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

The main complications of endoscopic retrograde cholangiography and sphincterotomy are bleeding, pancreatitis, perforation and sepsis. Two cases of unexplained prolonged cholestatic jaundice in patients who underwent endoscopic retrograde cholangiography (ERC) for biliary obstruction due to choledocholithiasis are reported. The patients were admitted because of right upper quadrant pain, vomiting and jaundice. Laboratory tests showed increased levels of total and conjugated serum bilirubin and increased alkaline phosphatase. Ultrasound examination showed cholelithiasis and choledocholithiasis with bile duct dilatation. ERC with sphincterotomy was performed and gallstones obstructing the common bile duct were removed endoscopically. Following ERC and despite complete patency of the biliary tree, a progressive increase of total and conjugated bilirubin and of alkaline phosphatase was noted, associated with itching and total stool discoloration. The insertion of nasobiliary drain did not improve the jaundice. Prednisolone treatment for 12 days was associated with progressive restoration of serum bilirubin alkaline phosphatase to normal levels. It was postulated that the radiocontrast material used may have acted toxically on the liver with disruption of the canalicular plasma membrane. It is proposed that intrahepatic cholestasis should be added in the list of complications of endoscopic retrograde cholangiography.
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PMID:Prolonged cholestatic jaundice after endoscopic retrograde cholangiography. 922 70

It's well known that patients was acquired immunodeficiency syndrome (AIDS) can develop various kinds of hepatobiliopancreatic diseases, for causes related to AIDS and for causes not related to HIV infection. The authors describe a case to their attention due to a suspected acute pancreatitis. The patient presented with abdominal pain, increased serum alkaline phosphatase and amylase levels. Serological test and stool concentration didn't show any opportunistic infection (Cytomegalovirus, Cryptosporidium). Abdominal ultrasonography showed enlargement of the head of the pancreas, gallbladder with biliary sludge, and a little dilatation of the biliary tree. The patient didn't feel better despite the medical treatment, so considering the probability of the migration of calculus, the patient underwent cholecystectomy. After the operation the patient felt better quickly. This case confirms the presence in HIV patients of pancreatitis for causes unrelated to AIDS like cholelithiasis as we showed, alcoholism, hypercalcemia, and the importance of an opportune surgical treatment that was resolutive.
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PMID:[Acute pancreatitis and AIDS]. 932 71

Dibutyltin dichloride (DBTC; 6 mg/kg body weight, i.v.) induced acute interstitial pancreatitis in rats. The course of the pancreatitis was examined within 28 days by light and electron microscopy as well as by pathobiochemistry (amylase, lipase, alkaline phosphatase, and bilirubin in serum; tin concentration in biliopancreatic juice, tissue, and concretions). The pathogenesis of the DBTC-induced pancreatitis in rats was studied by different experimental designs (in intact animals, after bile duct ligation, after surgical bypass of the bile duct). DBTC caused toxic necrosis of the biliopancreatic duct epithelium, which is then shed into the duct and forms obstructing plugs in the distal common bile duct. Interstitial pancreatitis occurred during the first 4 days, accompanied by significantly increased activities of serum alpha-amylase and lipase. After 7 days extensive infiltration of the pancreatic interstitium with mononuclear cells was observed. Twenty-eight days after administration of DBTC one-third of the rats showed periductal and interstitial fibrosis as well as an active inflammatory process in the pancreas. The findings suggest a twofold pathogenesis of the DBTC-induced pancreatitis: first, the cytotoxic effects on the biliopancreatic duct epithelium lead to epithelial necrosis with obstruction of the duct, subsequent cholestasis, and interstitial pancreatitis; and second, the hematogenic DBTC effects cause direct injury of pancreatic cells (mitochondrial damage, autophagy, cell necrosis) followed by interstitial edema and inflammation. Both processes lead to this special type of DBTC-induced acute pancreatitis with a tendency to a chronic course, when the obstruction of the duct and cholestasis persist.
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PMID:Acute interstitial pancreatitis in rats induced by dibutyltin dichloride (DBTC): pathogenesis and natural course of lesions. 936 Oct 94

