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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
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PMID:The hypocalcemia of acute pancreatitis. 114 52

Hypophosphatemia and decreased content of ATP, 2,3-DPG in erythrocytes were found in 147 patients operated upon organs of the abdominal cavity. Hypophosphatemia was more pronounced after operations for ulcer disease of the stomach and duodenum, acute pancreatitis and commissural ileus. An intravenous injection of potassium dihydrogen phosphate++ prevents the development of hypophosphatemia and concomitant decrease of the content of nonorganic phosphorus, ATP, 2,3-DPG in erythrocytes and may improve the postoperative period in these patients.
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PMID:[Correction of disorders of phosphorus metabolism after operations on the abdominal organs]. 165 8

To determine changes in parathyroid hormone secretion and target organ response caused by acute pancreatitis before the development of systemic toxic conditions, experimental acute pancreatitis was induced in rats with a choline-deficient, ethionine-supplemented diet. After 7 days, the rats were weighed and bled, and one kidney was assayed for 25-hydroxyvitamin D1 hydroxylase activity. Several manifestations of pancreatitis were observed in rats given the diet: weight loss (from 29.6 to 26.3 g vs that for control rats, from 29 to 52.8 g) and lower dietary intake (15.5 vs 47 g per rat per 7 days). Serum amylase levels fell from 1794 to 350 U/L in rats given the choline-deficient, ethionine-supplemented diet compared with levels of 1800 to 2100 U/L in control rats. The pancreases of rats given the choline-deficient, ethionine-supplemented diet showed degeneration, necrosis, and hemorrhaging. Serum levels of calcium, phosphorus, chloride, and parathyroid hormone did not change significantly throughout the experiment. Renal 25-hydroxyvitamin D1 hydroxylase activity was higher than in control rats (8.9 +/- 0.8 vs 7.6 +/- 0.6 fmol/mg of kidney per minute). Acute pancreatitis in this experimental animal model does not alter serum levels of calcium and parathyroid hormone or reduce target organ responsiveness to the hormone.
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PMID:Parathyroid hormone secretion and target organ response in experimental acute pancreatitis. 170 5

Serum calcium changes in severe pancreatitis were studied in 23 dogs. Twelve dogs underwent duodenotomy and served as controls. Pancreatitis was induced in the other 11 by autologous bile injection (1 ml/kg) into the pancreatic duct. Serum amylase, total calcium, ionized calcium, albumin, magnesium, chloride, phosphorous, parathyroid hormone (PTH), and calcitonin were measured at 0, 1/2, 1, 3, 6, 24, 48, and 72 hours after duodenotomy or bile injection. Serum amylase levels became significantly elevated in all dogs with pancreatitis at 30 minutes (p less than 0.01) and remained so throughout the entire experiment. Total calcium levels dropped significantly 30 minutes after pancreatitis was induced from 10.0 +/- 0.3 mg/dl compared with 8.8 +/- 0.4 mg/dl in control dogs (p less than 0.05) and remained statistically lower for as long as 1 hour. Ionized calcium levels were significantly lower than were those of control dogs at 1/2, 1, 3, and 6 hours (p less than 0.05). Serum magnesium and chloride levels showed no significant changes between both groups. The only significant difference in phosphorus values was at 6 hours when they were higher in dogs with pancreatitis than in controls (6.2 +/- 0.3 mg/dl versus 4.8 +/- 0.4 mg/dl; p less than 0.05). Serum albumin levels remained unchanged throughout the study except for 48 hours when they were significantly lower in animals with pancreatitis (p less than 0.02). PTH levels were significantly greater in dogs with pancreatitis than in controls at 1, 3, 6, and 24 hours (p less than 0.05). There was no significant difference in calcitonin levels between both groups. Ionized calcium is a more reliable indicator of calcium fluxes in acute experimental pancreatitis since it remains depressed longer than total serum calcium. The time course of PTH elevation indicates a reaction to hypocalcemia, and failure of PTH secretion is not the cause of hypocalcemia in pancreatitis. This study does not support elevation of calcitonin as a cause of hypocalcemia in acute pancreatitis.
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PMID:Serum calcium metabolism in acute experimental pancreatitis. 241 69

Acute haemorrhagic pancreatitis was induced in rats by injecting 0.2 ml of 5% (92.9 mmol/l) aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lysolecithin was separated from the pancreatic homogenate by thin-layer chromatography and quantified by phosphorus determination. The lysolecithin content increased rapidly, remained elevated for 12 h, and returned to the control level 24 h after the injection. Treatment with a trypsin inhibitor, aprotinin (Trasylol), given intraperitoneally and intravenously during 2 h postoperatively (800,000 units/kg of body weight) had no beneficial effects compared with physiological saline treatment. When the animals were treated similarly with a phospholipase A inhibitor, procaine hydrochloride (40 mg/kg of body weight), 45% of them survived 72 h (p less than 0.01). It was concluded that phospholipase A, which converts lecithin into lysolecithin, plays a significant role in the pathogenesis of acute pancreatitis.
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PMID:Experimental pancreatitis in the rat. The role of phospholipase A in sodium taurocholate-induced acute haemorrhagic pancreatitis. 616 66

