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

Since mumps virus seems to be one of the most likely candidates in viral etiology of insulin-dependent diabetes (IDDM) we studied the possible relationship of glucose tolerance (75 g oGTT), beta cell function, diabetes associated HLA antigens, haptoglobin phenotype, islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in 125 subjects with antecedent mumps infection. Impaired glucose tolerance (IGT) was diagnosed in 3.2% (n = 4) but onset of diabetes did not appear within 14 months after mumps infection. There was no relationship between glucose tolerance and complications of antecedent mumps infection (e.g. pancreatitis, meningitis, orchitis). The prevalence rate of ICA was 76%. ICSA were detectable in about 36% of children and 62% of the adults tested (p less than 0.01). There was no relationship between ICA/ICSA and diabetes-associated HLA antigens, haptoglobin phenotype or beta cell function (fasting C-peptide and insulin response to 75 g oGTT). However, adults with circulating ICA were characterized by a significantly lower insulin response to glucose. Fifty two "risk" subjects characterized by IGT, diabetes associated HLA antigen(s), ICA or ICSA either alone or combined were studied again 26 months after mumps infection. No symptomatic diabetes appeared and IGT was diagnosed in one case only. ICA and ICSA persisted in more than 50% of subjects in whom ICA or ICSA were present 14 months after mumps infection. Since the used immunological techniques do not clearly distinguish organ-specific from non-organ-specific antibodies the results must be interpreted with caution. To summarize, the preliminary results do not support a close temporal relationship between mumps infection and the onset of IDDM. The pathogenetic role of mumps virus and ICA/ICSA and their possible relation to a slow progressive beta cell destruction has still to be determined.
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PMID:Metabolic, hormonal, and immunological alterations in subjects with antecedent mumps infection. 391 1

In order to assess insulin sensitivity for glucose utilization in the other type of diabetes, insulin sensitivity tests were performed in subjects with pancreatitis, liver disease, steroid treatment and hyperthyroidism. Insulin sensitivity for glucose utilization decreased in subjects with liver disease, steroid treatment and hyperthyroidism irrespective of the presence or absence of glucose intolerance. Hyperinsulinism was associated in most of the subjects with liver disease and steroid treatment, but even in normo-insulinemic subjects, insulin insensitivity was observed. Obesity was associated with only 2 cases in both pancreatitis and liver diseases and therefore was excluded as a major cause for insulin insensitivity in subjects studied. In subjects with pancreatitis, insulin sensitivity was not significantly decreased. It is to be noted that 4 out of 5 subjects with diabetic OGTT (oral glucose tolerance test) exhibited normal insulin sensitivity. The results indicate that in pancreatitis, tissue insulin sensitivity for glucose metabolism is not altered and therefore can be used as a marker to differentiate the other type of diabetes due to pancreatitis from type 1 or 2 diabetes. Although hyperinsulinemia may be attributable to insulin insensitivity in subjects studied at least in part, steroid and thyroid hormone are thought to act directly antagonistically with insulin for glucose metabolism.
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PMID:Insulin sensitivity in pancreatitis, liver diseases, steroid treatment and hyperthyroidism assessed by glucose, insulin and somatostatin infusion. 614 89

19 subjects with an acute episode of pancreatitis, and 5 patients with chronic pancreatitis received intravenous glucose tolerance tests with measurement of glucose, insulin and glucagon. Patients recovering from acute pancreatitis demonstrated defects in their ability to dispose of a glucose load. 10 patients had overt glucose intolerance; of these, 4 were insulin-deficient, 3 had a loss of an acute insulin response to glucose, and 3 had marked hyperglucagonemia with normal to increased insulin levels. These abnormalities were seen in response both to intravenous glucose and intravenous arginine. Therefore, according to this study, at least three factors are clearly implicated in the production of glucose intolerance after an acute episode of pancreatitis: hypoinsulinemia, delayed insulin secretory response and hyperglucagonemia.
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PMID:Hormonal responses to intravenous glucose and arginine in patients with pancreatitis. 634 Nov 94

