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

Pancreatic stone protein, a novel protein isolated from pancreatic stones of patients suffering from chronic calcifying pancreatitis and secreted in normal human pancreatic juice, was measured by radial immunodiffusion in pure pancreatic juice. Patients with chronic calcifying pancreatitis of different etiologies had significantly lower levels of pancreatic stone protein when compared with other pancreatic diseases and controls. Pancreatic stone protein suppresses in vitro calcium carbonate precipitation and therefore stabilizes normally supersaturated pancreatic juice. The decreased pancreatic stone protein levels observed could be a key factor in the growth of calcium carbonate crystals and stone development during the course of chronic calcifying pancreatitis.
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PMID:Pancreatic stone protein. II. Implication in stone formation during the course of chronic calcifying pancreatitis. 392 21

The first lesion of chronic calcifying pancreatitis (CCP), the most frequent form of chronic pancreatitis is the formation in the ducts of plugs build up of protein and calcium carbonate which are at the origin of pancreatic calculi. Pancreatic juice is supersaturated in calcium carbonate. A novel protein, the pancreatic stone protein (PSP) has been purified from human pancreatic juice and its amino-acid composition has been determined. It is biosynthesized in the acinar cell as well as enzymes. PSP prevents the formation of calcium carbonate crystals in a supersaturated solution. Its secretion is decreased in patients presenting with CCP. It is proposed that this decrease plays an important part in the pathogenesis of CCP.
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PMID:[Pancreatic lithogenesis]. 396 39

Citrate, calcium and protein have been estimated in pure pancreatic juice after a secretin and a CCK injection in 4 patients presenting with alcoholic calcified pancreatitis (ACP), 10 controls without evidence of pancreatic disease, drinking more than 130 g alcohol/day, and 10 controls without evidence of pancreatic disease, drinking less than 20 g alcohol/day. Citrate is normally secreted in the pancreatic juice and this secretion increases in parallel with protein after CCK injection. Citrate secretion is significantly decreased in the two alcoholic groups. Calcium secretion is increased in the ACP, and reasons are presented to suggest that this may be due to lesions of the ducts. These modifications could play a role in the formation of pancreatic stones which are mostly built up of calcium carbonate.
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PMID:Citrate and calcium secretion in the pure human pancreatic juice of alcoholic and nonalcoholic men and of chronic pancreatitis patients. 401 38

To test the discriminatory potential of certain indices of pancreatic function we performed duodenal perfusion studies and measured trypsin, bicarbonate, and lactoferrin outputs, and plasma concentrations of pancreatic polypeptide and motilin in the basal state and during continuous intravenous stimulation with 100 ng kg-1h-1 Ceruletide and 1 CU kg-1h-1 secretin. The following groups were studied: 12 normal volunteers (NV), seven patients with chronic pancreatitis with steatorrhea (CPS), and seven without steatorrhea (CP). Stimulated trypsin outputs, after 45 min of stimulation, were the best discriminant among the groups (NV versus CPS, p less than 0.0005; NV versus CP, p less than 0.005; CP versus CPS, p less than 0.05). Basal trypsin outputs showed similar patterns but failed to discriminate between NV and CP. Bicarbonate outputs were less discriminatory than trypsin outputs. Lactoferrin outputs failed to discriminate, but transient high peak outputs occurred in the initial stimulation period in all four patients with calcific chronic pancreatitis, suggesting a washout phenomenon. Basal motilin levels were elevated in both groups of pancreatitis (p less than 0.05). Stimulated pancreatic polypeptide levels were lower in CPS (NV versus CPS, p less than 0.05) but higher in CP (NV versus CP, p less than 0.005). These differences were also apparent in the basal state. We conclude that the best discrimination among the three groups was achieved by measurement of trypsin outputs, after 45 min of stimulation. In addition, the pancreatic polypeptide response may be used as a marker of residual pancreatic function in chronic pancreatitis.
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PMID:Pancreatic exocrine and endocrine responses in chronic pancreatitis. 636 35