The present study was done to determine the additional influence of daily ethanol intake (15% in drinking water ad libitum) on long-term toxic effects of a single administration of dibutyltin dichloride (DBTC, 8 mg/kg b.w. i.v.) in pancreas and liver of rats. Pathohistological changes in pancreas, bile duct and liver as well as pathobiochemical parameters of pancreatitis (amylase and lipase activity), liver lesions (alkaline phosphatase activity and bilirubin) and fibrosis (hydroxyproline and hyaluronic acid) were measured 1 day and 1 to 24 weeks after DBTC- and DBTC/ethanol administration. DBTC alone induced in rats an acute interstitial pancreatitis as well as acute bile duct and liver lesions in the early experimental phase. Later on, the acute inflammatory processes in pancreas and liver took a chronic course resulting in pancreatic fibrosis and liver cirrhosis. Ethanol increased the toxic effects of DBTC on pancreas and liver during the acute and chronic course. In the acute phase lasting 1 day to 2 weeks, ethanol enhanced the DBTC toxicity on acinar cell and bilio-pancreatic duct epithelium as well as the formation of obstructive ductal plugs by necrotic cell debris. The obstruction and cholestasis in the DBTC/ethanol-group were significantly stronger as in the DBTC-group. The significant increase of hydroxyproline in urine and hyaluronic acid in serum of the DBTC/ethanol treated rats after 12 to 24 weeks was connected with a more severe chronic inflammatory fibrosis in pancreas and liver in comparison to the DBTC-treated group.
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PMID:The influence of ethanol on long-term effects of dibutyltin dichloride (DBTC) in pancreas and liver of rats. 958 82

A prospective study of patients with symptomatic cholelithiasis was undertaken to determine the effectiveness of identifying clinically significant choledocholithiasis with selective cholangiography. Between 1991 and 1995, 262 patients presented to the senior author (K.W.M.) with acute or chronic cholecystitis. Sixteen patients had a preoperative endoscopic retrograde cholangiopancreatography (ERCP) for an elevated alkaline phosphatase or total bilirubin greater than twice the normal value or an ultrasound finding suspecting choledocholithiasis. Ten of the ERCP patients had choledocholithiasis, with eight patients having successful clearance by ERCP. Ninety other patients had intraoperative cholangiography for abnormal serum liver biochemistries, a history of jaundice or pancreatitis, or a dilated common bile duct (CBD) (>6 mm) on ultrasound. Fourteen of the intraoperative cholangiography patients and the two remaining ERCP patients had choledocholithiasis requiring CBD exploration for clearance of their stones. There were no false-positive cholangiograms, and there were no bile duct injuries in this series. With 100 per cent follow-up of at least 2 years, only one patient required ERCP clearance of a retained CBD stone 13 months after cholecystectomy. The positive predictive value and the negative predictive value for the selective cholangiography criteria are 23 per cent and 99 per cent, respectively. In conclusion, clinically significant choledocholithiasis can be found effectively with selective cholangiography. Also, utilizing selective cholangiography reduces the number of routine cholangiograms by 60 per cent.
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PMID:A prospective experience with selective cholangiography. 965 77