The aim of this study was to determine whether diabetes could be ameliorated in totally pancreatectomized baboons by heterotopic intraperitoneal autotransplantation of the tail of the pancreas with the duct unligated. Twenty-five baboons were made diabetic by total pancreatectomy. Six untreated pancreatectomized animals survived a median of 5 days with mean (+/- SE) plasma glucose levels of 18 +/- 1.37 mmol/L and mean (+/- SE) potassium (K) values of 0.36 +/- 0.02% before death. Successful autotransplantation of the tail of the pancreas rendered pancreatectomized baboons consistently normoglycemic. Intravenous glucose tolerance tests performed 6 weeks after transplantation in 12 autograft recipients showed glucose intolerance in 12 of 14 recipients, and K values were significantly reduced to 1.03 +/- 0.015% (P less than 0.05). The K value of 40 normal baboons was 2.18 +/- 0.15. Histologic examination of successfully transplanted autografts of 12 animals at 6 weeks showed islets with intact beta and alpha cells, atrophy of the exocrine pancreas, graft fibrosis, and a cellular infiltration of the mononuclear type. The addition of a distal arteriovenous fistula to the graft did not reduce the incidence of graft vessel thrombosis, and all five animals died of hemorrhagic pancreatitis and venous thrombosis within 24 hours of transplantation.
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PMID:Intraperitoneal transplantation of vascularized segmental pancreatic autografts without duct ligation in the primate. 635 13

Diabetes and carbohydrate intolerance can occur in pancreatitis. Although one-half of patients with acute pancreatitis will have some evidence of glucose intolerance during their acute illness, few will require insulin administration on either a short- or long-term basis. The diabetes seen in acute pancreatitis is likely due to a combination of factors, including alerted insulin secretion, increased glucagon release, and decreased glucose utilization by the liver and peripheral tissue. Chronic pancreatitis is often associated with diabetes mellitus, with the incidence as high as 70 percent when pancreatic calcification is present. These patients tend to be very sensitive to the effects of insulin and hypoglycemia. This is probably secondary to concurrent hepatic disease, malnutrition, and a relative decrease in glucagon reserves. The diabetes seen in chronic pancreatitis is associated with decreased insulin production. Finally, although the endocrine pancreas may influence the exocrine gland through a portal system, primary diabetes mellitus probably does not result in clinically significant alterations in pancreatic exocrine function.
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PMID:Diabetes mellitus and the exocrine pancreas. 636 37

There is good evidence that viruses may play a role in some animal models of diabetes. Since mumps virus seems to be the most likely candidate, we studied the possible relationship of islet cell antibodies, islet cell surface antibodies and glucose tolerance in 86 children and adolescents in whom mumps infection had occurred 14 months previously. Impaired glucose tolerance was diagnosed in 3.5% (n = 3) but symptomatic diabetes did not appear. No relationship existed between complications of antecedent mumps infection (pancreatitis, orchitis, meningitis) and glucose tolerance. The prevalence of ICA and ICSA was 78% and 36%, respectively. The simultaneous prevalence of ICA and ICSA was 33%. The pathogenetic role of mumps infection and ICA/ ICSA and their possible relation to slow progressive beta cell destruction remains to be elucidated.
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PMID:Prevalence of islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in children and adolescents with antecedent mumps infection). 653 20

The clinical and epidemiological literature is reviewed as to metabolic effects of oral contraceptives (OCs). Both the estrogens and the progestins in OCs cause biochemical alterations which have metabolic consequences. Changes in glucose, lipid, and protein metabolism suggest that the dosage of both estrogens and progestins should be minimized as much as possible. All studies with OCs show no changes in glucose tolerance, but all do consistently show elevated plasma insulin levels as a result of OC usage. This occurs because the pill causes a decrease in insulin sensitivity in healthy women. Increases in age and weight, regardless of OC usage, will also cause an increase in glucose tolerance. Oral glucose tolerance deteriorates in all OC user groups, the greatest deterioration being in the high-dose estrogen users. Women with a history of gestational diabetes or impaired glucose tolerance should be considered high-risk pill users. Lipid abnormalities as a result of pill usage are primarily due to estrogen content. Fasting triglyceride levels are increased in all estrogen users. High-risk factors to be considered in OC prescription are: moderate obesity; diabetes; history of gestational diabetes; hypertension; history of pancreatitis, gallbladder or liver disease; physical evidence of xanthomatosis; age over 30 and smoker; age over 35; family history of hyperlipidemia; and family history of early atherosclerotic vascular disease. Many of the pill-induced protein synthesis changes are similar to those which occur during pregnancy. These, too, are due to estrogen content.
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PMID:Metabolic effects of the birth control pill. 702 12

