Cases reported "Pancreatic Diseases"

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1/14. Pancreatic arteriovenous malformation observed to bleed from the bile duct and a duodenal ulcer: report of a case.

    A 48-year-old man with recurrent episodes of biliary colic and subsequent pancreatitis was admitted to undergo a cholecystectomy. A gastroduodenal fiberscopic examination was performed because of massive melena on the seventh day after admission. It revealed a shallow ulcer on the posterior wall of a duodenal bulbus with rubor and an exposed vessel, which was clipped endoscopically to stop the bleeding. Further observations showed the papilla of Vater to be bleeding from the papilla. A contrast-enhanced abdominal computed tomography scan demonstrated a dilatation of the common bile duct and several dilated vasculatures around the portal vein, some of which drained into the portal vein. Based on the angiography findings, a diagnosis of arteriovenous malformation in the pancreas head was obtained and an embolization of the gastroduodenal artery was performed. Although the melena subsided, he underwent a pylorus-preserving pancreatoduodenectomy to prevent the recurrence of hemorrhaging. The histopathological findings of the bile duct revealed inflammatory cell infiltration and a detachment of the epithelium, except in a small part of the bile duct. A rupture of a damaged vessel inside the bile duct was observed, which was thought to be the cause of hemobilia. Sections of the pancreatic head demonstrated an inflammatory lesion with fibrosis and saponification as well as a large degree of arteriovenous anastomosis. The patient was discharged on the 35th day after the operation following an uneventful postoperative course.
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2/14. Hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for pancreatic stones.

    We present a patient with complication of huge hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for pancreatic lithotripsy. The hematoma measured 78-110mm. angiography showed a subcapsular hematoma, rather than a hematoma in the liver. In the arterial phase, the distal end of the small vessel showed spotty opacification similar to microaneurysma, suggesting that it was an injury caused by separation of the liver and its capsule, caused by the shock waves. The portal vein and hepatic vein were normal. After 8 weeks of conservative therapy, the hematoma was gradually absorbed and the patient was discharged. Eight months after the accident, the hematoma had decreased to 40mm in size. After 20 months, it was completely absorbed. The reported rate of renal subcapsular hematoma after ESWL for renal or ureter stones is 0.1%-0.7%. To date, however, only five cases of hepatic subcapsular hematoma after right renal stone disintegration have been reported. This is the first report of hepatic subcapsular hematoma after ESWL for pancreatic stones.
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3/14. Intrapancreatic duodenal duplication cyst with inversion of the superior mesenteric vessels: CT findings.

    We present a case of intrapancreatic duodenal duplication cyst and inversion of the superior mesenteric vessels. CT findings of this association are discussed.
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4/14. Fine needle aspiration diagnosis of isolated pancreatic tuberculosis. A case report and review of literature.

    CONTEXT: Tuberculosis is a common disease in the developing world and its incidence is slowly increasing in developed countries where a resurgence has been seen subsequent to the AIDS epidemic. Tuberculosis, in its extrapulmonary form, though emerging as a clinical problem, rarely affects the pancreas. The pancreas is biologically protected from being infected by mycobacterium tuberculosis. Pancreatic tuberculosis presents with a wide spectrum of symptoms such as abdominal pain, constitutional symptoms, obstructive jaundice, iron deficiency anemia, pancreatic abscess, massive gastro-intestinal bleeding, acute/chronic pancreatitis, secondary diabetes, splenic vein thrombosis and a pancreatic mass mimicking malignancy. It should be suspected clinically in patients having a pancreatic mass, particularly if the patient is young, not jaundiced, coming from an area of high tuberculosis endemicity and having a normal endoscopic retrograde cholangio-pancreatography. Its indolent course and vague symptomatology along with non-specific laboratory and radiological findings call for greater vigilance. CASE REPORT: We report a case of pancreatic tuberculosis which presented with pancreatic pain. Imaging techniques revealed a mass located in the head of the pancreatic gland. Fine needle aspiration cytology revealed caseating granulomas. The diagnosis of pancreatic tuberculosis was made and the patient was put on anti-tubercular therapy. Five months later, a repeat CT scan of the abdomen revealed resolution of the pancreatic lesion. CONCLUSION: The diagnosis of pancreatic tuberculosis is usually not suspected prior to laparotomy. Most patients have been diagnosed at laparotomy, thus fine needle aspiration cytology/biopsy is useful in obviating the need for major surgery with its accompanying morbidity. Exploratory laparotomy may be required in technically difficult cases due to risk of injury to the vessels in the vicinity of the mass.
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5/14. Oligoclonal T-cell populations in an inflammatory pseudotumor of the pancreas possibly related to autoimmune pancreatitis: an immunohistochemical and molecular analysis.

    Inflammatory pseudotumors (IPT), also known as inflammatory myofibroblastic tumors (IMT), are benign inflammatory processes that may have an infectious etiology and are very rare in the pancreatico-biliary region. Recent studies suggest a biological distinction between IPT and IMT, the latter being a true neoplastic process. We describe a case of pancreatic IPT, originally diagnosed as malignancy, which presumably recurred 4 months after the operation. Histologically, the tumor consisted of a smooth muscle actin and CD68-positive spindle cell population and a more abundant mononuclear inflammatory cell population, primarily composed of macrophages and t-lymphocytes. Inflammatory cells were the source of connective tissue growth factor and transforming growth factor-beta1 and tended to accumulate around nerves and blood vessels, as well as around residual pancreatic parenchymal elements, where an intense angiogenetic response was detected. comparative genomic hybridization analysis of the tumor showed no chromosomal imbalances. polymerase chain reaction-based analysis of T-cell receptor gamma gene rearrangement revealed an oligoclonal pattern. These findings suggest that the pathogenesis of aggressive cases of IPT could be related to the development of an intense and self-maintaining immune response, with the emergence of clonal populations of t-lymphocytes. The relation of the pancreatic IPT to autoimmune pancreatitis is emphasized.
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6/14. Laparoscopic spleen-preserving pancreatic tail resection for an intrapancreatic accessory spleen mimicking a nonfunctioning endocrine tumor: report of a case.