Acute haemorrhagic pancreatitis was induced in rats by injecting aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lecithin and lysolecithin were separated from pulmonary homogenate by thin layer chromatography and quantified by phosphorus determination. The ratio of lysolecithin to lecithin increased after the sodium taurocholate injection as well as after i.v. administration of porcine pancreatic phospholipase A2. It was concluded that phospholipase A2, released from pancreatic acinar cells into blood, may convert pulmonary lecithin into lysolecithin during acute pancreatitis. Destruction of pulmonary surfactant may contribute to the development of the adult respiratory distress syndrome as seen in patients suffering from severe acute pancreatitis.
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PMID:Experimental pancreatitis in the rat. Changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis. 685 89

A patient with a markedly elevated serum phosphorus level (23.9 mg/dL) is described, followed by a brief review of severe hyperphosphatemia. Elevated serum phosphorus levels may be artifactual or true. True hyperphosphatemia is usefully subdivided according to (a) whether phosphorus is added to the extracellular fluid from a variety of exogenous or endogenous sources, or (b) whether the urinary excretion of phosphorus is reduced from either decreased glomerular filtration or increased tubular reabsorption. Severe hyperphosphatemia, defined herein as levels of 14 mg/dL or higher, is almost invariably multifactorial--usually resulting from addition of phosphorus to the extracellular fluid together with decreased phosphorus excretion. The hyperphosphatemia of the patient described herein appeared to result from a combination of dietary phosphorus supplementation, acute renal failure, acute pancreatitis, and ischemic bowel disease, complicated by lactic acidosis.
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PMID:Review of the literature: severe hyperphosphatemia. 757 22

A surgical method is described which allows in vivo assessment of reversible rat pancreatic ischemia using 31P NMR spectroscopy at 2.0 T. Phosphorous-31 NMR spectra acquired during the ischemic period show the expected increase in inorganic phosphate with a concomitant decrease in ATP levels and pH as compared to controls. Upon reperfusion, inorganic phosphate and ATP returned to control levels while pH recovered to a more alkaline value. This method provides a means of studying in vivo changes in high energy metabolite associated with acute pancreatitis (AP) and maintains the secretory ability of the gland so that different forms of AP, such as those arising from pancreatic juice edema, can be studied.
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PMID:A method for in vivo assessment of reversible rat pancreatic ischemia using 31P NMR spectroscopy at 2.0 tesla. 779 56

The ability of high dietary carbohydrate to induce acute pancreatitis was investigated in groups of 16, 21-day and 15-month old rats fed different carbohydrate diets for 30 days. Significantly increased levels of serum amylase (2-fold), phospholipids (50%), phosphorus (2-fold), and lipoperoxides (8-fold) were observed in 15-month old rats fed a high-carbohydrate diet, compared to rats fed a diet with normal carbohydrate levels, indicating peroxidation of membrane lipids which caused final cell death and pancreatic lesion. Serum Cu-Zn superoxide dismutase activity was not altered. Daily administration of bovine Cu-Zn superoxide dismutase conjugated with polyethylene glycol prevented the serum level alterations and pancreatic lesions, indicating that the superoxide radical has a role in dietary carbohydrate-induced acute pancreatitis. No biochemical changes were observed in rats in which treatment was initiated on the 21st day of life indicating that this is an age-related lesion.
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PMID:High dietary carbohydrate and pancreatic lesion. 822 Feb 65

Migraine is periodical disorder which is characterized by recurrent headache seizures different in intensity, frequency and duration. Amylases L-1,4 glycol: gluckanohidrolises, (EC.3.2.1.1) are enzymes from hydrolase's group which dissolve starch meaning glycogen. Activity of amylases in serum grows: at acute pancreatitis, at carcinoma of pancreas, heavy necroses of pancreas. Total number of examinees was 92 out of which 45 were male (48.9 %) and 47 female or 51.1 %. Average age of the examines was 42.9. Neuroticism scale which was tested by Cornell scale was 55,03. Out of the total number of examinees 30 or 32,6 were non-smokers while 62 or 67,4 % smoked regularly. The aim of this work is to perform hematological-biochemical test of blood in patients with migraine. In the beginning of this research it was planned for all the patients to have hematological blood test done (sedimentation of erythrocytes, trombocytes, complete blood test and differential blood test) and biochemical blood test (hepatogram, transamynase, amylase, Lactal dehydrogenase, Alkalic phosphatase, ferrum in serum, Glucose, Cholesterol, Calcium and Phosphorus in serum. After reviewing the received values of hematological and biochemical tests, all values were within the borders of normal values. Amylases had higher values at 49 or 53,3 % of patients, and 43 or 46,7 % of patients had normal values of amylases. Normal values of amylases are to 220 U/l measured by I.F.C. at 37 degrees C. Medium value in tested group is 219.09. It means that every second examinee had increased values of amylase in blood; there is no statistics difference of amylase value between sexes.
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PMID:[Hematological-biochemical tests in patient with migraine]. 1642 33


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