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

Acute necrotizing pancreatitis developed in 5 of 405 patients who underwent renal transplantation. All five patients were taking immunosuppressive medication (azathioprine and steroids). Three patients also received rabbit antithymus serum. Alcohol ingestion or cholelithiasis did not play any causative role in the pancreatitis, which began between 7 days and 13 months after renal transplantation. The delay from the time of admission for pancreatitis to surgical exploration was a mean of 17 days. Operative findings included pancreatic necrosis, hemorrhage and abscess formation. All five patients died of the complications of necrotizing pancreatitis--persistent sepsis, respiratory and renal failure, upper gastrointestinal bleeding and disseminated intravascular coagulation. This review demonstrates that prolonged conservative therapy in renal transplant patients with necrotizing pancreatitis is associated with high mortality. The authors believe that earlier surgical intervention will lead to increased survival.
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PMID:Necrotizing pancreatitis in renal transplant patients. 618 Aug 18

Acute necrotizing pancreatitis in opossums after bile and pancreatic duct ligation (BPDL) is a useful experimental corollary of gallstone-induced acute pancreatitis in humans. In experimental and human acute pancreatitis, a loss of segregation of the lysosomal enzyme cathepsin B and the zymogen proenzyme trypsinogen (colocalization) is implicated as the triggering event of disease pathogenesis, as cathepsin B can activate trypsinogen. The object of this study was to quantitate acinar cell necrosis and to study subcellular distribution of cathepsin B in BPDL-induced acute necrotizing pancreatitis in opossums. Bile and pancreatic ducts were ligated separately (no bile reflux) in four opossums while ducts were dissected in four sham controls. Opossums were killed 24 hr after operation. Three equidistant cross-sectional portions of each opossum pancreas were submitted to histologic examination. In blinded fashion, each focus of acinar cell necrosis was photographed and quantitated with digitizing morphometry. Numerical density (foci/cm2) and areal density (x10(3) micron 2/cm2) of focal acinar cell necrosis were determined. Differentially centrifuged pancreatic homogenates were assayed for cathepsin B, the lysosomal marker enzyme N-acetylglucosaminidase, and amylase. Morphometric quantitation of acinar cell necrosis confirmed development of acute necrotizing pancreatitis after 24 hr of BPDL in opossums. However, colocalization was not observed after BPDL, as evidenced by an absence of subcellular shift of cathepsin B activity (and N-acetyl-glucosaminidase activity) from the lysosome-enriched to the zymogen-enriched subcellular fraction. Amylase activity was increased in subcellular fractions after BPDL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ligation-induced acute pancreatitis in opossums: acinar cell necrosis in the absence of colocalization. 753 Mar 9

Impairment of pancreatic microcirculation has often been advocated as one pathogenic mechanism in necrotizing pancreatitis. In contrast, data on pancreatic capillary perfusion in edematous pancreatitis are scarce. It was the aim of this experimental study to compare changes in pancreatic microcirculation in edematous and necrotizing pancreatitis. Twelve rabbits were allocated to two groups. Two different models of acute pancreatitis were used. Edematous pancreatitis was elicited by intravenous administration of cerulein (25 micrograms/kg/hr) (N = 6). Necrotizing pancreatitis of the biliary type was induced by pressure-controlled intraductal infusion of a mixture of taurocholate, trypsin, and blood (N = 6). Pancreatic microcirculation was quantified by means of intravital microscopy assessing functional capillary density, blood cell velocity, and distribution of the plasma marker FITC-dextran 70. Systemic hemodynamics were maintained at baseline values by fluid administration. Regardless of edema or necrosis, pronounced extravasation of FITC-dextran was recorded in the early stage of pancreatitis. In cerulein-induced pancreatitis, hyperemia developed as indicated by an increase in blood cell velocity in the presence of homogeneous capillary perfusion. In contrast, a progressive reduction of the number of perfused capillaries was detected in necrotizing pancreatitis. In conclusion, pancreatic microvascular perfusion may be regarded as an important pathogenetic factor for the determination of acute pancreatitis.
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PMID:Impact of microcirculatory flow pattern changes on the development of acute edematous and necrotizing pancreatitis in rabbit pancreas. 799 90