    Laparoscopic surgery is now performed for several pancreatic disorders, such as benign tumors of the pancreatic body or tail, which are a good indication for laparoscopic resection. However, the risk of pancreatic fistula after distal pancreatectomy, performed laparoscopically or by open surgery, is a topic of debate. We report the case of a 61-year-old man in whom a routine follow-up computed tomography (CT) scan showed a solid, well-defined mass, 1.5 cm in diameter, in the pancreatic tail. The mass was homogeneously enhanced from the early phase to the super-delayed phase on enhanced CT. We suspected a nonfunctioning endocrine tumor of the pancreas, and surgery was performed laparoscopically. After dissecting the pancreatic tail away from the splenic hilum and the splenic vessels, it was resected using only a linear stapler. The histological diagnosis was an intrapancreatic accessory spleen. The patient was discharged on postoperative day 14, but was readmitted 6 days later because of a pancreatic fistula, which was treated by CT-guided percutaneous drainage.
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7/14. amyloidosis of pancreatic islets in primary amyloidosis (AL type).

    Seven cases of primary amyloidosis (AL-type) were studied immunocytochemically for the possible involvement of pancreatic islets. The two cases with extensive organ involvement by AL-amyloidosis revealed amyloid deposits in pancreatic islets by routine HE and congo red staining, which were positive for amyloid p and amyloid a, but were only focally positive for light chains kappa and lambda. Positive staining for amyloid p and amyloid a was also noted in the scattered pancreatic acinar tissues, and this positive staining was not specifically located in pancreatic islets as seen in type 2 diabetes mellitus. It is concluded that amyloid deposits in pancreatic islets occur in systemic AL-amyloidosis by a different mechanism from type 2 diabetes. Islet amyloidosis in AL-amyloidosis appears to deposit via circulation, depositing in both pancreatic islets and acinar tissue through blood vessels. In type 2 diabetes, beta islet cells die by cytotoxic effects of smaller amylin (islet amyloid polypeptide, IAPP) aggregates, and the interstitial space created by the necrotic beta cells is replaced by larger IAPP aggregates, to form complex, polymerized islet amyloid. In AL-amyloidosis, the amount of amyloid and light chain deposits in pancreatic islets is much less than that of the other organs and appears to have no connection to type 2 diabetes because the patients did not present diabetes or hyperglycemia. However, considerable islet amyloidosis can be seen in severe AL-type amyloidosis.
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8/14. Two case reports of macrovascular complications in fibrocalculous pancreatic diabetes.

    Fibrocalculous pancreatic diabetes (FCPD) is a form of diabetes secondary to chronic, non-alcoholic pancreatitis in tropical countries. Being a secondary form of diabetes, vascular complications are believed to be rare. In this paper we present two case reports of macrovascular complications (myocardial infarction and gangrene). This shows that large vessel disease does occur in FCPD.
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9/14. Pancreatic lithiasis: a rare cause of gastrointestinal hemorrhage.

    The rare instance of a gastrointestinal hemorrhage caused by a lithiasis of the duct of Wirsung is described. The world literature records only 13 other cases. Pancreatic calculi cause hemorrhage by either migrating through the pancreatic parenchyma to perforate the duodenum, ulcerating the vessels of the periductal parenchyma, or rupturing the pancreas. The usual sign of this complication of chronic calcifying pancreatitis, difficult to diagnose, is repeated gastrointestinal hemorrhages and sometimes pain, as in epigastric colitis. The immediate therapy is control of the hemorrhage. With transcatheter occlusive techniques, radical surgery can be postponed until it is more tolerable.
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10/14. Severe hemorrhage associated with pancreatic pseudocysts: report of two cases.

    Severe hemorrhage from pancreatic pseudocysts is a rare condition that poses a diagnostic and therapeutic challenge. Two cases of preoperative intracystic bleeding and massive postoperative gastrointestinal hemorrhage observed during the last year form the basis of the present report. In the first patient, transcystic suture ligation of the bleeding vessel was necessary to control this life-threatening and dramatic condition--External drainage of the cyst was followed by an uneventful postoperative course. In the second patient, massive gastrointestinal bleeding occurred after cysto-gastrostomy, and neither endoscopy nor arteriography was able to identify the source. Despite aggressive medical and surgical therapy, the patient died. Massive intracystic or gastrointestinal hemorrhage caused by rupture of pseudoaneurysms into pancreatic pseudocysts still remains a rare but severe condition, difficult to treat and affected by high mortality rates. angiography should be performed routinely in the preoperative assessment of pancreatic pseudocysts, even when the other diagnostic techniques do not raise the suspicion of pseudoaneurysm formation. After internal drainage procedures early surgery is recommended whenever GI bleeding occurs in the postoperative course.
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