Should anticoagulants be administered for portal vein thrombosis associated with acute pancreatitis?

Venous complications in patients with acute pancreatitis typically occur as a form of splenic, portal, or superior mesenteric vein thrombosis and have been detected more frequently in recent reports. Although a well-organized protocol for the treatment of venous thrombosis has not been established, anticoagulation therapy is commonly recommended. A 73-year-old man was diagnosed with acute progressive portal vein thrombosis associated with acute pancreatitis. After one month of anticoagulation therapy, the patient developed severe hematemesis. With endoscopy and an abdominal computed tomography scan, hemorrhages in the pancreatic pseudocyst, which was ruptured into the duodenal bulb, were confirmed. After conservative treatment, the patient was stabilized. While the rupture of a pseudocyst into the surrounding viscera is a well-known phenomenon, spontaneous rupture into the duodenum is rare. Moreover, no reports of upper gastrointestinal bleeding caused by pseudocyst rupture in patients under anticoagulation therapy for venous thrombosis associated with acute pancreatitis have been published. Herein, we report a unique case of massive upper gastrointestinal bleeding due to pancreatic pseudocyst rupture into the duodenum, which developed during anticoagulation therapy for portal vein thrombosis associated with acute pancreatitis.     

A case of a duodenal duplication cyst presenting as melena

Duodenal duplication cysts are benign rare congenital anomalies reported mainly in the pediatric population,but seldom in adults.Symptoms depend on the type and location and can present as abdominal pain,distension,dysphagia or dyspepsia.They have been reported to be responsible for duodenal obstruction,pancreatitis and,in rare cases,gastrointestinal bleeding.We present a case of a duodenal duplication cyst in a 43-year-old man presenting as melena.Initial gastroduodenoscopy and colonoscopy did not reveal any bleeding focus.However,the patient began passing melena after 3 d,with an acute decrease in hemoglobin levels.Subsequent studies revealed a duplication cyst in the second portion of the duodenum which was surgically resected.Histology revealed a duodenal duplication cyst consisting of intestinal mucosa.There was no further bleeding and the patient recovered completely.In rare cases,duodenal duplication cysts might cause gastrointestinal bleeding and should be included in the differential diagnosis.     

Zollinger-Ellison Syndrome Unresponsive to Cimetidine

A patient with Zollinger-Ellison syndrome appeared initially to respond to cimetidine with a reduction in gastric acid secretion. Symptoms immediately improved but after three days recurred with increasing severity. Intravenous cimetidine had only a short-lived and partial inhibitory effect on the rate of acid production and because of continuing pain and progressive bleeding from his duodenal ulcer, total gastrectomy was performed. Evidence of the effect of atropine and of oral and intravenous cimetidine is presented. Despite recent optimism, cimetidine is not always adequate treatment for Zollinger-Ellison syndrome.     

A case of an intraluminal duodenal diverticulum managed with endoscopic incision and ligation using needle-knife and detachable snare]

An intraluminal duodenal diverticulum (IDD) is a rare congenital anomaly consisted of a sac-like mucosal projection within the second portion of the duodenum. Even though most of cases are asymptomatic, patients may develop recurrent abdominal pain, pancreatitis, and gastrointestinal bleeding. We report a case of symptomatic IDD which presented as acute pancreatitis and obscure gastrointestinal bleeding. Diagnosis was made by typical findings of upper GI series and coronal reformatted CT images. Although surgical resection is the treatment of choice, endoscopic incision and ligation with detachable snare was performed which led to a good result.     

The Zollinger-Ellison syndrome in a child

The Zollinger-Ellison syndrome was encountered in a boy aged 11 years who presented with a bulbar duodenal ulcer causing intractable pain and bleeding. The diagnosis was made by finding an overnight fasting gastric secretion of 1,300 ml containing 134 m-equiv/HCl, and little change of secretion after maximal histamine stimulus. A circumscribed non-beta islet cell pancreatic tumour was excised, with antrectomy. Postoperative acid secretion was normal and the boy was well after being followed up for 15 months. The diagnosis and management are discussed, as the view that total gastrectomy must be performed in all cases of the Zollinger-Ellison syndrome is questioned.     

Massive intraperitoneal bleeding from tryptic erosions of the splenic vein Another cause of sudden deterioration during recovery from acute pancreatitis

Acute bleeding is a rare, but frequently fatal complication of pancreatitis. Bleeding into the gastrointestinal tract may occur owing to gastric or duodenal erosions, peptic ulcers, or varices in the esophagus, stomach, or colon following splenic vein thrombosis, or intraperitoneally from eroded vessels in pancreatic pseudocysts or expanding pseudoaneurysms. We report a novel case of massive intraperitoneal bleeding owing to tryptic erosions of the splenic vein in a patient recovering from acute pancreatitis. Diagnosis of the bleeding was made by ultrasound and ultrasound-guided blood aspiration. The source of the bleeding was identified intraoperatively, and a left-sided pancreatectomy and a splenectomy were performed.     

