Cases reported "Pancreatic Diseases"

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1/8. Intrapancreatic accessory spleen. A rare cause of a pancreatic mass.

    CONCLUSION: The clinical significance of intrapancreatic accessory spleens resides in the mimicry of pancreatic cancer. Radionuclide tests (octreotide scan and Tc99m sulfur colloid scan) should be undertaken to distinguish these lesions from neuroendocrine tumors, hypervascular metastases and pancreatic carcinoma. If the tests are equivocal, diagnostic laparotomy or laparoscopy is recommended. BACKGROUND: Despite its relatively common occurrence, intrapancreatic ectopic splenic tissue is rarely detected owing to its asymptomatic nature. methods: We report a case of a clinically asymptomatic patient in which abdominal computed tomography (CT) scans revealed a mass of 1.5 cm in diameter in the distal pancreas. The tumor markers CA 19-9 and carcinoembryonic antigen (CEA) were slightly elevated, and pancreatic neoplasm was suspected. RESULTS: Left pancreatic resection and splenectomy were performed. The removed specimen disclosed the presence of an accessory spleen within the pancreatic tail.
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2/8. Epithelial splenic cysts in an intrapancreatic accessory spleen and spleen.

    A rare case of cysts simultaneously occurring in the intrapancreatic accessory spleen and spleen in a 49-year-old female is reported. The patient underwent distal pancreatomy for a cystic tumor of the pancreas, and a splenectomy. A multilocular cyst (4.3 x 2.6 cm) in an accessory spleen at the pancreas tail, and a solitary cyst (1.2 x 0.9 cm) of the spleen were found. The cyst in the intrapancreatic accessory spleen was lined by non-keratinizing stratified squamous epithelium, and the spleen cyst by a single layer of flat epithelium; these lining cells were positive for alcian blue stain and periodic acid-schiff reaction, and were immunohistochemically positive for cytokeratin, HBME-1 and Sialyl-Tn. Epithelial membrane antigen, carcinoembryonic antigen and CA19-9 were positive in the accessory spleen cyst but were negative in the spleen cyst. An electron microscopic examination of the flat epithelium of the spleen cyst revealed numerous microvilli on the surface, cytoplasmic microfilaments, and a number of tight junctions between adjacent cells. These features suggested that the two cysts differ in nature, and origin; the accessory spleen cyst may be an embryonic inclusion of the pancreas duct while the spleen cyst may be an inclusion cyst of the mesothelium.
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3/8. Pancreatic involvement in co-infection visceral leishmaniasis and hiv: histological and ultrastructural aspects.

    The involvement of the gastrointestinal tract in the co-infection of hiv and Leishmania is rarely reported. We report the case of an hiv-infected adult man co-infected with a disseminated form of leishmaniasis involving the liver, lymph nodes, spleen and, as a feature reported for the first time in the English literature, the pancreas. light microscopy showed amastigote forms of Leishmania in pancreatic macrophages and immunohistochemical staining revealed antigens for Leishmania and also for hiv p24. Microscopic and ultrastructural analysis revealed severe acinar atrophy, decreased zymogen granules in the acinar cytoplasm and also nuclear abnormalities such as pyknosis, hyperchromatism and thickened chromatin. These findings might correspond to the histologic pattern of protein-energy malnutrition in the pancreas as shown in our previous study in pancreas with AIDS and no Leishmania. In this particular case, the protein-energy malnutrition may be due to cirrhosis, or, Leishmania or hiv infection or all mixed. We believe that this case represents the morphologic substratum of the protein energy malnutrition in pancreas induced by the hiv infection. Further studies are needed to elucidate these issues.
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4/8. An autopsy case of pancreatic and ectopic nesidioblastosis.

    We report an autopsy case of pancreatic and ectopic nesidioblastosis. A five-month-old Japanese girl was born at 35 weeks gestation, and showed clinical symptoms of hyper-insulinemic hypoglycemia before death. At autopsy a tumorous nodule was observed at the portion of the jejunum, 90 cm from Treitz's ligament. The nodule measured 30 x 20 x 20 mm. The ectopic pancreas, also revealed nesidioblastosis histologically. Immunohistologically, both nesidioblastoses were stained positive for chromogranin a, insulin, glucagon and somatostatin. The proliferating cell nuclear antigen (PCNA) and Ki-67 indices were less than 4% in the nesidioblastosis. To our knowledge, this is the first reported case of nesidioblastosis demonstrating proliferating activity with PCNA and Ki-67, and is the third reported case of nesidioblastosis arising in the pancreas and ectopic pancreas.
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5/8. Characterization of T lymphocytes infiltrating human pancreas allograft affected by isletitis and recurrent diabetes.