Acute pancreatitis remains a serious illness. Most patients with persisting organ failure have necrotizing rather than interstitial pancreatitis. Necrotizing pancreatitis can be distinguished from interstitial pancreatitis on incremental dynamic bolus CT scan. Infected necrosis can be diagnosed by guided percutaneous aspiration with Gram stain and culture. The treatment is surgical debridement. Patients with sterile necrosis associated with organ failure may have a high mortality rate. It remains unclear at present whether such patients should be treated by early surgical debridement or continuation of medical therapy. Measures that may be helpful in the future in reducing morbidity and mortality include the use of newer inhibitors of proteases and phospholipase-A2, inhibitors of other mediators of inflammation, and methods to improve the microcirculation of the pancreas.
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PMID:Acute pancreatitis: medical and surgical management. 804 17

Endoscopic retrograde cholangiopancreatography (ERCP) is complicated by acute pancreatitis in up to 12% of the examinations. One possible mechanism for this complication is the cannulation-induced sphincter of Oddi spasm with temporary pancreatic duct obstruction. Nifedipine is known to relax the sphincter of Oddi, thus possibly inhibiting or reducing post-ERCP +/- endoscopic sphincterotomy (EST) pancreatic irritation. To test this hypothesis 166 adult patients undergoing ERCP +/- EST were randomized to receive nifedipine (n = 82) 20 mg 3 times at 8-hour intervals during the day of ERCP +/- EST or placebo (n = 84) in a double-blind manner. Clinical pancreatitis developed in 6 patients (4%), in 3 patients in each group. Necrotizing pancreatitis developed in 3 patients, 2 (2%) in the nifedipine group and 1 (1%) in the placebo group. Overall 60 patients (36%) needed medication for post-ERCP +/- EST epigastric pain, 27 (33%) in the nifedipine group and 33 (39%) in the placebo group. Of the 87 patients, who did not need any pain medication before ERCP +/- EST, 34 (39%) needed pain medication after ERCP +/- EST. 14/47 (30%) in the nifedipine group and 20/40 (50%) in the placebo group (p = 0.044). Serum total amylase activity (median) increased from 189 U/l (range 39-11,950 U/l) before ERCP +/- EST to 299 U/l (range 43-11,824 U/l) at 12 h (p < 0.001) and 247 U/l (range 34-15,950 U/l) at 24 h (p < 0.001), with no differences between the two groups. Median serum C-reactive protein concentration and blood leukocyte count remained unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective randomized trial of the effect of nifedipine on pancreatic irritation after endoscopic retrograde cholangiopancreatography. 831 38

The influence from anti-inflammatory drugs on cellular damage of pancreatic acinar cells after induction of an acute pancreatitis (AP) in a rat model was investigated. Necrotizing pancreatitis was induced by retrograde instillation of trypsin solution in the pancreatic duct (group I). The severity of inflammation was determined using morphological and histological parameters 6, 24, and 48 h after induction of the necrotizing pancreatitis. After isolation of acinar cells, the degree of damage was measured by trypan blue exclusion--a parameter of membrane permeability--as well as accumulation of rhodamine 6G--a parameter of the mitochondrial membrane potential. In groups II-V, rats were treated with the anti-inflammatory drugs indomethacine, hydrocortisone, cimetidine, and acetylsalicylic acid (ASS) before induction of AP. There was no significant benefit from therapy in either group regarding cell membrane damage, cellular energy metabolism, or histology.
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PMID:Survival and morphology of isolated pancreatic acinar cells from rats with induced acute pancreatitis are not improved with anti-inflammatory drugs. 853 Aug 30