A case of Zollinger-Ellison syndrome produced by gastrinoma in the duodenum accompanied with multiple endocrine neoplasia type 1

A case of Zollinger-Ellison syndrome produced by gastrinoma in the duodenum accompanied by multiple endocrine neoplasia type-1 (MEN-1) is reported. A 46 year-old female underwent distal gastrectomy due to gastric ulcer 5 years ago. As ulceration of the residual stomach recurred, further examination was performed. Hyperprolactinemia, hypergastrinemia, primary hyperparathyroidism, pancreatic tumor, and duodenal carcinoid were evident, and the diagnoses of Zollinger-Ellison syndrome and MEN-1 were established. The origin of the gastrin secretion was suspected to be from the pancreatic tumor, so sampling of the portal blood was performed. As lesion on the gastrinoma in the pancreas could not be identified, total parathyroidectomy was performed for primary hyperparathyroidism. The level of the gastrin secretion, however, remained high. Partial resection of the duodenum for the duodenal carcinoid and a distal pancreatectomy were carried out concurrently. Immunohistochemical study of the anti-gastrin antibody revealed duodenal tumor cells. Initially, the gastrinoma was thought to be in the pancreas, however, the lesion accompanied with MEN-1 and the Zollinger-Ellison syndrome had occurred in the duodenum.     

Pseudo Zollinger-Ellison syndrome in a patient with duodenal stenosis caused by tuberculosis

We report the case of a 32-year-old Indian man with symptoms suggesting Zollinger-Ellison syndrome including abdominal pain, esaphagitis, duodenal stenosis that did not improve with antisecretory medication, elevated fasting gastrin serum levels that increased after intravenous secretin injections, elevated chromogranin A serum levels and tumoral aspect of pancreatic uncus on CT scan examination. A pancreaticoduodenectomy was performed. Histological examination of the resected specimen showed that there was no endocrine tumour of the pancreas or the duodenum, but identified marked lesions of follicular and caseous tuberculosis. The final diagnosis retained pseudo Zollinger-Ellison syndrome due to gastric outlet obstruction caused by duodenal stenosis of a tuberculosis origin.     

Duodenal ulcer and pancreatitis associated with pancreatic arteriovenous malformation

Arteriovenous malformation (AVM) of the pancreas is a rare condition that may cause severe gastrointestinal bleeding. We describe a 54-year-old man with a 7-year history of recurrent duodenal ulcer due to AVM in the pancreatic head. We recommended pancreatoduodenectomy because of recurrent haemorrhage from the duodenal ulcer, but the patient refused surgery on several occasions. He was admitted to our hospital complaining of severe upper abdominal pain radiating to the back and was diagnosed with acute pancreatitis. He agreed at that stage to the surgical treatment. The resected specimen contained a highly vascular malformation in the pancreatic head and ulceration in the adjacent descending duodenum. Histopathological examination revealed numerous vascular structures with dilated and tortuous vessels in the pancreatic head, confirming the presence of AVM. Moreover, oedema, inflammatory cell infiltration, haemorrhage and necrosis were evident, confirming the presence of acute pancreatitis.     

Recurrent Massive Upper Gastrointestinal Hemorrhage Due to Strongyloides stercoralis Infection

A 29-yr-old black male immigrant from Africa presented with recurrent life-threatening upper gastrointestinal bleeding due to massive duodenal infection by Strongyloides stercoralis. The diagnosis was missed by repeated examinations of fresh stool specimens for ova and parasites and by an initial esophagogastroduodenoscopy. The diagnosis was made by pathologic examination of a duodenal biopsy and of a duodenal aspirate obtained at a second esophagogastroduodenoscopy. This has been previously reported as a cause of massive upper gastrointestinal hemorrhage in four cases. Patients with obscure gastrointestinal bleeding who have travelled or lived in an endemic area should have a duodenal aspiration performed at esophagogastroduodenoscopy.     

Duodenal obstruction following acute pancreatitis caused by a large duodenal diverticular bezoar

Bezoars are concretions of indigestible materials in the gastrointestinal tract. It generally develops in patients with previous gastric surgery or patients with delayed gastric emptying. Cases of periampullary duodenal divericular bezoar are rare. Clinical manifestations by a bezoar vary from no symptom to acute abdominal syndrome depending on the location of the bezoar. Biliary obstruction or acute pancreatitis caused by a bezoar has been rarely reported. Small bowel obstruction by a bezoar is also rare, but it is a complication that requires surgery. This is a case of acute pancreatitis and subsequent duodenal obstruction caused by a large duodenal bezoar migrating from a periampullary diverticulum to the duodenal lumen, which mimicked pancreatic abscess or microperforation on abdominal computerized tomography. The patient underwent surgical removal of the bezoar and recovered completely.     

