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

Lipase, in contrast to amylase, is completely reabsorbed by the proximal tubules after glomerular filtration. Therefore, no lipase is detectable in the unconcentrated urine according to the current opinion. The handling of lipase (detected with an enzyme-immunoassay) by the kidney was investigated in comparison with creatinine, amylase, and beta-2-microglobulin by clearance studies in acute pancreatitis (n = 10), burn injury (n = 4), glomerular proteinuria (n = 8), and controls without evidence of pancreatic or renal diseases (n = 5). In initial stages of acute pancreatitis a measurable clearance of lipase (mean: 49.6 microliters/min, range: 0.5-234) was found in association with corresponding increased clearances of beta-2-microglobulin (mean: 10.5 ml/min, range: 0.02-58.9) and of amylase (mean: 8.9 ml/min, range: 2.4-22.6) in nine of ten patients. This finding is consistent with a defect of tubular function. However, regression analysis failed to show a significant correlation between lipase and beta-2-microglobulin clearance. Repeated measurements during the course of pancreatitis in seven patients showed reversibility of tubular dysfunction. In patients with burn injury a similar elevation of clearances of beta-2-microglobulin and of amylase was found, but tubular dysfunction in this condition was not associated with lipasuria. In glomerular proteinuria a lipase clearance was found in two of five cases with moderate, and in the other three cases with severe impairment of creatinine clearance. beta-2-microglobulin clearance was normal in the former and only slightly elevated in the latter group. In conclusion lipase is measurable in the urine of most patients with acute pancreatitis as a result of a reversible tubular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1987
PMID:Lipasuria in acute pancreatitis: result of tubular dysfunction? 244 47

Pancreas divisum, a congenital variant of pancreatic ductal anatomy first described by Opie in 1903, has only recently been thought of as a cause of pancreatitis. The majority of reported patients presenting are middle-aged, with the exact pathogenesis not clearly understood. The reason for this late clinical presentation of a congenital abnormality is also not clear. However, reports of children with recurrent pancreatitis and an associated pancreas divisum have now appeared. None had any identifiable cause of pancreatitis. Pancreas divisum was diagnosed or suspected preoperatively in two, with findings on endoscopic retrograde cholangiopancreatography (ERCP) and gastroduodenoscopy. All findings were confirmed at operation. All underwent surgical treatment with good results within 6 months. Review of the literature showed eight patients younger than 18 years with pancreas divisum and pancreatitis requiring operation. All had good results after surgical repair. It appears that this anomaly can be associated with recurrent pancreatitis in children. Children with recurrent pancreatitis with no obvious cause should be evaluated for pancreas divisum and, if it is found, be surgically treated. The role of ERCP, while not clearly defined, may become critical in the evaluation of pancreas divisum in children.
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PMID:Pancreas divisum and pancreatitis in children. 244 15

Organophosphates (OPs) cause irreversible inhibition of cholinesterases (ChEs) and profound cholinergic stimulation. There are major differences in the response of the dog and cat pancreas to the in vivo administration of Diazinon (O,O-diethyl O-2-isopropyl-4-methyl-6-pyrimidyl phosphothioate), a butyrylcholinesterase (BuChE) inhibitor. Acute edematous pancreatitis is found in the dog but not in the cat. The present experiments were designed to see what effect OP had in vitro on pancreatic exocrine function of dog, cat, and guinea pig, and whether the effects were consistent with an anti-ChE activity. A water-soluble OP agent, tetraisopropyl pyrophosphoramide (iso-OMPA) at 10(-3) M, which like Diazinon inhibits BuChE, was used. Minced pieces of fresh whole pancreata 3 mm in size were taken from 3 dogs, 4 guinea pigs, and 2 cats. The tissues were placed in flasks containing Eagle's solution and gassed with 100% O2. Cumulative amylase release was measured by Phadebas method up to 3 h. At half-maximal acetylcholine (ACH) concentration (10(-5) M), the canine pancreas pretreated with iso-OMPA (10(-3) M) showed a 42-87% greater release of amylase than tissues receiving ACH alone (p less than 0.001). The same potentiated response to ACH was seen in guinea pig pancreas pretreated with iso-OMPA (p less than 0.001), but iso-OMPA pretreatment did not augment the ACH response in the cat. Atropine pretreatment effectively blocked all ACH responses, and there was no effect seen with iso-OMPA alone. In the dog, iso-OMPA in combination with half-maximal carbachol (10(-6) M), or in combination with half-maximal cholecystokinin (CCK-8) stimulation (10(-9) M), provided no potentiated amylase release.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1987
PMID:Effect of the organophosphate iso-OMPA on amylase release by pancreatic lobules of dog, guinea pig, and cat. 244 88

