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

There is evidence that the pancreatic duct plays an important role in the evolution of necrotizing pancreatitis. We hypothesized that occlusion of the pancreatic duct and its smaller ductules with prolamine (Ethibloc) in opossums at risk of severe necrotizing pancreatitis would have a beneficial effect on the progression of the disease. Sixteen opossums underwent bile duct ligation below the entrance of the pancreatic duct. They were divided into four groups at 6 days. Group I (control, n = 5) opossums were killed for histologic observation of the degree of necrosis of the pancreas; group II (n = 5) underwent external drainage of the pancreatic biliary duct; group III (n = 4) had external biliary drainage and ligation of the pancreatic duct; group IV (n = 7) was treated with external biliary drainage and ligation of the main pancreatic duct after instillation of prolamine. Serum amylase, lipase, and calcium values were determined. The pancreas was examined by inspection and histologically at the time of death, and the severity of the disease was determined by quantitation of pancreatic tissue necrosis. All animals in groups II and III died 8 to 14 days after bile duct ligation, and all had severe necrotizing pancreatitis. All animals in group IV survived and were killed at 2 to 10 weeks after prolamine (Ethibloc) injection into the pancreatic duct. A mild edematous pancreatitis was observed in all seven animals. Prolamine (Ethibloc) provided dramatic protection from progressive necrosis. This study does not provide an explanation, but it allows for speculation that ductal injection interrupted the deleterious effect of proteolytic enzymes and their leakage into the interstitial space of the pancreas.
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PMID:Role of pancreatic duct occlusion with prolamine (Ethibloc) in necrotizing pancreatitis. 244 41

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.
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PMID:Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats. 245 25

The aim of this experimental study was to demonstrate that the mortality of calcium chlorine induced acute pancreatitis in the dog was decreased by the intraductal injection of solid substances. Seventy-two dogs were used. In the control group (n = 5) the mortality was 100%. Three different drugs were used for the intraductal injection: Ethibloc (n = 37), Tissucol (n = 10) and silicones (n = 10). The mortality rate has been respectively of 13.5, 10 and 10%. In order to define at which level of the pancreatic duct the obstruction had a maximum efficiency, 10 dogs underwent a distal ligation of the pancreatic duct after induction of the pancreatitis. The mortality rate in this group was 100%. It can be therefore concluded that only the complete obstruction of the pancreatic duct decreases the mortality rate in this experimental model.
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PMID:[Experimental acute necrotico-hemorrhagic pancreatitis in dogs. Treatment by intraductal block]. 246 92

The content of pancreatic enzymes, cyclic nucleotides and prostaglandins (PG) in the duodenal contents was measured in 77 patients with chronic pancreatitis and in 20 healthy individuals. Pancreatitis exacerbation was attended by a decrease in enzymatic activity, in bicarbonate, cAMP and cGMP production. The content of PGE in pancreatic secretion remained normal, that of PGF2 alpha was elevated. Stimulation of the exocrine part of the pancreas by means of euphylline, pentagastrin and calcium was accompanied by the rise of the content of cyclic nucleotides rather than of PG. Suppression of enzymatic secretion by contrykal was followed by the reduction in the content of the cyclic nucleotides and PGE. The data suggest that cyclic nucleotides and PG are involved in the mechanism by which the external secretion of the pancreas is impaired in patients with chronic pancreatitis.
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PMID:[Prostaglandins and cyclic nucleotides in chronic pancreatitis]. 247 Dec 85

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.
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PMID:Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning. 247 70

A study on the effect of zinc feeding on the survival rate as well as the levels of trypsinogen, alpha 2-macroglobulin, zinc, calcium, and magnesium in the plasma, pancreata, and livers of BALB/c mice fed a choline-deficient diet supplemented with 0.5% DL-ethionine (CDE diet) was undertaken. Feeding them a zinc-excess diet significantly increased the survival rate of mice with pancreatitis induced by CDE diet feeding. Trypsinogen concentrations in plasma and pancreas increased in mice fed a CDE diet and further increased in mice fed a zinc-deficient diet. The plasma alpha 2-macroglobulin levels in mice fed a zinc-deficient diet decreased compared to those fed a zinc-adequate or a zinc-excess diet. In mice with pancreatitis, zinc and calcium concentrations of pancreata increased and magnesium concentrations decreased compared to those of normal controls. The calcium concentrations in both livers and pancreata increased, but magnesium concentrations in these tissues decreased. These results suggest that altered mineral metabolism in the pancreas may have contributed to the pathophysiology of the mice with acute pancreatitis and that zinc supplementation in the diet may be therapeutic for pancreatitis.
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PMID:Role of zinc in treatment of experimental acute pancreatitis in mice. 248 Aug 71

Cells of the murine hemopoietic cell line FDC-P1 were multiply infected with a retroviral construct containing cDNA encoding the leukemia inhibitory factor (LIF) to produce cells secreting high levels of LIF. Injection of these cells to unirradiated or irradiated syngeneic DBA/2 mice resulted in animals engrafted with LIF-producing cells in the marrow, spleen, and lymph nodes and with elevated serum LIF levels. These mice developed within 12-70 days a fatal syndrome characterized by cachexia, excess new bone formation, calcification in heart and skeletal muscle, pancreatitis, thymus atrophy, and abnormalities in the adrenal cortex and ovarian corpora lutea. Injection of mice with control FDC-P1 cells led to comparable organ engraftment, but the mice developed none of these lesions. The observations suggest that LIF may be a potent cachexia-inducing agent and may have marked effects on osteoblasts and calcium metabolism.
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PMID:Fatal syndrome in mice engrafted with cells producing high levels of the leukemia inhibitory factor. 256 39

