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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 32 histologically documented cases of heterotopic pancreas was found in a review of the records of the department of pathology at the Chang Gung Memorial Hospital between 1977 and 1987. This review was done to ascertain the clinical significance of this uncommon entity. In 14 patients (44%), the aberrant pancreatic tissue was symptomatic; in the other 18 (56%), it was found incidentally. In the symptomatic group, the heterotopic pancreatic tissue was found in a duplication cyst of the ileum in one patient, in the common bile duct in one, in a Meckel's diverticulum in four, in the stomach in three, in a congenital duodenal diaphragm in one, in the duodenum in three, and in the ileum in one. The majority of heterotopic pancreatic tissue in the asymptomatic group was encountered in the jejunum (15 patients). Symptoms were related to complications, including obstruction of the common bile duct, mucosal ulcer with hemorrhage, intussusception, and intestinal obstruction, but not to pathologic conditions of the pancreas itself, such as pancreatitis or pancreatic cyst or neoplasm. In all of the clinically significant cases, the clinical symptoms disappeared completely after surgical removal of the aberrant tissue. In 28 cases (87%), diagnosis was made by frozen section during operation. Preoperative diagnosis of aberrant pancreas was not made in any of the cases. Histologically, all cases showed pancreatic excretory ducts; in 31 cases (97%), exocrine glands were present, and in 27 cases (84%), islets of Langerhans were discernible. There was no relationship between symptoms and the presence of islets, acini, or ducts. Mallory's phosphotungstic acid-hematoxylin stain was used to demonstrate zymogen granules in the acinar cells, and insulin, glucagon, and somatostatin were demonstrated with the horseradish peroxidase-antihorseradish peroxidase immunocytochemical staining technique; islets of Langerhans were also identified. Technetium Tc 99m scintigraphy was used to detect the bleeding source in a Meckel's diverticulum and an enteric duplication associated with ectopic gastric mucosa.
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PMID:Pancreatic heterotopia: a reappraisal and clinicopathologic analysis of 32 cases. 305 29

We report on a patient with a carcinoid tumour of the ampulla of Vater and review the 33 known cases of the literature with regard to clinical presentation, morphology and therapy. As it is apparent from the location of the tumour, obstructive jaundice, pancreatitis and nonspecific upper abdominal complaints are the most frequent symptoms. The ampullary carcinoid belongs histogenetically to the APUD cell system with the ability of multiple endocrine activity. The expression of somatostatin peptide and neuron-specific enolase are the most common histopathological findings. A systemic function of these hormones, however, has not yet been shown. For diagnostic purposes in surgical pathology we found synaptophysin and chromogranin A to be important markers. For surgical treatment, partial duodenopancreatectomy remains the current therapy of choise, if the tumour exceeds two centimeters in diameter.
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PMID:[Carcinoid tumor of the ampulla of Vater. Morphology, diagnosis and therapy of a rare papilla tumor]. 305 8

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p less than 0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a "multistep" process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.
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PMID:Aberrant expression of class II major histocompatibility complex molecules by B cells and hyperexpression of class I major histocompatibility complex molecules by insulin containing islets in type 1 (insulin-dependent) diabetes mellitus. 330 84

In 3 healthy men and 4 healthy women, and in 5 men and 2 women with confirmed chronic relapsing pancreatitis (CRP) the inhibitory effect of somatostatin cn pancreatic exocrine function and insulin secretion stimulated with pancreozymin and secretin was determined. In all 7 patients with CRP the volume of pancreatic juice and the bicarbonate and amylase and protein output after stimulation were lower than in healthy subjects, and somatostatin had a reduced inhibitory effect on both the basal secretion and particularly on the pancreozymin-secretin-stimulated secretion. A similarly lower inhibitory effect of somatostatin on the secretin-pancreozymin induced increase in blood insulin (IRI) level was observed in these patients. The presented data suggest that the damaged pancreas reacts less effectively not only to the stimuli enhancing its exocrine and endocrine secretory activity, but also to the stimuli inhibiting this activity. This observation may be of practical value for the evaluation of the functional efficiency of the pancreas.
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PMID:Reduced inhibitory effect of somatostatin on the exocrine function of the pancreas and on serum insulin (IRI) levels in chronic relapsing pancreatitis. 608 15