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.
Pancreas 1988
PMID:Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology. 245 72

This study was undertaken to investigate serially the development, progression, and healing of acute pancreatitis which was induced in rats by the closed duodenal loop technique. Edematous changes appeared within 2 to 4 h. Pancreatic blood flow increased at 1 h and tended to decrease after 3 h. After injection of fesin into the loop, fesin appeared in the periacinar space and acinar cells after 4 h. Electron microscopy showed that partial destruction of the plasma membrane occurred and serum amylase increased considerably at the same time, suggesting that the initial inflammatory changes caused the release of pancreatic enzymes at approximately 4 h. After elimination of the causal factors, edematous pancreatitis healed completely but hemorrhagic acute pancreatitis was not completely healed 6 months later.
Pancreas 1988
PMID:Serial histologic study of the development, progression, and healing of acute pancreatitis in the rat. 245 73

Asperlicin (ASP), a new, nonpeptidal cholecystokinin (CCK) receptor antagonist isolated from the fungus Aspergillus alliaceus, has an affinity that is 300-400 times greater than that of proglumide for gallbladder, ileal, and pancreatic CCK receptors. The long in vivo half-life and high selectivity for peripheral CCK receptors make ASP suitable for investigations on the physiological and pharmacological actions of CCK. Endogenous CCK has been postulated to participate in the pathogenesis of acute hemorrhagic pancreatitis (AHP) in rats and mice. We examined the effects of ASP in rats on the early course (6 h) of AHP induced by a retrograde infusion of sodium taurocholate (NaTC) into the common bile-pancreatic duct. An i.v. bolus injection of ASP (either 10 mg/kg or 30 mg/kg) in dimethyl sulfoxide (DMSO) given 1 h prior to AHP induction failed to significantly alter pancreas weights, serum amylase concentrations, or pancreatic histopathology when compared with AHP control rats treated with vehicle alone. However, rats given 2 i.p. injections of ASP (either 20 mg/kg/injection or 40 mg/kg/injection) in DMSO: olive oil 1 h before and 2 h after induction of AHP exhibited significantly reduced serum amylase concentrations. Additionally, rats given the high dose i.p. injections of ASP also had significantly reduced pancreas weights and less severe pancreas histopathology compared with AHP control animals. These data indicate that endogenous CCK participates in the pathogenesis of NaTC-induced AHP in the rat.
Pancreas 1988
PMID:Asperlicin, a nonpeptidal cholecystokinin receptor antagonist, attenuates sodium taurocholate-induced acute pancreatitis in rats. 245 74

This study describes the effect on the function and structure of the saline-perfused cat pancreas of factors implicated in the pathogenesis of pancreatitis (bile acid, ethanol, pancreatic enzymes) after their addition to the perfusion fluid or their instillation into the pancreatic duct. Instillation of trypsin or chenodeoxycholic acid, but not ethanol, into the pancreatic duct resulted in a profound suppression of secretory function. The leakage of perfusion fluid and amylase from the gland was also abruptly increased. Intraarterial perfusion of trypsin also inhibited secretin-induced flow and cholecystokinin evoked enzyme secretion. Intraarterial bile acid inhibited fluid flow but augmented enzyme secretion in a concentration-dependent manner. In addition, massive or focal parenchymal necrosis was caused by sustained intraarterial perfusion of bile acid or trypsin, respectively. Elastase and phospholipase A had little influence on pancreatic function or structure when added to the perfusion fluid. These findings show that pancreatic structure and function can be disturbed by potentially toxic factors administered not only via the ductal system but also via the vascular route, and consequently suggest that an "internal reflux" mechanism could be involved in the pathogenesis of pancreatitis in addition to a "ductal reflux" mechanism.
Pancreas 1988
PMID:Analysis in the isolated perfused cat pancreas of factors implicated in the pathogenesis of pancreatitis. 245 94