Over an 18 month interval at the University of Louisville Affiliated Hospitals, 40 patients were evaluated in a nonrandomized prospective study to determine the value of methylthionine chloride / tetramethylthionine chloride (methylene blue--MB) as an aid for the rapid intraoperative identification of parathyroid hyperplasia of end-stage renal disease (ESRD). Patients assigned to the MB infusion subgroup had infusion of 1 per cent MB (5.5 milligrams per kilogram) over a time interval of 25 to 60 minutes (mean of 43.9) prior to anesthetic induction. A total of 159 glands were identified in both the control and MB infusion groups (3.98 glands per patient) of which the predominant histopathologic diagnosis on frozen section was chief cell hyperplasia (78.3 per cent). Of 91 hyperplastic glands submitted for analysis after subtotal parathyroidectomy in those in the MB infusion group, 82 glands (90.1 per cent) were observed to have positive staining with identifiable differentiation from surrounding tissues. Analyses of the correlation of the serum calcium value and probability of MB staining or its relation to serum intact parathyroid hormone (intact-PTH) values were not statistically significant (p greater than 0.05, correlation coefficient equals 0.149). Furthermore, no relationship existed between the glandular size (millimeter to the third power) and probability of MB staining (chi-square equals 1.750, p greater than 0.05) or between hyperplastic size and serum intact-PTH value (correlation coefficient equals 0.068). Conversely, analysis of MB gland staining with regard to intact PTH concentration disclosed 59 of 59 glands stained intensely with MB when intact-PTH concentration was not less than 700 picograms per milliliter (p less than 0.01). Non-staining of hyperplastic parathyroid tissue was observed in 28.1 per cent of glands submitted for histopathologic analysis in which preoperative intact PTH values were more than 699 picograms per milliliter. Time of operation was reduced from 119.0 +/- 47.53 minutes (mean +/- S.E.M.) in control patients to 92.1 +/- 20.12 minutes (mean +/- S.E.M.) for the MB infusion group (V per cent equals 21.85, p less than 0.01). Furthermore, this technique appears to have value in the detection of ectopically located parathyroid tissue as demonstrated by the in vivo staining of seven ectopic glands in six patients of the infused group. Complications were restricted to the patients in the MB infusion group (21.7 per cent) and included: pseudo-cyanosis in three; pain in the infusion site in two, wound hematoma in one patient, pancreatitis in one and angina in one.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intraoperative localization of parathyroid glands using methylthionine chloride / tetramethylthionine chloride in secondary hyperparathyroidism. 257 72

The mechanism of hypocalcemia in acute pancreatitis remains unknown despite continued investigative work over the past several decades. Because acute pancreatitis is accompanied by multiple systemic manifestations and alterations of plasma membranes, the possibility that an abnormal translocation of calcium from extracellular to intracellular compartments could play a role in hypocalcemia of acute pancreatitis was investigated in dogs. Acute pancreatitis was induced by injecting bile into the pancreatic duct. Plasma calcium, magnesium, and amylase concentrations were determined. Calcium and magnesium contents were also measured in biopsy specimens of pancreas, liver, skeletal muscle, and kidney before and after induction of acute pancreatitis. As expected, hypocalcemia and hyperamylasemia occurred 6 hours after induction of pancreatitis, and persisted throughout the experiment, 13 to 25 hours. Plasma magnesium concentration fell at 6 and 18 hours, and returned to an almost normal level by the end of the study. A significant elevation in calcium content of pancreas (71%), liver (24%), and muscle (112%), and 25% reduction of calcium in kidney were observed in dogs with histologic signs of pancreatitis. However, tissue magnesium concentration fell in pancreas (18%) but remained unchanged in the other tissues investigated. No significant changes in any variables were detected in sham-operated animals. In another group of dogs in which the accessory pancreatic duct was not occluded when bile was injected, the histologic lesions were extremely mild, although the plasma calcium concentration and the pancreatic calcium and magnesium contents were altered just as much as in the severely affected dogs. Data suggest that the hypocalcemia of acute pancreatitis may be the result, at least in part, of accumulation of calcium in soft tissues. The decreased calcium content in kidney could be related to hypocalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Soft tissue calcium and magnesium content in acute pancreatitis in the dog: calcium accumulation, a mechanism for hypocalcemia in acute pancreatitis. 258 33

Acute pancreatitis is not the cause but may be a complication of chronic pancreatitis. Different forms of chronic pancreatitis are described. The most frequent type in all climates, chronic calcifying pancreatitis, has different causes but similar pathological changes. It is a lithiasis in which a new family of molecules. PSP, a calcium stabilizer, plays a dominant role. Studies of chronic pancreatitis have now reached the stage of molecular biochemistry.
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PMID:Pathogenesis and epidemiology of chronic pancreatitis. 265 60


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