Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 a study of pancreases from 75 patients who died at presentation of Type I diabetes there was selective destruction of beta cells associated with islet inflammation (insulitis). According to a recent hypothesis, aberrant expression of Class II major histocompatibility complex (MHC) products on a target cell may allow presentation of organ specific surface antigen(s) to potentially autoreactive T helper lymphocytes and thus lead to autoimmunity. Aberrant expression of Class II MHC was demonstrated immunohistochemically on beta cells in 21 out of 23 patients with recent onset diabetes. No such expression was seen on the other pancreatic endocrine cells. Ninety-four per cent of insulin-containing islets in these patients had marked hyperexpressions of Class I MHC affecting all endocrine cells in these islets. Insulin deficient islets were not thus affected. Both these abnormalities of MHC expression appeared to precede insulitis within a given islet and appeared to be unique to Type I diabetes, being absent in pancreases of patients with Type II diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to beta cells in Type I diabetes may be a 'multistep' process in which abnormalities of MHC expression are crucial events.
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PMID:C. L. Oakley lecture (1987). The pathogenesis of beta cell destruction in type I (insulin-dependent) diabetes mellitus. 330 29

The experiments on normal mongrel dogs and those with chronic experimental pancreatitis were performed to reveal the early changes of the endocrine pancreas function. The concentration of immunoreactive insulin and glucagon were studied in afferent vessels of the organ after intraarterial glucose-loading during pancreatic perfusion in situ. The data obtained have shown that in chronic pancreatitis the maximum secretion of insulin is decreased and delayed, as compared to normal animals. At the same time insulin-glucagon secretion ratio remains unchanged. That was indicative of the normal alpha-cell function at the early stages of the disease.
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PMID:[Characteristics of endocrine disorders in the early stages of the development of chronic experimental pancreatitis]. 331 35

Plasma vasoactive intestinal peptide (VIP) concentrations of normal individuals and patients with pancreatitis were studied using a VIP RIA kit. The inter-assay and intra-assay variation of this kit were between 2.1 and 9.4%. The VIP levels increased in the acute phase of acute pancreatitis and patients with chronic pancreatitis. The VIP concentration increased during the first 30 min of glucose tolerance test, but this increase was much smaller than that in insulin. These results suggest that this kit is useful for physiologic and pathologic changes in the VIP level.
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PMID:Fundamental and clinical evaluation of vasoactive intestinal peptide (VIP) in pancreatitis by radioimmunoassay kit. 331 28

The operation of total pancreatectomy is performed rarely. Its role in the management of patients with chronic pancreatitis remains to be elucidated. We have reviewed our series of 29 total pancreatectomies for benign disease [14 women median age 39 years; 15 men median age 34 years]. Twelve underwent standard total pancreatectomy, in 17 duodenum preserving total pancreatectomy (DPTP) was performed. There was one death (mortality 3.4%). In no patient was the total pancreatectomy the first operative procedure. The patients were compared with age and sex matched diabetic control subjects selected on a best fit basis from the diabetic clinic database. The aetiology of the pancreatitis was idiopathic nine, pancreas divisum nine, alcohol eight and other causes three. The indication for surgery was pain 27, acute pancreatitis one and cholangitis with pancreatitis one. The complications of the procedures were mainly caused by infection [wound three, chest six and central line sepsis four] and in two there was a leak from the duodenum; no patient required re-operation. The postoperative stay [standard total, median 21 days (range 13-98) DPTP median 31 days (range 17-49)] has lengthened over the period due to greater attention to analgesic, diabetic and enzyme deficiency control before discharge. In standard total pancreatectomy there were five major hypoglycaemic episodes with only two in 17 DPTP patients. The per cent ideal body weight, the insulin requirement and the HbAl compared less well in standard total pancreatectomy group compared with controls than did DPTP. With both groups large doses of enzyme replacement were required, and this proved of importance in diabetic control. Our experience with total pancreatectomy suggests that pain will be improved in over 80% of patients and that the results of surgery will improve with prolonged follow up provided attention is given to analgesic abuse, enzyme deficiency and diabetes.
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PMID:Total pancreatectomy for chronic pancreatitis. 335 68