Somatostatin and its analogue octreotide have a profound inhibitory effect on the endocrine and exocrine secretions of the pancreas, stomach, and small intestine. Previous studies have been inconclusive about the possible therapeutic effect of somatostatin and its analogues in the treatment of pancreatitis. This study assessed the effect of the long acting somatostatin analogue, octreotide, in two models of experimental pancreatitis in rats. Necrotizing pancreatitis was induced by pancreatic injection of 5 ml taurocholate, 5% in male Wistar rats. In a second model mild edematous pancreatitis was induced by intravenous injection of caerulein at a supramaximal dose, 6 micrograms/kg/hr, for 5 hr. Compared to untreated rats, treatment with octreotide either prior to or following the induction of necrotizing pancreatitis resulted in less hypocalcemia (P < 0.05) and acidosis (P < 0.05), and prevented the increase in pancreatic weight (P < 0.05). Amylase levels remained high. After 20 days, there was less pancreatic damage, lower mortality rates (P < 0.05), and increase in body weight (P < 0.05). In the model of milder pancreatitis, octreotide treatment attenuated the increase in pancreatic weight (P < 0.05) and pathological damage (P < 0.05). We concluded that the somatostatin analogue octreotide has a beneficial effect in the treatment of experimental acute pancreatitis.
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PMID:Effect of the somatostatin analogue octreotide on experimental pancreatitis in rats. 863 40

Acute necrotizing pancreatitis involves high mortality. When diagnosed, the disease implies a choice of suitable timing and proper technique of surgical approach. The experience on 16 patients with acute necrotizing pancreatitis, 9 males and 7 females, mean age of 54.7 +/- 3.3 years, is presented in this study. Necrosectomy and continuous local lavage of abdominal collections and pancreatic necrotic surfaces was the most appropriate surgical treatment. The method seems able to remove necrosis and active biological compounds and would appear to achieve a limited mortality and morbidity. Necrosectomy and postoperative local lavage represent a therapeutic effective procedure.
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PMID:[The role of necrosectomy and continuous peritoneal lavage in the treatment of acute necrotic-hemorrhagic pancreatitis]. 876 89

Acute necrotising pancreatitis is associated with an unacceptably high mortality for which no satisfactory remedy exists. Emblica officinalis (E.o.) is a plant prescribed in Ayurveda, the Indian traditional system of medicine, for pancreas-related disorders. This study was carried out to evaluate the protective effect of E.o. against acute necrotising pancreatitis in dogs. Pancreatitis was induced by injecting a mixture of trypsin, bile and blood into the duodenal opening of the pancreatic duct. Twenty eight dogs were divided into 4 groups (n = 6-8 each): GpI--control, GpII--acute pancreatitis, GpIII--sham-operated, GpIV--pretreatment with 28 mg E.o./kg/day for 15 days before inducing pancreatitis. Serum amylase increased from 541.99 +/- 129.13 IU/ml to 1592.63 +/- 327.83 IU (p <0.02) 2 hrs after the induction of pancreatitis in GpII. The rise in serum amylase in both GpIII and GpIV was not significant. On light microscopic examination, acinar cell damage was less and the total inflammatory score was significantly lower in the E.o. treated group as compared to GpII. Electron microscopy confirmed this and showed an increased amount of smooth endoplasmic reticulum and small, condensed granules embedded in a vacuole. More studies are needed to explore the clinical potential of E.o. and its mechanism of action.
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PMID:Emblica officinalis: a novel therapy for acute pancreatitis--an experimental study. 885 50

Pancreatitis may be acute or chronic, mild or severe. Acute necrotizing pancreatitis remains the most serious form of acute pancreatitis and accounts for the majority of complications. Although there is an established nomenclature for pancreatitis and pancreatic fluid collections, such as pancreatic pseudocysts, it is not widely understood or recognized by physicians, including gastroenterologists. Because nonspecialists will be increasingly called upon to treat and appropriately refer patients with pancreatitis and its complications for more specialized care, it is important to understand the evolving treatment options for managing these patients. This article addresses and summarizes pancreatitis and its complications, particularly pancreatic collections.
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PMID:The diagnosis and management of fluid collections associated with pancreatitis. 968 31


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