Scavengers of toxic oxygen reduction products have been reported to reduce the inflammatory reaction in some models of pancreatitis. In a blinded study, the effect of parenteral pretreatment with superoxide dismutase plus catalase was compared with placebo on pancreatitis induced in rats by infusion of 0.25% or 2% sodium taurocholate into the hepatopancreatic duct. The degree of inflammation was assessed by macroscopic examination of the pancreas, dry/wet weight ratios of pancreatic specimens, amylase activity in plasma and peritoneal exudate, the weight of the exudate, and its content of total protein. All parameters were indicative of a more severe inflammation in rats given the higher concentration of sodium taurocholate. The only significant effect of the superoxide dismutase plus catalase treatment was a moderate reduction of the dry/wet weight ratio, i.e., pancreatic edema, in rats given 2% sodium taurocholate. Our results indicate that toxic oxygen reduction products, available for interception by parenterally administered superoxide dismutase plus catalase, are of only minor importance in the pathogenesis of sodium taurocholate-induced pancreatitis in the rat.
Pancreas 1988
PMID:Parenteral superoxide dismutase plus catalase diminishes pancreatic edema in sodium taurocholate-induced pancreatitis in the rat. 246 Aug 55

We have recently reported successful 72-h preservation of the canine pancreas with a new cold-storage solution developed at the University of Wisconsin (UW solution). Over 10 mo, we performed 11 combined pancreas-kidney and 4 isolated-pancreas transplants with this solution. In situ cooling of the donor pancreas was performed with 1000 ml of UW solution followed by ex vivo perfusion with an additional 250-500 ml. Graft preservation times ranged from 3 to 19 h (mean 10.2 h). Pancreas transplants were vascularized whole-organ grafts with pancreaticoduodenocystostomy. Early graft function was excellent as assessed by immediate insulin independence, high urinary amylase and low serum amylase levels, and a technetium perfusion index indicating good pancreatic blood flow. There were no episodes of primary nonfunction, graft pancreatitis, or vascular thrombosis. Actuarial patient and graft survival at 1 mo was 92.9%. We conclude that UW solution provides excellent early graft function for up to 19 h of cold storage. Based on previously reported data on its efficacy in liver and kidney preservation, UW solution seems ideally suited as a universal intra-aortic flush and cold-storage solution.
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PMID:Use of UW solution in pancreas transplantation. 246

Acute edematous pancreatitis was produced in rats by subcutaneous administration of caerulein. Pancreas weight, pancreas histology and plasma amylase were used as endpoints to quantitate the severity of the syndrome. A caerulein dose of 10 micrograms/kg.hour produced the most severe pancreatitis, whereas at 5 micrograms/kg.hour the values were half-maximal. The pancreatic lesions were characterized by edema, formation of cytoplasmic vacuoles, leukocytic infiltration, necrosis, and with time (12-hour caerulein infusion) dilated acini. Cholecystokinin octapeptide also produced pancreatitis when given at ten times the dose required for caerulein (50 micrograms/kg.hour instead of 5 micrograms/kg.hour). Carbachol did not induce pancreatitis. Two prostaglandins, 16,16-dimethyl prostaglandin E2 injected subcutaneously and prostaglandin E2 infused subcutaneously, dose dependently prevented caerulein-induced pancreatitis (pancreatic edema, leukocytic infiltration, and necrosis) and reduced the number and size of intracellular vacuoles. The ED50 were 15 to 25 micrograms/kg for 16,16-dimethyl prostaglandin E2 and 90 micrograms/kg.hour for prostaglandin E2. Neither prostaglandin, given at doses inhibiting the development of pancreatitis, prevented the retardation of gastric emptying caused by caerulein, a finding suggesting that the prostaglandins may act specifically on the effect of caerulein on the pancreas but not on caerulein receptors in gastric smooth muscle. Indomethacin, an inhibitor of prostaglandin synthesis, and methscopolamine bromide, an anticholinergic agent, had no effect on caerulein-induced pancreatitis. We concluded that prostaglandins of the E type prevent the development of caerulein-induced pancreatitis. The mechanism by which prostaglandins protect the pancreas may involve stabilization of lysosomes within the acinar cells and inhibition of intracellular activation of pancreatic digestive enzymes.
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PMID:Prevention by prostaglandins of caerulein-induced pancreatitis in rats. 246 59


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