The effect of somatostatin on the secretory process of the rat exocrine pancreas has been studied using a combined in vivo- in vitro system. Somatostatin in a concentration of 5 x 10(-6) g/kg/h was infused alone or in combination with low (5 x 10(-7) g/kg/h) and high (5 x 10(-6) g/kg/h) doses of synthetic caerulein. All aspects of the secretory process were then studied in vitro using isolated pancreatic lobules. Somatostatin inhibits both basal and stimulated discharge of enzymes and newly synthesized proteins thus leading to increased enzyme content. The stimulatory action of low doses of caerulein is nearly totally blocked, however, the induction of an acute non-hemorrhagic interstitial pancreatitis due to supramaximal doses of caerulein is not prevented, but only reduced in its severity. Furthermore, somatostatin infusion following the induction of pancreatitis has a beneficial effect on recovery, since increase levels of pancreatic enzymes in blood are quickly reduced and cellular infiltration of the diseased pancreas is nearly prevented.
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PMID:Effect of somatostatin on rat exocrine pancreatic secretory process in normal and diseased state. 610 23

Plasma immunoreactive glucagon, C-peptide and substrates (glucose, lactate, and alanine) were measured in 21 pancreatectomized patients and 28 patients with chronic calcifying pancreatitis during arginine infusion. Results were compared with those obtained in control and in insulin-dependent diabetic subjects, and in pancreatectomized subjects receiving a combined infusion of glucagon and arginine or somatostatin and arginine. Plasma immunoreactive glucagon in the pancreatectomized patients was 230 +/- 26 pg/ml (control subjects 100 +/- 13 pg/ml, p less than 0.001), but was unchanged following arginine or somatostatin. Following ethanol extraction of plasma it became undetectable. Similar results were obtained in patients with chronic pancreatitis. In contrast to the insulin-dependent diabetic subjects, no changes in blood glucose, lactate, and alanine concentrations were found during arginine infusion in the pancreatectomized or pancreatitis patients. Addition of glucagon restored the metabolic response to arginine in the pancreatectomized patients. Our results confirm previous smaller studies that in pancreatectomized patients, A cell function is absent or insignificant.
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PMID:Absence of islet alpha cell function in pancreatectomized patients. 612 Aug 75

Patients with chronic recurrent pancreatitis were examined for the blood content of insulin, glucagon, somatostatin (SS), somatotropin (STH), cAMP and cGMP. The blood content of insulin, glucagon and STH was normal, that of SS and cAMP elevated, and that of cGMP lowered. In severe pancreatitis, the endocrine part of the pancreas was activated. The relationship was established between the level of amylasemia and the activity of islet cells and the blood content of cGMP. The compensatory importance of hypersecretion of SS and glucagon for pancreatitis exacerbation is demonstrated. The role of cyclic nucleotides in the pancreatic activity is discussed.
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PMID:[Pancreatic hormones and cyclic nucleotides in the blood in chronic recurrent pancreatitis]. 615 52

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52

The endocrine secretory function of rat pancreases in which pancreatitis had been induced by feeding rats a 0.5% ethionine diet was investigated. Despite loss of 50% of exocrine tissue and widespread destruction of acinar structure, pancreatic insulin and glucagon contents and 4-h fasting plasma insulin levels in vivo did not differ significantly from those of food-restricted, weight-matched controls. Plasma glucose concentrations (fasting and after oral glucose) were significantly lower than control. In isolated, perfused ethionine-treated pancreases secretin failed to stimulate insulin secretion, whereas basal insulin secretion and insulin responses to glucose, arginine, gastric inhibitory polypeptide, vasoactive intestinal peptide (VIP), and somatostatin were similar to those of controls. Basal glucagon secretion was elevated in ethionine-treated pancreases, and glucagon outputs in response to arginine, VIP, and somatostatin showed a consistent trend toward higher levels than those of controls. These findings demonstrate that ethionine-induced pancreatitis selectively impairs islet secretory function. These effects may be due to damage to islet cell membranes by exocrine enzymes and/or a direct pathogenic action of ethionine on the islets.
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PMID:Altered insulin and glucagon secretion in perfused ethionine-treated rat pancreases. 675 65

Despite improving results, the management of exocrine complications after pancreas transplantation remains problematic. During a 30-month period, we performed 65 pancreas transplants with bladder drainage. A total of 23 patients (35%) were managed with a long-acting somatostatin analogue (Sandostatin) for persistent hyperamylasemia or allograft pancreatitis. Sandostatin was begun at a mean of 29 days after transplant with a mean duration of therapy of 13 days. Sandostatin therapy was associated with significant reductions in the serum, urine, and peritoneal fluid amylase levels (p < 0.05). Sandostatin also caused a decrease in cyclosporine levels during oral cyclosporine use. In patients receiving Sandostatin, pancreas allograft survival was 83%. We conclude that pancreatitis remains a major cause of morbidity after pancreas transplantation. The selective use of Sandostatin can result in excellent graft salvage with low morbidity. Sandostatin appears to be safe and effective in reducing the exocrine output of the denervated pancreas allograft but also reduces cyclosporine levels.
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PMID:Selective use of Sandostatin in vascularized pancreas transplantation. 750 9


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