easily suffer COP due to the stenosis of the pancreatic ductal opening caused by the duodenal mastoiditis or paramastoiditis. The local plasty surgery to correct the stenosis at the pancreatic ductal opening and improve the drainage of the pancreatic duct is an easy and effective management.     

Effect of platelet-activating factor antagonists (BN-52021, WEB-2170, and BB-882) on bacterial translocation in acute pancreatitis

Bacterial translocation is an important source of pancreas infection in acute pancreatitis. The effect of platelet-activating factor (PAF) in the pathogenesis of acute pancreatitis has been proved in various studies. The aim of this study was to determine whether potent PAF antagonists influence bacterial translocation in acute pancreatitis. Acute pancreatitis was induced in 62 Wistar rats by injection of 2.5% sodium taurocholate into the biliopancreatic duct. The rats treated with PAF factor antagonists received intravenous injection of WEB-2170 (10 mg/kg), lexipafant (5 mg/kg), and BN-52021 (5 mg/kg) 30 minutes before induction of acute pancreatitis. Six hours after induction of acute pancreatitis, bacteriologic cultures and histologic scoring of tissues were performed. There was a statistically significant reduction in bacterial translocation to the mesenteric lymph nodes and liver but not to the pancreas of the rats treated with PAF antagonists. No significant increase in the intestinal bacterial population of any group was found. There were no statistical differences between the pancreatic histologic scores of the groups. PAF antagonists reduced bacterial translocation to distant sites other than the pancreas, preventing the bacterial dissemination that occurs in the early phase of acute pancreatitis and may have beneficial effects on the evolution of this disease.     

Pancreas divisum and the dominant dorsal duct syndrome

Pancreas divisum, the most frequent congenital malformation of the pancreas, results from the absence of embryologic fusion of the dorsal and ventral pancreatic ducts which keep an autonomy of drainage. The dorsal pancreatic duct is dominant and drains the major part of the pancreatic fluid through a non adapted accessory papilla. The high prevalence of pancreas divisum in patients presenting recurrent acute pancreatitis, the presence of obstructive pancreatitis electively located on the dorsal pancreatic duct and the results of the treatments targeted on the accessory papilla are the arguments pleading for the pathogenic character of the pancreas divisum. Currently, the diagnosis of pancreas divisum is based on magnetic resonance imaging. For symptomatic patients (after exclusion of patients with intestinal functional disorders), results of endoscopic sphincterotomy or surgical sphincteroplasty are favourable in 75% of patients with recurrent acute pancreatitis. They are worse in patients with chronic pain. Surgical sphincteroplasty must be discussed in the same manner as the endoscopic treatment for sometimes avoiding multiplication of the procedures.     

Complete obstruction of the lower common bile duct caused by autoimmune pancreatitis: is biliary reconstruction really necessary?

Recent observations suggest that an immune response is involved in the development of chronic pancreatitis. We report a case of autoimmune pancreatitis in a patient who showed complete obstruction of the lower common bile duct. A 63-year-old man was admitted to a local hospital, complaining of appetite loss and back pain. The patient had obstructive jaundice, and percutaneous transhepatic gallbladder drainage was performed. Fluorography through the biliary drainage catheter showed complete obstruction of the lower common bile duct. The patient had no history of alcohol consumption and no family history of pancreatic disease. Physical examination revealed an elastic hard mass palpable in the upper abdomen. Abdominal ultrasound and abdominal computed tomography (CT) scans showed enlargement of the pancreas head. While autoimmune pancreatitis was highly likely, due to the patients high serum immunoglobulin level, the possibility of carcinoma of the pancreas and/or lower common bile duct could not be ruled out. Laparotomy was performed, and wedge biopsy samples from the pancreas head and body revealed severe chronic pancreatitis with infiltration of reactive lymphocytes, a finding which was compatible with autoimmune pancreatitis. Cholecystectomy and biliary reconstruction, using choledochojejunostomy, were performed, because the complete bile duct obstruction was considered to be irreversible, due to severe fibrosis. After the operation, prednisolone (30mg/day) was given orally for 1 month, and the entire pancreas regressed to a normal size. Complete obstruction of the common bile duct caused by autoimmune pancreatitis has not been reported previously; this phenomenon provides an insight into autoimmune pancreatitis and provokes a controversy regarding whether biliary reconstruction is needed for the treatment of complete biliary obstruction caused by autoimmune pancreatitis.     

False pancreas divisum. Acquired pancreatic duct obstruction simulating the congenital anomaly.