症状性十二指肠憩室的临床特点分析

目的探讨症状性十二指肠憩室病例的临床、内镜及影像学表现、治疗方法,并分析其临床意义。方法回顾性分析武汉大学人民医院2008年1月-2011年1月症状性十二指肠憩室病例,分析其临床表现、内镜及影像学表现、治疗方法等临床资料。结果共35例患者诊断为症状性十二指肠憩室,其中腹痛者15例、呕吐者2例、呕血或黑便者12例、黄疸患者6例,腹痛患者4例有反复发作史、黑便患者2例。所有病例中并发十二指肠憩室炎5例、急性胰腺炎1例、胆总管结石6例、肠梗阻1例、上消化道出血12例。35例症状性十二指肠憩室分别位于十二指肠球部9例、降部22例、水平部4例,其中单发25例、多发10例。经由消化道钡餐检查发现十二指肠憩室13例、胃镜9例、经内镜逆行胰胆管造影(endoscopic retrograde cholangio-pancreatography,ERCP)7例,双气囊小肠镜2例、腹部CT检查4例。结论十二指肠憩室症状不典型,对于不明原因上腹痛、消化道出血及胰腺炎患者,需考虑此病因,可行相关检查明确,治疗上除内科保守外还可以进行内镜下或者手术治疗。     

Hemorrhage from the upper gastrointestinal tract as a cause of sudden death

During the period from 1971 to 1988 there were 212 fatalities out of 24,822 obductions because of gastrointestinal bleeding. Bleeding from oesophagus varices was most often found, followed by bleeding from duodenal ulcer (16%), gastric ulcer (14%) and haemorrhagic gastritis (11%). The sex-ratio was 2:1 in favour of men. In most cases alcohol related problems were found (with organic diseases such as fat liver, liver cirrhosis, pancreatitis as well as social deprivation, sometimes with acute alcoholization.     

Massive intraperitoneal bleeding from tryptic erosions of the splenic vein. Another cause of sudden deterioration during recovery from acute pancreatitis.

Acute bleeding is a rare, but frequently fatal complication of pancreatitis. Bleeding into the gastrointestinal tract may occur owing to gastric or duodenal erosions, peptic ulcers, or varices in the esophagus, stomach, or colon following splenic vein thrombosis, or intraperitoneally from eroded vessels in pancreatic pseudocysts or expanding pseudoaneurysms. We report a novel case of massive intraperitoneal bleeding owing to tryptic erosions of the splenic vein in a patient recovering from acute pancreatitis. Diagnosis of the bleeding was made by ultrasound and ultrasound-guided blood aspiration. The source of the bleeding was identified intraoperatively, and a left-sided pancreatectomy and a splenectomy were performed.     

Zollinger-Ellison syndrome type 1: clinical and pathological correlations in a case

Some patients with the Zollinger-Ellison syndrome appear to have hypergastrinaemia and hyperplasia of the antral G cells but no tumour. This subgroup has been classified as Zollinger-Ellison syndrome type 1. We have treated such a patient by vagotomy and antrectomy, the fasting plasma gastrin and acid secretion subsequently returning to normal.A 17-year-old male had a four-year history of duodenal ulcer. Gastric secretion tests showed acid hypersecretion. Fasting plasma gastrin was 8350 pg/ml (normal 50-170 pg/ml). At laparotomy duodenal ulceration was confirmed but no pancreatic or other tumours were found. Truncal vagotomy and antrectomy was performed with distal pancreatectomy. Immunofluorescent staining showed hyperplasia of G cells in the resected antrum but a normal pancreas and duodenum.Six months after operation he was symptom free and acid secretion was reduced by 92%. The fasting plasma gastrin at two months was <50 pg/ml.These findings suggest that type 1 Zollinger-Ellison syndrome may be a clinical entity.     

Secretin-Induced Gastrin Response in the Zollinger-Ellison Syndrome and Chronic Duodenal Ulcer Patients before and after Cimetidine Treatment

A secretin provocative test was performed in 16 patients with chronic duodenal ulcer and in five patients with the Zollinger-Ellison syndrome. In four chronic duodenal ulcer patients a second secretin test was done during acute iv cimetidine administration. There were only slight variations of gastrin compared with the first test. A third test was done on the same four chronic duodenal ulcer patients after 1 month's po cimetidine treatment (1 g/day); gastrin at 0 time was significantly higher than in the previous two tests (p < 0.01). Integrated gastrin response after secretin was significantly lower in the third test than in the first (p < 0.05). In two Zollinger-Ellison syndrome patients treated with 1.0 and 1.4 g/day cimetidine for 3 months, gastrin at 0 time was not markedly increased, whereas compared with the first test gastrin levels were higher at each time after secretin. These data suggest that previous cimetidine treatment does not alter, and may even increase, the diagnostic sensitivity of the secretin test.     