It is suggested that the important drugs rifampicin and halothane and the raised glucose levels in diabetes mellitus exert injurous effects on cells through a lysosomal mechanism. Further evidence is given of by time rifampicin induction of beta-glucuronidase and beta-N acetylglucosaminidase and its possible relation to hepatitis and pancreatitis. On the basis of preliminary data halothane may cause hepatitis connected to lysosomal enzyme release in the presence of other aggravating factors common to the perioperative period. The onset of diabetic vascular complications may be related to the similar raised levels of lysosomal enzymes found in insulin, drug and diet controlled disease. Release of these enzymes into plasma may be a marker of important changes in the lysosome, whether due to enzyme induction or damage, and could be a primary mechanism of many disease processes including some thought to be mainly autoimmune in character. Routine estimation in the clinical laboratory along with existing cytoplasmic and microsomally derived enzymes in the chemical screen would be a useful way of surveying lysosomal changes in the wide spectrum of disease in a general hospital.
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PMID:Rifampicin, halothane and glucose as mediators of lysosomal enzyme release and tissue damage. 341 3

The concentration of somatotropic hormone (STH) was measured by radioimmunoassay in 108 patients with acute and chronic pancreatitis and in 15 healthy persons. In addition, to study the reserve capacity of the somatotropic function of the pituitary, insulin hypoglycemia was employed. It was established that during exacerbation, the pancreatitis patients manifested an increase in the hormone content. In the patients suffering from acute pancreatitis, the STH level returned to normal following treatment. In chronic pancreatitis, the hormone concentration remained elevated after treatment. No correlation was discovered between alterations in the STH level and the activity of pancreatic enzymes. The data obtained point to a definite role of STH in the pathogenesis of chronic pancreatitis.
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PMID:[Secretion of somatotropic hormone in patients with pancreatitis]. 351 16

Reported are eight patients with idiopathic chronic pancreatitis and two patients with alcoholic pancreatitis who had near total distal pancreatectomy for disabling pain and underwent simultaneous segmental pancreatic autotransplantation of the body and tail of the gland to the femoral area in an attempt to prevent or delay the onset of diabetes. The median follow-up period was 31 months, and follow-up study in nine patients ranged from 24 to 54 months. Patency of the grafts was determined by angiography and selected percutaneous venous assays for insulin. Islet cell function was determined by oral glucose tolerance tests, intravenous (I.V.) glucose tolerance tests, and I.V. glucagon stimulation studies. Segmental autotransplantation was technically successful in eight patients, only one of whom required insulin (at 2 years after grafting). The other seven patients with technically successful grafts have remained insulin independent, including two patients who later underwent pyloric preserving pancreatoduodenectomy for completion pancreatectomy. Variable pain relief was observed in patients who underwent near total pancreatectomy, but pain was unrelieved in those patients who underwent limited distal resection. Patients with idiopathic pancreatitis appear to have better pain relief and preservation of endocrine function than alcoholic patients. Segmental pancreatic autotransplantation prevents or delays the onset of diabetes mellitus and should be considered as an alternative for those patients who require extensive pancreatic resection for chronic pancreatitis.
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PMID:Segmental pancreatic autotransplantation with pancreatic ductal occlusion after near total or total pancreatic resection for chronic pancreatitis. Results at 5- to 54-month follow-up evaluation. 352 8

Satisfactory results were obtained in 5 type I diabetic recipients of 6 human pancreas transplantations. We chose the three following options: diversion of the pancreatic juice by a pancreaticojejunostomy, simultaneous kidney transplantation from the same donor and cyclosporin A as the basic drug in the immunosuppressive regimen. Further conclusions were also drawn from our experience. Firstly, biological data alone might not be relevant for donor selection: histologic examination of the non transplanted cephalic portion of the donor pancreas is needed to rule out pancreatitis. Secondly, donor management usually needs large amounts of fluids and blood. Finally, besides the general rules of recipient management common to kidney transplantation, pancreas transplantation further requires heparinization, insulin therapy and parental nutrition during the immediate postoperative period.
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PMID:Six human pancreas transplants: results and perioperative management. 352 91

The release of insulin and glucagon in cirrhotic rats was examined. Rats were made cirrhotic by a combination treatment of carbon tetrachloride (CCl4) and phenobarbitone. Liver cirrhosis was verified by histologic findings. Both basal and stimulated release of insulin from isolated pancreatic islets, in vitro, were decreased significantly in cirrhotic rats, as compared with control rats. Basal, but not stimulated, levels of glucagon, in vitro, were reduced significantly in cirrhotic rats. Circulating levels of plasma insulin, glucagon, glucose, bilirubin, and amylase levels were unaffected in cirrhotic rats when compared with control rats. There were no signs of pancreatitis. The results indicated that the release of insulin and glucagon is depressed in cirrhotic rats and in rats treated with phenobarbitone and CCl4. Clearance of circulating insulin and glucagon by the liver was apparently reduced, since circulating levels of insulin and glucagon were unaltered in all treated rats.
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PMID:Insulin and glucagon production in experimental cirrhosis. 354 4


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