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

The influence of the secretory state of the pancreas on the development of pancreatitis in an isolated, ex vivo, perfused canine pancreas model was evaluated. Free fatty acid infusion was used to induce pancreatitis, and secretin, glucagon, and atropine were administered to influence the secretory state. Despite a 40-fold difference in hourly secretory output, the development of pancreatitis as judged by weight gain, hemoconcentration, amylase value, and arterial blood pressure response was similar in the stimulated, basal, and suppressed states. This study casts further doubt on the role of hypersecretion in the pathogenesis of acute pancreatitis.
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PMID:Experimental pancreatitis: influence of secretory state of the pancreas. 615 93

The known suppressive actions of glucagon on the secretion of pancreatic enzymes and of gastric acid, and the reported effectiveness of glucagon in treating acute pancreatitis, prompted the authors to carry out a prospective, randomized, double-blind, controlled trial of this hormone. Sixty-six patients with acute pancreatitis admitted to the surgical service of the Vancouver General Hospital were randomized into two groups of 33, receiving either glucagon or placebo in addition to their conventional therapy. The two groups were comparable with respect to the cause of the pancreatitis and the severity of the disease. Glucagon did not reduce the patients' analgesic requirements or the duration of abdominal signs, ileus, hyperamylasemia or hospital stay. Of the 66 patients, 4 died. Three of these were in the group receiving glucagon. The authors conclude that, contrary to theoretical expectations and the results of past uncontrolled trials, glucagon has no beneficial effect on the clinical course or outcome of acute pancreatitis, irrespective of the etiology or severity of the disease.
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PMID:Glucagon therapy in acute pancreatitis: prospective randomized double-blind study. 616 Sep 1

A double blind study testing the effect of long-acting zinc-protamine-glucagon (7.5 mg every 12 hours for 4--5 days) was carried out in acute pancreatitis. There were 32 patients in ZP-glucagon- and 39 patients in the placebo group. The results show that glucagon had a slightly favourable effect on the general clinical course of the disease but they do not give enough evidence for routine use of glucagon in pancreatitis.
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PMID:The effect of zinc-protamine-glucagon in acute pancreatitis. 616 89

The literature on the medical management of pancreatitis is reviewed. Reference is made to successful results obtained in 30 personal cases with a semimedicamentous protocol, in which an antipancreatitic activity in the true sense was obtained by administering aprotinine and glucagon. Eight subjects presented acute or recrudescent chronic forms, 12 pancreatitis combined with cholelithiasis, 5 secondary forms following penetrating duodenal ulcers, and 5 forms arising after stomach, duodenal or bile duct surgery. The evaluation of each case is described and the conclusion is drawn that intensive, timely medical therapy will secure resolution in the majority of cases.
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PMID:[Clinical and therapeutic studies of pancreatitis]. 616 57

Partial pancreatic duct obstruction due to gallstone migration has been suggested as an important step in the pathogenesis of gallstone, pancreatitis. Since gallstone migration often follows a meal, pancreatic secretory stimulation is also present. Utilizing the isolated perfused canine pancreas, an experimental model of gallstone pancreatitis was developed by partial obstruction of the main pancreatic duct and secretin stimulation (POSS). In control glands (n=6) perfused for a four-hour period, gross appearance remained normal, weight gain (8 g) was minimal, and mean amylase (875 Caraway units/dl) remained within normal limits. POSS glands (n=9) became markedly edematous during the perfusion period, with significant weight gain (47 g) and hyperamylasemia (7200 Caraway units/dl). Steroid-treated (n=6) and Trasylol-treated (n=6) POSS glands became edematous, and mean weight gain and hyperamylasemia were similar to those seen in untreated POSS glands. Glucagon-treated POSS glands (n=6) became edematous, but mean weight gain (24 g) was significantly decreased compared with that of untreated POSS glands. Mean amylase elevation was unchanged (8536 Caraway units/dl). POSS glands treated with albumin (n=6) remained normal in gross appearance, mean weight gain (12 g) was minimal and mean amylase (3120 Caraway units/dl) was significantly decreased compared to that of untreated POSS glands. The failure of Trasylol to ameliorate the injury response and the effectiveness of albumin were interpreted as evidence against enzyme extravasation and for capillary injury as the initial step in the pathogenesis of gallstone pancreatitis.
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PMID:Experimental gallstone pancreatitis. Pathogenesis and response to different treatment modalities. 617 93