Eight patients with recurrent acute pancreatitis were found by ERCP to have foreshortening of the duct of Wirsung simulating the radiographic appearance of the congenital anomaly pancreas divisum. In contrast to 44 patients with true pancreas divisum, who were predominantly young (mean 32 years), nonalcoholic (42/44), and female (34/44), patients with false pancreas divisum were older (mean 48 years), male (7/8), and alcoholic (5/8). False pancreas divisum is most often an acquired obstructing lesion resulting from irremediable injury to the pancreatic duct during acute pancreatitis, often associated with pseudocyst formation and subsequent healing by scar at the site of duct injury. Appreciation of the radiographic differences between pancreatograms in true and false pancreas divisum and the different findings at operation allow for proper selection of therapy. Whereas accessory papilla sphincteroplasty appears to be effective for recurrent pancreatitis associated with true pancreas divisum, false pancreas divisum requires distal pancreatectomy or pancreaticojejunostomy to overcome the irreversible obstruction of the main pancreatic duct.     

Pancreatic duct obstruction itself induces expression of alpha smooth muscle actin in pancreatic stellate cells

BACKGROUND: Pancreatic stellate cells (PSCs) are thought to be responsible for pancreatic fibrosis. Although fibrosis is a major characteristic of chronic pancreatitis (CP) induced by pancreatic duct obstruction, it is unclear whether pancreatic duct obstruction itself activates PSCs. METHODS: To test the hypothesis that pancreatic duct obstruction activates PSCs, clinical and experimental analyses were performed using alpha smooth muscle actin (alpha-SMA) as a marker of their activation. In clinical analysis, surgical specimens from the patients with pancreatic cancer or cancer of the papilla Vater were classified into two groups with or without duct obstruction. alpha-SMA expression was examined on these specimens, and the difference between two groups was evaluated. In animal experiment, duct ligation-induced pancreatitis was developed in rats by ligating the secondary pancreatic duct in duodenal segment, and the expression of alpha-SMA was examined. RESULTS: In clinical analysis, the specimens from the pancreas with duct obstruction (14 cases) expressed alpha-SMA significantly stronger than those from the pancreas without duct obstruction (7 cases). All specimens in the former expressed alpha-SMA, but 4 specimens from the latter did not at all (P < 0.05). In animal experiment, alpha-SMA expression was detected 7 days after the ligation and was increased on the 10th day. CONCLUSIONS:We can assume that pancreatic duct obstruction itself activates PSCs. This mechanism may play roles in the development of CP from multiple origins.     

Chronic obstructive pancreatitis after healing of a necrotic pseudocyst

Seven patients presented with chronic pancreatitis localized upstream to a complete stenosis of the main pancreatic duct in its median part. This stenosis seemed to be secondary to the healing of a necrotic pseudocyst after either acute pancreatitis (four patients) or blunt abdominal trauma (three patients). In five patients, after spontaneous regression of the clinical symptoms of the initial pseudocyst, a silent period which ranged from 2 to 5 months was followed by recurrent attacks of pain of lesser intensity and shorter duration (less than 2 days) than observed during the evolution of the initial pseudocyst. These attacks of pain decreased spontaneously with time, probably because of the atrophy of the left part of the pancreas drained by the obstructed duct (in 6 months to 2.5 years). In 2 patients, the initial pseudocyst was revealed at the same time as the obstructive pancreatitis.The histologic features of chronic obstructive pancreatitis have been described. Fibrosis uniformly spread throughout the diseased pancreas with uniform atrophy of the exocrine parenchyma. Dilated ducts showed far less damages than in chronic calcifying pancreatitis. Since spontaneous clinical healing may be observed, surgical treatment is often useless. Only in patients with severe or frequent attacks is a Roux-Y anastomosis with the dilated part of the main pancreatic duct indicated rather than a risky left pancreatectomy.     

T cell lymphoplasmacellular and eosinophilic infiltration of the pancreas with involvement of the gallbladder and duodenum in non-alcoholic duct-destructive chronic pancreatitis

