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

Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
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PMID:The effect of glucagon on the exocrine pancreas. A review. 36 5

One hundred patients with acute pancreatitis are studied. The results in 90 cases were "favorable or very favorable", in ten cases "unfavorable or death". Various different characterisitics were analyzed statistically in relationship to the two types of outcome: sex, clinical histories, and results of physical examination. Furthermore, the individual relationships between age, main initial analytic parameters, and later development were determined. In our experience neither age nor sex, considered individually, showed a significant relationship to the seriousness of the disease. Having had pancreatitis previously proved to be a favorable factor (p less than 0.005). None of the other factors in the case histories showed any bearing of the later course of the condition. Findings in physical examination which were signs of unfavorable prognosis included jaundice (p less than 0.001), low blood pressure (p less than 0.001), tachycardia (p less than 0.005), intestinal paresia (p less than 0.001), pain following decompression (p less than 0.025), and abdominal tenderness (p less than 0.05). Abnormalities in ECG (p less than 0.005), marked leukocytosis (p less than 0.0005), hyperglycemia (p less than 0.02), hypocalcemia (p less than 0.05), and high values for the coefficient of amilase/creatinine clearance (p less than 0.01) also suggested an unfavorable course.
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PMID:[Early prognosis of acute pancreatitis (author's transl)]. 45 91

Lethal nosocomial mucormycosis developed in three previously well individuals while they were receiving intensive care for acute hemorrhagic pancreatitis, for cardiogenic shock, and for a ruptured intra-abdominal aortic aneurysm. In two cases, the condition was first seen as progressive cavitary pneumonia refractory to antibacterial therapy; Mucoraceae was identified in all three patients only at autopsy. Each patient had received large doses of corticosteroids and broad-spectrum antibiotics, and all had suffered from respiratory failure, acute renal failure with acidosis, and severe hyperglycemia in association with total parenteral nutrition. Mucoraceae should be regarded as an additional nosocomial pathogen in the setting of advanced life-support care.
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PMID:Mucormycosis. A complication of critical care. 64 64

It is evident that ethanol by itself or one of its metabolites produces alterations in transport, metabolism and disposition of carbohydrates. Ethanol acts via changes in the redox state of co-factors; e.g. ethanol-induced hypoglycemia is due, partly, to the inhibition of hepatic gluconeogenesis by ethanol as a consequence of the increased NADH2/NAD ratio in patients whose glycogen stores are already depleted. On the other hand, hyperglycemia has also been described in patients with alcoholism. Although its mechanism is still obscure, abnormal hormonal secretion of insulin, catecholamines and glucocorticoids has been incriminated. Finally, structural changes of the liver and pancreas such as cirrhosis and pancreatitis produced by chronic alcohol consumption should also be considered as pathogenetic factors in a variety of clinical states involving deranged carbohydrate metabolism.
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PMID:Alcohol induced changes of carbohydrate metabolism [author's transl]. 70 66

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Alloxan diabetes was induced in inbred rats that then were divided into four groups consisting of unoperated diabetic controls, sham-operated diabetic controls, rats given pancreaticoduodenal isografts, and rats given duct-ligated pancreas isografts. The animals were studied for from 18 months (controls) to two years (transplants) and the following important results were obtained: 1) In striking contrast to the diabetic controls, pancreas transplants of both types produced immediate and permanent relief of hyperglycemia, immediate and lasting elevation of serum insulin levels, a normal weight and growth curve, and good health for two years. Removal of the graft was followed by recurrence of severe diabetes. 2) Pancreas transplants of both types prevented the widespread and severe renal, ophthalmic and neural lesions of diabetes that were found in the diabetic controls. 3) The duct-ligated pancreas graft and pancreaticoduodenal transplant were equally effective in controlling diabetes. Ligation of the pancreatic duct was not followed by significant morphologic or clinical evidence of pancreatitis or by loss of endocrine function. 4) Portal venous drainage of the pancreas transplant was unnecessary for good endocrine function.
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PMID:Long term studies of pancreas transplantation in experimental diabetes mellitus. 109 93

The finding that diabetic microangiopathy is caused by accumulation of multiple layers of basal lamina and experiments in which similar basal lamina layering is produced when new cell generations repopulate preexisting basal lamina scaffolding (from which previous cell generations have shed) indicate, that the rates of cell death and cell replenishment are accelerated in diabetics. Because the lesions are focal and regional and develop at different ages and in different time sequences, we have proposed that the accelerated cell turnover is probably caused by increased vulnerability of diabetic cells to injury which in turn may represent the expression of a genetically transmitted defect. To test whether this aberration can be detected in vitro, we examined the replicative life-span of skin fibroblasts from three nondiabetics, three age- and sex-matched diabetics and one individual with acquired hyperglycemia due to pancreatitis. Cells of diabetics exhibited about half the number of population doublings as cells from nondiabetics (0.01 less than P less than 0.025). Cells of the individual with pancreatitis generated a normal number of cell doublings. The interpretation that fits best with all data is that decreased replicative life span of diabetic fibroblasts in vitro is also an expression of increased susceptibility of diabetics' cells to injury and dying.
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PMID:Restricted replicative life-span of diabetic fibroblasts in vitro: its relation to microangiopathy. 110 56

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.
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PMID:Glucagon secretion in acute and chronic pancreatitis. 120 May 23

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

Non-insulin-dependent (type II) diabetes mellitus is an inherited metabolic disorder characterized by hyperglycemia with resistance to ketosis. The onset is usually after age 40 years. Patients are variably symptomatic and frequently obese, hyperlipidemic and hypertensive. Clinical, pathological and biochemical evidence suggests that the disease is caused by a combined defect of insulin secretion and insulin resistance. Goals in the treatment of hyperglycemia, dyslipidemia and hypertension should be appropriate to the patient's age, the status of diabetic complications and the safety of the regimen. Nonpharmacologic management includes meal planning to achieve a suitable weight, such that carbohydrates supply 50% to 60% of the daily energy intake, with limitation of saturated fats, cholesterol and salt when indicated, and physical activity appropriate to the patient's age and cardiovascular status. Follow-up should include regular visits with the physician, access to diabetes education, self-monitoring of the blood or urine glucose level and laboratory-based measurement of the plasma levels of glucose and glycated hemoglobin. If unacceptably high plasma glucose levels (e.g., 8 mmol/L or more before meals) persist the use of orally given hypoglycemic agents (a sulfonylurea agent or metformin or both) is indicated. Temporary insulin therapy may be needed during intercurrent illness, surgery or pregnancy. Long-term insulin therapy is recommended in patients with continuing symptoms or hyperglycemia despite treatment with diet modification and orally given hypoglycemic agents. The risk of pancreatitis may be reduced by treating severe hypertriglyceridemia (fasting serum level greater than 10 mmol/L) and atherosclerotic disease through dietary and, if necessary, pharmacologic management of dyslipidemia. Antihypertensive agents are available that have fewer adverse metabolic effects than thiazides and beta-adrenergic receptor blockers. New drugs are being developed that will enhance effective insulin secretion and action and inhibit the progress of complications.
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PMID:Non-insulin-dependent (type II) diabetes mellitus. 174 94


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