Glucose intolerance is well known in acute pancreatitis. The question of this study was to clarify, if fat used partly instead of glucose in the parenteral nutrition of these patients allows to reduce the insulin necessary to control the blood glucose. A second question was if hypertriglyceridemia is caused by long term infusion of fat in such patients. 10 patients with acute necrotising pancreatitis were divided in two groups: group I (5 patients) were infused with a parenteral nutrition with fat, group II (5 patients) with a parenteral nutrition without fat. As parameters the amount of insulin needed to maintain the blood glucose at levels less than 200 mg% and the serum triglycerides were used. The blood glucose was controlled three times a day. For statistical evaluation the Student-t-test was used. The patients in group I (parenteral nutrition with fat) were infused 44 days and received insulin on 40 days. 69 units insulin/day were needed with a glucose dose of 243 g/day. The insulin dose per 100 g glucose was 29.9 U. The fat dose was 74 g/day. Group II (parenteral nutrition without fat) was infused 45 days and received insulin on 38 days. 103 units insulin/day were needed metabolized 295 g of glucose. The insulin per 100 g glucose was 28.7 units. The dose of insulin per 100 g glucose was not different between the two groups. In 1 patient a hypertriglyceridemia occurred after infusion of fat and disappeared immediately after withdrawal of the fat infusion. In the other patients no hypertriglyceridemia occurred during fat infusion. The parenteral infusion of fat has no influence on the glucose intolerance of patients with acute necrotising pancreatitis.
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PMID:[Effect of parenteral administration of fat on the glucose and fat metabolism in acute pancreatitis]. 704 43

Once thought to be solely a disease of insulin deficiency, diabetes mellitus now is recognized as a disorder with multiple pathogenetic mechanisms. Newer terminology identifies those uncommon patients with true insulin deficiency as having insulin-dependent diabetes (IDDM), while the majority of patients with diabetes have some residual insulin secretion but may have a disorder of insulin receptor number or affinity. These patients have non-insulin dependent diabetes (NIDDM). Other patients may have gestational diabetes, impaired glucose tolerance, a potential for glucose intolerance, or a previous history of diabetes. A few patients will have diabetes secondary to a known cause, such as pancreatitis or Cushing's syndrome. Understanding this nosological approach to diabetes should enhance the clinician's decisions regarding therapy.
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PMID:Classification and pathogenesis of the diabetes syndrome: a historical perspective. 705 Feb 15

Cholecystokinin (CCK) receptor antagonists are shown to have therapeutic as well as preventive effects in some types of acute pancreatitis. However, there is a possibility that administration of CCK receptor antagonists with a high inhibitory potency on the endocrine pancreas to patients with acute pancreatitis exacerbates the associated glucose intolerance. In the present study we simultaneously examined the effects of the newly developed benzodiazepine derivative FK480 and proglumide-related antagonist KSG-504 on CCK octapeptide (CCK-8)-stimulated exocrine and endocrine function in the isolated perfused rat pancreas. FK480 and KSG-504 inhibited CCK-8-stimulated pancreatic juice flow, protein output, and insulin release in a dose-dependent manner. FK480 was approximately 10 times more potent than KSG-504 in inhibiting exocrine and endocrine secretion. Both antagonists inhibited CCK-8-stimulated insulin release more potently than exocrine secretion. FK480 caused a dose-dependent residual inhibition of exocrine secretion after its removal from the perfusate, whereas insulin release was only slightly impaired even at the highest dose. In contrast, termination of KSG-504 infusion resulted in an immediate increase in both exocrine and insulin responses without causing any residual inhibition. With regard to the residual inhibition, therefore, KSG-504 had no significant influences on exocrine and insulin release, whereas FK480 inhibited exocrine secretion more potently than insulin response. These results suggest that FK480 might become a useful therapeutic agent for pancreatitis with respect to its long-duration inhibitory effect on exocrine secretion and short-duration inhibitory effect on insulin release.
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PMID:Different inhibitory effects of the newly developed CCK receptor antagonists FK480 and KSG-504 on pancreatic exocrine and endocrine secretion in the isolated perfused rat pancreas. 771 33


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