Cases reported "Pancreatic Diseases"

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1/40. nesidioblastosis, myelodysplastic syndrome and nodular diabetic glomerulosclerosis in an elderly nondiabetic woman: an autopsy report.

    nesidioblastosis as the cause of hyperinsulinaemic hypoglycaemia in an adult is rare. We report here an additional case of nesidioblastosis, which resulted in fatal hyperinsulinaemic hypoglycaemia in a 72-year-old woman with an underlying myelodysplastic syndrome. The diagnosis of nesidioblastosis was established only after post-mortem examination with a careful exclusion of minute insulinoma. To our surprise, the renal pathology disclosed typical diabetic nodular glomerulosclerosis in the same patient who had no previous history of diabetes mellitus (DM). nesidioblastosis has been reported to cause 'reversal' of Type 1 DM and insulinoma causing 'reversal' of Type 2 disease. We therefore hypothesize that our patient might have had an undiagnosed DM in the past, which resulted in the typical diabetic nodular glomerulosclerosis. The nesidioblastosis caused a 'reversal' of DM and even the ultimate development of hyperinsulinaemic hypoglycaemia.
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ranking = 1
keywords = diabetes mellitus, diabetes, mellitus
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2/40. Endoscopic retrograde pancreatographic findings of pancreatic lipomatosis.

    Pancreatic lipomatosis is characterized by fatty infiltration or replacement of the pancreas, and has been associated with many conditions. We recently experienced two cases of pancreatic lipomatosis in patients with pancreatic pseudocyst and a case of lipomatosis in diabetes mellitus. In these patients, abrupt obstruction of the main pancreatic duct with smooth tapering is a typical endoscopic retrograde pancreatography (ERP) finding of pancreatic lipomatosis and must be differentiated with pancreatic carcinoma.
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ranking = 1
keywords = diabetes mellitus, diabetes, mellitus
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3/40. Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family.

    The mitochondrial (mt) 3243 dna mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 dna mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnosed with chronic pancreatitis with pancreatic calcifications and pancreatic duct dilation, although she was completely asymptomatic and with no signs of steatorrhoea. She did not have gallstones and the common bile duct was normal. A possible etiopathogenic pathway for pancreatitis could be a suppressive effect of the mt 3243 mutation on the oxidative phosphorylation in affected mitochondria. Although pancreatitis and pancreatic dysfunction in association with the mt 3243 mutation, especially in patients with comorbidity of MELAS and diabetes, has previously been described as a rare manifestation, this case is specific because of the discrepancy of advanced morphological pancreatic alterations and complete lack of pancreatogenic symptoms.
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ranking = 3.1347267010309
keywords = diabetes
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4/40. Hypothalamic and pancreatic lesions with diabetes mellitus.

    A case is reported of a neoplasm of mixed mesenchymal and neuroepithelial origin consisting of plasmacytoma, lymphoma, ganglioneuroma, and astrocytoma in the same mass. The tumour arose in the hypothalamus of a 43 year old diabetic woman who also had alpha cell hyperplasia and beta cell hypoplasia of the islets of langerhans. It is suggested that both hypothalamic and pancreatic lesions produced diabetes mellitus in this patient.
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ranking = 5
keywords = diabetes mellitus, diabetes, mellitus
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5/40. Hypoglycaemia from islet cell hyperplasia and nesidioblastosis in a patient with type 2 diabetes mellitus--a case report.

    INTRODUCTION: We report the first case of hypoglycaemia from beta cell hyperplasia with nesidioblastosis in an Asian adult with pre-existing type 2 diabetes. CLINICAL PICTURE: A 57-year-old Chinese woman presented with hyperinsulinaemic hypoglycaemia despite discontinuation of oral hypoglycaemic agents 4 months after diagnosis of type 2 diabetes. Preoperative portal venous sampling suggested regionalisation to the neck of the pancreas. Intraoperative ultrasound and palpation of the fully mobilised pancreas were non-localising. TREATMENT: A subtotal 85% pancreatectomy was performed with success. OUTCOME: histology showed no evidence of tumour, but revealed islet hyperplasia and nesidioblastosis. Her diabetes was subsequently well controlled on metformin therapy. CONCLUSION: Endogenous hyperinsulinism from beta cell hyperplasia with nesidioblastosis may rarely occur in type 2 diabetics. However, this remains a diagnosis of exclusion that is confirmed only on surgical pathology. In affected individuals, preoperative portal venous sampling may be falsely localising, especially if selective sampling of the smaller peri-pancreatic veins is omitted. Definite treatment involves pancreatectomy, although the extent of surgical resection is not well established.
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ranking = 5.3434543004418
keywords = diabetes mellitus, diabetes, mellitus
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6/40. adult-onset nesidioblastosis causing hypoglycemia: an important clinical entity and continuing treatment dilemma.