Significance and regulation of gastric secretion of platelet-activating factor (PAF-Acether) in man

Platelet-activating factor (PAF) has been implicated in the pathogenesis of acute inflammatory and ulcerative diseases of the upper gastrointestinal tract. In the present study, we compared the gastric output of PAF and its precursors with gastric acid output, in patients with various upper gastrointestinal tract diseases and healthy controls. PAF and precursors were also extracted from gastric biopsies from subjects with chronic gastritis and/or gastric colonization byHelicobacter pylori. Under basal conditions, hourly gastric PAF output increased in esophagitis and erosive gastritis, but not in duodenal ulcer or Zollinger-Ellison syndrome. In the gastric juice of duodenal ulcer patients, PAF output rose after secretin, but in patients with Zollinger-Ellison syndrome, PAF was only detected when gastric acid secretion had been reduced by antisecretory drugs and no concurrent changes were observed in serum gastrin levels. After pentagastrin, patients and controls exhibited a significant decrease in PAF output and a negative correlation was found between PAF and acid outputs (r=–0.57,p<0.01). When PAF was incubated with gastric juicein vitro, it underwent degradation irrespective of the medium pH. We found no relation between the outputs of PAF and precursors and the severity of gastritis or gastric colonization byH. pylori. Overall, these results suggest that PAF might be released in the stomach by gastric epithelial cells and could be responsible for mucosal injury of the upper gastrointestinal tract.     

Neuroendocrine islet cell tumour producing gastrin and ACTH in a patient with calcifying chronic pancreatitis.

A patient with a calcifying chronic pancreatitis was found to have a neuroendocrine islet cell tumour (a previously unreported association). The tumour secreted both gastrin and ACTH leading to clinical manifestations of both the Zollinger-Ellison syndrome and Cushing's syndrome.     

Overt gastrointestinal bleeding in haematologic neoplasms

BACKGROUND AND AIM: Patients with acute leukaemia suffer from various haemorrhages, most frequently due to thrombocytopenia. We could not reach any information regarding the frequency of gastrointestinal bleeding in acute leukaemia and decided to search this complication in patients with acute and chronic leukaemias and myeloproliferative disorders, retrospectively. PATIENTS AND METHODS: During a 6-year period, 291 patients with acute leukaemia, 52 patients with chronic leukaemia and 108 patients with myeloproliferative disorders had been followed. Thirty-two cases of overt gastrointestinal haemorrhage episodes (25 upper, 7 lower) were observed during the mentioned period. RESULTS: The frequency of bleeding episodes was 7.1% (32/451) in haematologic malignancies as a whole, 5.8% (17/291) for acute leukaemia, 1.9% (1/52) for chronic leukaemia and 13% (14/108) for myeloproliferative disorders. If the patients with myeloproliferative disorders in blastic phase were analysed separately, the ratio was 30% (6/20). Oesophagogastroduodenoscopy, which could be performed in 8 of 25 upper gastrointestinal haemorrhage episodes, revealed erosive gastritis in five patients and duodenal ulcers in three patients. Neutropenic enterocolitis was the underlying cause in all of the seven patients with lower gastrointestinal haemorhage. Five out of the seven patients had acute leukaemia. In 7 bleeding attacks, out of 32, the ultimate result was death. Generally, the haemorrhage was only a contributing cause of mortality. All of the mortality cases were patients with acute leukaemia. CONCLUSION: Especially, the patients with myeloproliferative disorders are prone to develop gastrointestinal haemorrhage. The manifestation is generally as upper gastrointestinal bleeding due to gastric erosions and duodenal ulcers. Lower gastrointestinal bleeding is frequently a problem of the patients with acute leukaemia. It is commonly a sign of neutropenic enterocolitis.     

Helicobacter pylori and Zollinger-Ellison syndrome

Helicobacter pylori (previously Campylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship between H. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency of H. pylori infection in Zollinger-Ellison syndrome and also what effect H. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome. H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins of H. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients had H. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P less than 0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr; median 52.7. Acid secretion was lower in the H. pylori-infected patients than the uninfected patients (BAO 24.5 +/- 6.5 vs 45.4 +/- 6.6, and MAO 44.3 +/- 11.8 vs 67.9 +/- 10.7, for H. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P less than 0.05). The present results indicate that H. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO with H. pylori suggests that these findings may be related.