    We studied a human leukocyte antigen-identical pancreas graft transplanted into an insulin-dependent (type I) diabetic patient shortly after onset of recurrent diabetes to characterize the putative autoreactive T lymphocytes mediating the lesion. The immunohistopathological analysis revealed the presence of isletitis and a selective loss of beta-cells. The isletitis was mostly constituted by CD8 /T-lymphocyte receptor alpha,beta (TCR alpha,beta ) T lymphocytes surrounding and infiltrating the affected islets. CD4-/CD8-/TCR gamma, delta T lymphocytes were observed within the islets. Incubation of the tissue in 15% interleukin 2 induced the migration and initial expansion of the infiltrating cells (66% CD3 lymphocytes) for up to 2 wk; most T lymphocytes in this initial isolate were CD4 (92% CD4 and 7% CD8 ). Long-term anti-CD3 stimulation of this T-lymphocyte population induced the selective growth of CD8 /TCR alpha,beta (75%) and CD4-/CD8-/TCR gamma,delta (all V1 delta ) (17%) T lymphocytes. Therefore, this strategy selectively expanded the T lymphocytes, found to be the predominantly islet-infiltrating cells, rather than the lymphocytes predominating in the initial isolate. Anti-CD3 did not stimulate growth of T lymphocytes in cultures of three isletitis-free pancreas graft biopsies. In a control experiment with a CD4( )-rich T-lymphocyte population, long-term anti-CD3 stimulation and cloning of cytomegalovirus (CMV)-primed peripheral blood mononuclear cells from a CMV subject selectively induced the growth of CD4 T-lymphocyte clones, all CMV specific.(ABSTRACT TRUNCATED AT 250 WORDS)
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6/8. Presence of autoimmunity to pancreatic antigens in a patient with fibrocalculous pancreatic diabetes.

    A case of fibrocalculous pancreatic diabetes (FCPD) is reported for which antibody and cellular immune characteristics were determined. The patient, a Thai woman, had serum islet cell antibodies (ICA) that were detected by both immunoperoxidase staining and an indirect enzyme-linked immunosorbent assay (ELISA). serum anti-human insulin antibodies were negative by a displacement ELISA. Lymphoproliferation assay against pancreatic antigen prepared from a blood group O cadaveric donor was positive. Increased CD8 lymphocytes were observed using direct immunofluorescence staining and flow cytometry. CD4 T lymphocytes, B lymphocytes and NK cells were within normal levels. These findings provide evidence for autoimmunity to pancreatic antigens in a patient with fibrocalculous pancreatic diabetes.
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7/8. Mucinous ductal ectasia of the pancreas: a premalignant disease and a cause of obstructive pancreatitis.

    Five cases of localized ectasiae of pancreatic ducts associated with epithelial mucinous metaplasia have been previously reported by Itai et al. (radiology 1986; 161:697-700). During a 1-year period, we collected four new observations of patients presenting with recurrent attacks of pancreatic pain due to similar clusters of cystlike dilated ducts communicating with the main pancreatic duct and lined by a columnar epithelium interspersed with numerous goblet cells. Duct lumina were filled with mucous. carcinoembryonic antigen levels were high in the pure pancreatic juice, but normal in the blood. Sonography and CT scan showed cystlike, intrapancreatic defects localized three times in the head of the pancreas and once in the body. Endoscopic retrograde cholangiopancreatography (ERCP) showed a huge dilation of some collateral ducts filled by radiolucent defects. The main pancreatic duct was dilated proximally to pathological ducts in three cases. Neither pancreatic stones nor exocrine insufficiency could be demonstrated 7 years after the clinical onset; one case presented with an in situ carcinoma. Since mucinous ductal ectasia is a precancerous state, surgery is mandatory. ERCP is probably the best method of diagnosis.
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8/8. Fatal cyclophosphamide-induced congestive heart failure in a 10-year-old boy with Shwachman-diamond syndrome and severe bone marrow failure treated with allogeneic bone marrow transplantation.

    A 10-year-old boy with Shwachman-diamond syndrome and severe bone marrow failure was treated with high-dose cyclophosphamide, busulfan, and antithymocyte globulin followed by an infusion of human leukocyte antigen-identical, mixed lymphocyte culture (MLC) non-reactive sibling bone marrow. He developed cardiac arrhythmias and intractable hypotension and died on day 23 posttransplant. autopsy findings were consistent with cyclophosphamide-induced pancarditis. The bone marrow showed signs of early engraftment. Allogeneic bone marrow transplantation may be a treatment alternative for Shwachman-diamond syndrome with severe bone marrow failure. However, fatal posttransplant pancarditis due to doses of cyclophosphamide not usually associated with cardiac death may be an unanticipated problem. Further trials of bone marrow transplantation as therapy for this syndrome may be warranted, perhaps using lower doses of cyclophosphamide or substituting for it other immunosuppressive and myelosuppressive agents.
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