    HYPOTHESIS: nesidioblastosis is an important cause of adult hyperinsulinemic hypoglycemia, and control of this disorder can often be obtained with a 70% distal pancreatectomy. DESIGN: The records of all adult patients operated on for hypoglycemia between 1974 and 1999 were reviewed retrospectively. patients with the pathologic diagnosis of nesidioblastosis were contacted for follow-up (1.5-21 years) and are presented. patients' results were compared with those of 36 other individuals with this disorder who were previously reported in the literature. SETTING: The University of chicago Medical Center (chicago, Ill), a tertiary care facility. patients: A consecutive sample of all patients operated on for hypoglycemia. INTERVENTIONS: Seventy percent distal pancreatectomy for all patients with nesidioblastosis, and maintenance therapy with verapamil hydrochloride for 2 patients. MAIN OUTCOME MEASURES: achievement of normoglycemia with and without medication, development of insulin-dependent diabetes mellitus, pancreatic exocrine insufficiency, and need for reoperation. RESULTS: Of 32 adult patients who underwent surgical exploration for hyperinsulinemic hypoglycemia at our institution, 27 (84%) were found to have 1 or more insulinomas, and 5 (16%) were diagnosed with nesidioblastosis. Each patient with nesidioblastosis underwent a 70% distal pancreatectomy. Follow-up duration for the 5 patients ranged from 1.5 to 21 years, with 3 patients (60%) asymptomatic and taking no medications, and 2 patients (40%) experiencing some recurrences of hypoglycemia. The 2 patients with recurrences are now successfully treated with a calcium channel blocker, an approach, to our knowledge, never before reported for adult-onset nesidioblastosis. CONCLUSIONS: nesidioblastosis is an uncommon but clinically important cause of hypoglycemia in the adult population, and must always be considered in a patient with a presumptive preoperative diagnosis of insulinoma. This study indicates that a 70% distal pancreatectomy is often successful in controlling hypoglycemia, and rarely results in diabetes mellitus. However, the optimal treatment of this disorder remains to be determined.
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ranking = 2.1675493561655
keywords = diabetes mellitus, diabetes, insulin-dependent, mellitus
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7/40. Lipomatous pseudohypertrophy of the pancreas: further evidence of advanced hepatic lesion as the pathogenesis.

    An 80-year-old Japanese man with liver cirrhosis was suspected of having lipomatous pseudohypertrophy of the pancreas on the basis of results of ultrasonography and a computed tomography scan. He eventually died of hepatic failure. He had no obesity, diabetes mellitus or pancreatic symptoms during his entire clinical course. autopsy results confirmed lipomatous pseudohypertrophy of the pancreas, cholecystolithiasis, and postnecrotic liver cirrhosis associated with submassive hepatic necrosis was suspected. Although the pathogenesis of lipomatous pseudohypertrophy of the pancreas is not clear, the findings in the present case provide further evidence to support the hypothesis that advanced hepatic lesions cause this lesion.
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ranking = 1
keywords = diabetes mellitus, diabetes, mellitus
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8/40. Fibrocalcific pancreatic diabetes in a young Ethiopian man.

    An eighteen year old Ethiopian patient was admitted to Jimma teaching hospital, after presenting with classical hyperglycemic symptoms associated with abdominal pain, chronic diarrhea, cachexia, and radiological appearance of extensive pancreatic calcification. These clinical and radiologic findings correlated with the well-described entity of Fibrocalcific pancreatic diabetes, which has never been reported from ethiopia before.
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ranking = 2.2390905007364
keywords = diabetes
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9/40. 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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ranking = 0.44781810014727
keywords = diabetes
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10/40. 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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ranking = 2.4066398569019
keywords = diabetes, insulin-dependent
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