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

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

The case history of a patient who presented with diabetic ketoacidosis and was subsequently found to have hyperparathyroid crisis complicated by acute necrotizing pancreatitis and phosphate depletion syndrome is reviewed. The interaction of these diseases and their treatment is discussed. The simultaneous presentation of hyperparathyroid crisis and acute necrotizing pancreatitis is rare, and no instance of survival has been reported previously.
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PMID:Hyperparathyroid crisis and acute necrotizing pancreatitis presenting as diabetic ketoacidosis. 677 34

Initial steps of the experimental pancreatitis were characterized by an increase in glycerophosphate accumulation as well as in activity of glycerokinase, glycerophosphate dehydrogenase and glycerol dehydrogenase; content of free glycerol and dihydroacetone phosphate was also increased. Within the subsequent periods the patterns studied exhibited normalization except of glycerokinase and glycerophosphate dehydrogenase activity of which was distinctly decreased as compared with the controls.
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PMID:[Impairment of glycerophosphate and glycerol turnover in myocardium under conditions of experimental pancreatitis]. 679 79

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Pancreatic blood flow was measured with 15-micrometer radioactive microspheres. Measurements of pancreatic adenosine triphosphate (ATP) and creatine phosphate (CP) were made under normal conditions and during acute hemorrhagic pancreatitis. Basal ATP and CP concentrations were 5.82 +/- 0.25 and 5.30 +/- 0.31 mmol/g wet tissue, respectively. Hemorrhagic pancreatitis was characterized by a severe reduction in pancreatic blood flow, followed by a 45% fall of ATP and a 70% lowering of CP. These results suggest that inadequate pancreatic tissue perfusion during acute pancreatitis results in a marked depletion of high-energy phosphate stores. We suspect this energy depletion reflects the progression of the disease from edematous to hemorrhagic pancreatitis and causes irreversible damage of pancreatic tissue.
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PMID:Correlation of pancreatic blood flow and high-energy phosphates during experimental pancreatitis. 711 26

A 32-year-old man with insulin-dependent diabetes secondary to chronic calcifying pancreatitis of alcoholic origin in whom hypocalciuria (22 to 88 mg/24 hours) was discovered by chance, renal function being normal. Plasma phosphate levels were between 25 and 35 mg/l and the level of parathyroid hormone was at the upper limit of normal. Cervicotomy led to the discovery of three parathyroid glands which were removed. Their weight was increased and their histological appearance normal. The fourth parathyroid was not seen. Hypercalcaemia and hypocalciuria were found during the operation and persis 3 years after, with none of the usual causes being found. This patient has a certain number of characteristics reminiscent of familial hypercalcaemia-hypocalciuria syndrome: high plasma calcium levels associated with low calciuria despite normal renal function and a plasma parathyroid level normal in most cases. The physiopathology of this syndrome remains unknown. Its course is benign, without renal complications. Partial parathyroidectomy is ineffective.
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PMID:[An unrecognised cause of hypercalcaemia: hypercalcaemia-hyocalcluria syndrome]. 736 69

Pancreatitis is accepted as an uncommon complication of parathyroid surgery, but it has been suggested that up to 35% of patients may experience hyperamylasaemia after parathyroidectomy indicating subclinical inflammation of the pancreas. A series of 26 patients undergoing parathyroidectomy were studied by preoperative biochemical analyses repeated 24 and 48 h postoperatively allowing changes in calcium metabolism and serum and urinary amylase levels to be documented. Of the patients, 21 also underwent a CT scan of the pancreas between 24 and 48 h after operation. Despite highly significant changes in serum parathormone, calcium and phosphate levels postoperatively, there was no evidence in any patient of acute pancreatic inflammation or hyperamylasaemia. Twenty-one patients underwent unilateral neck exploration, and we suggest that the absence of any detectable amylase elevation supports the suggestion that such elevation may reflect an increase in salivary isoamylase as a result of extensive neck dissection, rather than reflecting a subclinical pancreatitis. The development of postparathyroidectomy pancreatitis appears to be an all or nothing phenomenon of unknown aetiology.
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PMID:Does subclinical pancreatic inflammation occur after parathyroidectomy? 754 Aug 15