Diabetic ketoacidosis (DKA) is the commonest endocrine emergency encountered in clinical practice. Although in the last 3 decades the average worldwide immediate mortality has decreased from 10% to 5%, survival has not improved strikingly. The pathogenesis of DKA is currently attributed to a combination of two hormonal abnormalities--a relative insulin insufficiency and stress hormone excess (glucagon, catecholamines, cortisol and growth hormone). Withdrawal of exogenous insulin, pancreatic beta cell failure and insulin resistance are factors leading to relative insulin insufficiency. Factors leading to stress hormone excess include fasting, stress and dehydration. The combination of these two hormonal abnormalities leads to impaired carbohydrate utilization and ketonaemia which in turn results in metabolic acidosis with loss of water through acidotic breaths, rise in plasma lipids, hyperglycaemia and glycosuria leading to osmotic diuresis and further loss of water, excretion of partly neutralised ketoacids via the kidney with loss of cations (Na+ and K+). A net increase in protein catabolism which leads to an increased amino acid flux from muscle and an enhanced load of gluconeogenic precursor to the liver and a rise in blood pyruvate and lactate concentration. The prevention of either of these hormonal abnormalities will prevent the development of DKA. The successful outcome in the treatment of DKA is clearly related to the prompt recognition of the diagnosis and the precipitation factors, the severity of the initial metabolic derangements, the judicious use of fluid and electrolyte replacement, the choice, route and dosage of the insulin therapy and above all the close monitoring and meticulous clinical care of the patient throughout the entire course of the treatment. Current acceptable treatment of DKA include the following: adequate fluid replacement: low dose insulin therapy at frequent intervals; adequate potassium replacement from time of first insulin therapy with ECG monitoring; bicarbonate replacement if pH less than 7.1; broad spectrum antibiotics if infections is suspected and other supportive measures. The role of phosphate and magnesium replacement is still controversial. An awareness of the complications during the treatment of DKA including cerebral edema (paradoxical acidosis), altered central nervous system oxygenation, vascular thrombosis, shock, myocardial infarction, pancreatitis, infection, inhalation of vomitus , overhydration, underhydration , hypoglycaemia, hyperkalemia and hypokalemia all certainly help improve the morbidity and mortality of DKA.
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PMID:Current concepts of the pathogenesis and management of diabetic ketoacidosis (DKA). 633 Dec 71

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

We describe the results of metabolic studies in a 17-year-old woman with diabetes mellitus which was the initial manifestation of idiopathic chronic calcifying pancreatitis (CCP). These studies were done on 2 occasions, 5 months and 5 years after the onset of diabetes, when her diabetes could be managed by glibenclamide and insulin, respectively. Five months after the onset of diabetes, oral glucose produced a small increase in insulin and a paradoxical rise in both glucagon immunoreactivity (GI) and growth hormone (GH). BY contrast, arginine-stimulated responses of the three hormones were normal. No increase in GI and a blunted rise in GH resulted from an insulin-induced decrease in blood glucose. Five years later, when CCP was demonstrated by roentogenologic examinations and tests of pancreatic exocrine function, oral glucose was followed by a flat and depressed response of C-peptide immunoreactivity and a markedly elevated response of gut glucagon-like-immunoreactivity (gut GLI). There were delayed and extremely low responses of pancreatic polypeptide to a test meal, irrespective whether or not her diabetes required treatment with insulin. These results demonstrate that CCP can cause diabetes in adolescents, as it does in adults, and that the adolescent woman described here had impaired responses of PP and gut GLI as well as insulin, GI and GH, especially to changes in blood glucose levels.
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PMID:Diabetes mellitus secondary to idiopathic chronic calcifying pancreatitis in an adolescent woman. 635 71

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

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


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