Background Non-alcoholic duct destructive chronic pancreatitis is a rare entity with specific pathological features. The majority of the patients are from Japan. We report a case with involvement of the distal bile duct, the gallbladder, the duodenum and the ampulla, and present a review of patients from Europe and the USA since 1997.Case presentation A 56-year-old man presented with a 3-month history of mild acute pancreatitis and obstructive jaundice, followed by increasing weight loss, lethargy and epigastric pain. CT showed a mass in the head of the pancreas. ERCP demonstrated a smooth stricture of the intra-pancreatic main bile duct and an irregular, incomplete, stricture in the main pancreatic duct. A pancreatic cancer could not be reliably excluded, and, therefore, he underwent a pylorus-preserving Kausch–Whipples pancreatoduodenectomy.Results Histopathology showed typical peri-ductal T cell-rich lymphoplasmacellular and eosinophilic infiltration of the pancreas, with involvement of the distal bile duct but, also, unusual inflammatory infiltration of the gallbladder, the duodenum and the ampulla.Conclusion The inflammatory process in non-alcoholic duct-destructive chronic pancreatitis can affect the entire pancreato-biliary region and mimics pancreatic cancer. Currently, there are no definitive criteria for pre-operative diagnosis, so it is very difficult for one to avoid resection.     

Intraductal papillary-mucinous tumor of the pancreas head with complete absence of the ventral pancreatic duct of Wirsung

A case of intraductal papillary mucinous tumor of the pancreas with complete absence of the ventral pancreatic duct of Wirsung is presented. A 74-year-old Japanese man was admitted to our hospital because of elevated serum amylase concentration. Abdominal computed tomography (CT) scanning revealed diffuse dilatation of the main pancreatic duct and a diffuse and uncircumscribed area with heterogeneous density in the pancreas head. Endoscopic retrograde cholangiopancreatography revealed that the main pancreatic duct was connected with an accessory papilla and was diffusely dilated, without any irregularity of the duct wall being observed in the entire length of the duct. The common bile duct was detected only by cannulation through Vaters papilla, and no pancreatic duct or its communicating branch was found. Some branches, directed to the dorsal portion of the pancreas head, were found arising from the accessory pancreatic duct. Intraductal ultrasound examination performed through the accessory papilla and the common bile duct revealed a small tumor with a heterogeneous echo level in the pancreas head. From these findings, intraductal papillary-mucinous tumor (IPMT) occurring in the pancreas head was diagnosed, and pylorus-preserving pancreaticoduodenectomy was performed. The resected specimen revealed IPMT in the pancreas head. A roentgenographic study of the resected specimen revealed a defect caused by the tumor located in the pancreatic duct connected with the accessory papilla and showed that there was complete absence of the pancreatic duct connected with Vaters papilla. Surgical resection enabled us to completely analyze the duct system of pancreas divisum. Although it is not known whether there is a relationship between the pathogenesis of IPMT and embryological anomaly of the pancreatic duct system, this case may provide an insight into the pathogenesis of IPMT.     

Obstructive pancreatitis: unusual causes of chronic pancreatitis

Fifty-eight consecutive surgical pancreatic resections for chronic pancreatitis were examined. Eight cases were identified with obstructive pancreatopathy; all underwent pancreato-duodenectomy. Histological examination revealed that obstruction in three cases was due to duodenal wall cysts, and in two patients it was associated with pancreas divisum (the accessory papilla was obstructed by a neuroendocrine tumour in one case and by ectopic pancreatic tissue in the other). One case each was due to obstruction of an anomalous duct by vegetable matter, to segmental pancreatitis, and to an intraductal carcinoma. Obstructive pancreatitis has many causes and diligent pre-operative assessment is required as surgical resection may be beneficial. Special efforts should be made to identify ductal anomalies, duodenal cysts, ectopic pancreatic tissue, and small ampullary tumours of exocrine and endocrine origin in order to define the aetiology of pancreatitis.     

Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis

HYPOTHESIS: Bile and pancreatic juice exclusion from gut activates acinar stress kinases and exacerbates gallstone pancreatitis as evidenced by the ameliorating effects of replacement therapy in an experimental model of duct ligation-induced acute pancreatitis. In the early stages of gallstone pancreatitis, bile-pancreatic juice cannot enter the gut. Enteral exclusion worsens pancreatitis by causing feedback hyperstimulation of the exocrine pancreas that activates acinar cell stress kinases. Investigations using a unique surgical model, the Donor Rat Model, showed that duodenal replacement of bile-pancreatic juice in rats with duct ligation attenuates pancreatic stress kinase activation, reduces pancreatic cytokine production, and ameliorates pancreatic morphologic changes. These findings suggest that exclusion-induced acinar hyperstimulation, in the presence of duct obstruction, exacerbates acute pancreatitis via stress kinase activation. Although acinar hyperstimulation has often been implicated in the pathogenesis of acute pancreatitis, the lack of supporting evidence remains a conspicuous void. The proposed hypothesis draws on fresh evidence to present a new paradigm that reexamines the role of exocrine pancreatic hyperstimulation in gallstone pancreatitis pathogenesis.