We review the pathogenesis of cholesterol gallstones, which occur in five steps: 1) metabolic; 2) chemical; 3) nucleation, 4) growing and maturation of gallstones; 5) clinical. It is emphasized that in the third step it could occur an arenous precipitate formed by cholesterol crystals, calcium bilirrubinate granules, calcium phosphate, or fatty acids anions and calcium, and mucin, called "biliary sludge", which has been associated with cholecystitis and pancreatitis. We describe the gallbladder motor abnormalities that occur during the lithogenesis and the diagnostic approach through scintigraphy and real time ultrasound. We review the pancreatobiliary dyskinesia, a condition associated with the postcholecystectomy syndrome. This later condition can result from anatomic stenosis or dyskinetic dysfunction of the sphincter of Oddi. Likewise, it is pointed out that at the present time, the manometric evaluation of the sphincter of Oddi is the gold standard in the diagnostic approach of this condition.
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PMID:[Laboratory studies and special tests for assessing gallbladder and bile duct function]. 774 24

In order to investigate the changes in phosphoglucose metabolism in acute experimental pancreatitis, the authors utilized the measuring cell NMR spectroscopy. The experimental pancreatitis had been evoked by both the method of ligature of lateral pancreas ducts and that of the duodenal blind loop. These methods evoke a morphological response, namely edematous and necrotizing pancreatitis. Gradual reduction of macroergic phosphate binds and augmentation of anorganic phosphates represent the principal change in NMR spectrum. The clinical picture provides evidence of the exhaustion of highly energetic phosphate compounds which are necessary for the maintenance of integrity of the pancreas tissue in acute experimental pancreatitis. The discussion includes the possibilities and limitations of the NMR spectroscopy.
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PMID:[31P NMR spectroscopy in acute experimental pancreatitis]. 781 17

Many previous reports using experimental animal models of pancreatitis have suggested that oxygen free radicals play an important part in initiation and development of pancreatitis. Infiltration of inflammatory cells--that is, neutrophils, lymphocytes, and monocytes--has been seen in damaged pancreatic glands of animal models and patients with pancreatitis. As neutrophils are known to be the highest producer of oxygen free radicals among these inflammatory cells, it seems plausible that oxygen free radicals produced by neutrophils have some pathoaetiological meaning in pancreatitis. This study measured the superoxide production by neutrophils obtained from patients with acute and chronic pancreatitis and then examined the effects of pancreatic enzymes on superoxide production. Patients showed significantly higher superoxide production by 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) stimulated neutrophils than healthy controls. Among the three pancreatic enzymes, amylase, trypsin, and elastase, elastase was the only one that increased the superoxide production by PMA stimulated neutrophils, by an increment of 1.5-fold. It also increased the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase prepared from PMA stimulated neutrophils by a factor of 2.1. High affinity and low affinity binding sites for elastase on neutrophils were identified. These results suggest that elastase plays a part in the development of pancreatitis by enhancing superoxide production of neutrophils.
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PMID:Specific interaction of pancreatic elastase and leucocytes to produce oxygen radicals and its implication in pancreatitis. 782 93

In a population of 716 patients with end-stage renal disease (ESRD), 46 patients (6.4%) were identified as having pancreatitis. Pancreatitis was significantly more common in those with alcohol abuse, systemic lupus erythematosus (SLE), and polycystic kidney disease. It was not significantly associated with hyperlipidemia, biliary tract disease, or hypercalcemia. Acute pancreatitis occurring before the patient developed ESRD was mainly alcohol-related and did not appear to be a significant risk factor for future episodes of pancreatitis during dialysis. Chronic calcific pancreatitis diagnosed before ESRD was almost invariably due to alcohol abuse, and tended to be a marker for recurrent acute exacerbation after development of ESRD, whether alcohol consumption continued or not. Pancreatitis occurring for the first time after ESRD in patients on dialysis was generally benign, and was usually accompanied by an uneventful recovery and few recurrent episodes. However, a significant elevation of the calcium x phosphate product was observed in these patients, occurring in about half the patients without any known precipitating factor. After kidney transplantation, the development of pancreatitis was associated with higher morbidity and mortality. Chronic calcific pancreatitis diagnosed after ESRD occurred only in patients with SLE; reported here for the first time, it may be a manifestation of long-standing disease, chronic steroid therapy, or both.
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PMID:Pancreatitis in patients with end-stage renal disease. 830 63


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