Previous studies have shown dissolution of human pancreatic stones in vitro by citrate solution which bind considerable amounts of ionized calcium. Pancreatic citrate secretion has been demonstrated in canine and human pancreatic juices. This study compares pancreatic citrate secretion of chronic alcohol-fed dogs with controls in response to graded doses of caerulein, in order to evaluate possible differences in factors favouring pancreatic lithogenicity. The dose-response-relation of citrate outputs after graded doses of caerulein revealed significantly reduced maximal secretory capacity of citrate in alcoholic dogs. Protein concentrations in juices from alcoholic dogs were reduced for all doses of caerulein but protein outputs were not different. Bicarbonate concentrations and outputs, as well as volumes, were significantly greater in alcoholic dogs. Linear relation were found between citrate and protein secretion. Chronic alcohol consumption in the dog leads to reduced citrate secretion, which is consistent with recent results in humans suffering from chronic calcifying pancreatitis, who secrete significantly less citrate than healthy subjects. The decrease of calcium-chelating citrate could be an additional factor causing increased calcium levels in the pancreatic juice of chronic alcoholics, a circumstance that might favour protein-plug formation and subsequently pancreatic stone formation.
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PMID:Pancreatic citrate and protein secretion of alcoholic dogs in response to graded doses of caerulein. 668 1

Basal and stimulated (secretin/CCK pancreozymin) duodenal aspirates were analyzed for flow rate and the protein and bicarbonate concentrations in 7 non-alcoholic controls and in 7 subjects with type IV hyperlipoproteinemia. Basal volume and bicarbonate concentration did not differ in the two groups. In the hyperlipoproteinemia patients, basal protein concentration and flow rates were significantly different from controls (p = 0.0143 and p = 0.0182 respectively). The bicarbonate flow rate is also increased in hyperlipoproteinemia. The data obtained after stimulation were similar for protein and HCO3 in both groups. These findings are identical to those observed by SARLES in alcoholic and hypercalcemic animals and in man. It is possible, but not yet proven, that hyperlipoproteinemia pancreatitis is due to protein precipitates in the pancreatic canaliculi.
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PMID:[Disturbance of exocrine secretion by the human pancreas in hyperlipoproteinemia]. 691 5

Perfusion of the pancreatic duct with acidified aspirin in cats increased the permeability of the duct to HCO3-. Intravenous administration of the synthetic prostaglandin analog 16,16 dimethyl prostaglandin E2 (PGE2) prevented this permeability change. The effect was dose-related and at the highest dose (50 microgram/kg/hour) was essentially complete. The beneficial effect of the PGE2 was apparent even when it was given after the duct had been exposed to aspirin. PGE2 had no effect on pancreatic water or electrolyte secretion in the unstimulated nonsecreting gland. No histologic changes in the pancreatic ducts were seen after exposure to aspirin, PGE2 or both. The effectiveness of PGE2 in restoring membrane permeability towards normal suggests the possibility of its therapeutic role in pancreatitis.
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PMID:Effect of 16, 16 dimethyl prostaglandin E2 on aspirin-induced permeability changes in the pancreatic duct. 745 23

Eighteen patients with acute hemorrhagic necrotizing pancreatitis who survived from operation were followed up for 12 to 43 months. Late complications including pancreatic external fistula, pseudocyst, hyperglycemia, etc were reviewed. The pancreatic juice was collected through endoscopic cannulation. The volume and HCO3- concentration of the pancreatic juice and three kinds of pancreatic enzymes were measured. The results demonstrated that inspite of anatomic abnormality or functional impairment of the pancreas, the pancreatic insufficiency rarely manifested to be marked because of the compensative ability of the viable exocrine pancreas.
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PMID:Long-term results of surgical treatment for acute hemorrhagic necrotizing pancreatitis. 824 20

This paper explores the unifying aetiopathology between disorders of the immune system and the CNS, using a case example. An adolescent had a 2-year history of chronic-active Epstein-Barr virus infection and recurrent acute pancreatitis that resolved following a course of immunotherapy. Subsequently, she redeveloped acute symptoms of infectious mononucleosis and pancreatitis, along with manic depression, and then made a complete recovery with combination of lithium carbonate and electroconvulsive therapy. On follow-up, lithium carbonate effectively controlled the previous neuroimmune dysfunction.
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PMID:A neuroimmune hypothesis for the aetiopathology of viral illness and manic depression: a case report of an adolescent. 883 48

We report a 12-year-old boy receiving long-term peritoneal dialysis who developed marked hypercalcemia and pancreatitis. Hypercalcemia was successfully treated by conducting dialysis with non-calcium-containing dialysate fluid. Factors predisposing to the development of hypercalcemia included the presence of adynamic bone disease and the use of vitamin D and calcium carbonate therapy. This case is presented to emphasize potential complications that can be associated with the adynamic bone lesion in patients on peritoneal dialysis.
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PMID:Hypercalcemia and pancreatitis in a child with adynamic bone disease. 909 Jun 72


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