Overproduction of tumor necrosis factor (TNF-), interleukin-1beta (IL-1beta), and nitric oxide (NO) is believed to be detrimental during the progression of acute pancreatitis, yet little is known about the hepatic production of these mediators and their role in mediating pancreatitis-induced hepatic dysfunction. Rats were randomized to receive a single intraperitoneal injection of the macrophage-pacifying compound, CNI-1493 (1.0 mg/kg), or vehicle 1 hour before the induction of retrograde bile salt pancreatitis. Sham-operated animals served as controls. Animals were killed 18 hours later, with serum and livers harvested to determine the degree of hepatocellular injury and the induction of TNF-, IL-1beta, and inducible nitric oxide synthase (iNOS). In addition, serum TNF- and nitrites (end-product of NO breakdown) were determined in each group to assess the mechanism of action of CNI-1493. TNF-, IL-1beta, and iNOS gene expression (by reverse-transcription polymerase chain reaction) as well as aspartate transaminase (AST), alanine transaminase (ALT), and lactic dehydrogenase (LDH) (but not alkaline phosphatase [ALP]) increased following the development of pancreatitis (all P < .05). Macrophage pacification significantly prevented the induction of TNF- and IL-1beta mRNA (but not iNOS), resulting in lessened serum AST, ALT, and LDH (all P < .05). Serum TNF- protein and nitrites correlated with gene induction in that both were increased following the onset of pancreatitis, and TNF- protein production was significantly attenuated in animals receiving CNI-1493. Hepatocellular, but not bile duct, injury occurs during experimental pancreatitis that is associated with hepatic TNF-, IL-1beta, and iNOS mRNA gene induction, as well as TNF- protein and nitrite production. Preventing the production of TNF- and IL-1beta by macrophage pacification attenuates the hepatocellular damage, suggesting that these mediators play a role in pancreatitis-induced hepatic injury.
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PMID:Macrophage pacification reduces rodent pancreatitis-induced hepatocellular injury through down-regulation of hepatic tumor necrosis factor alpha and interleukin-1beta. 979 13

In this study we examined the effects of continuous calcium channel blocker (CCB) infusion on pancreatic duct-ligated acute pancreatitis (AP) in rabbits. Thirty rabbits were used for this study. Animals in group 1 (n = 10), which served as a control group, underwent dummy operations and received 0.5 microliter/h normal saline via the internal jugular vein. Animals in group 2 (n = 10) with artificially-induced pancreatitis received the same dosage of saline in the same manner. Animals in group 3 (n = 10) with artificially-induced pancreatitis received 180 micrograms/kg/h CCB (Verapamil) via the jugular vein starting from just before pancreatic duct ligation. AP histology score, plasma amylase levels and liver function tests were measured after 48 h. Verapamil infusion did not prevent the rise in plasma amylase levels, nor did it prevent pancreatic inflammation and damage. Serum levels of serum glutamate pyruvate transaminase, serum glutamate oxalacetate transaminase and alkaline phosphatase were significantly elevated in group 2 and significant reductions were seen in the Verapamil treated animals (group 3). The findings in this study imply that a continuous 180 micrograms/kg/h dose Verapamil infusion does not ameliorate the pathogenesis of pancreatitis induced by ligation of pancreatic duct but do not rule out a dose-dependent protective effect. Meanwhile, the lowering of liver function test scores should be considered the beneficial effect of CCBs, and this should be investigated in further studies.
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PMID:Continuous calcium channel blocker infusion in experimentally induced acute pancreatitis: effects on pancreas and liver function. 987 64

The neutrophils functional state was studied in 101 patients with an acute destructive pancreatitis (DP), complicated by parapancreatitis, in 20 patients with edematic pancreatitis and in 25 healthy persons using cytochemical reactions with determination of the enzymes activity of alkaline phosphatase, myeloperoxidase, and also of lysosomic-cation proteins, phospholipids and glycogen. The enzymatic contents of neutrophils changes in acute period of destructive pancreatitis (DP) are causing their function inhibition, promoting the infection complications occurrence. The neutrophils functional activity indexes may be used in early diagnosis and prognostication of the DP course.
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PMID:[Diagnostic and prognostic significance of the blood neutrophils functional activity in patients with an acute destructive pancreatitis]. 1124 48

This prospective study was performed to assess the predictive ability of the various indicators of common bile duct (CBD) calculi, individually or in combination, by analyzing 88 patients with gallstone disease. The patients were classified into two groups according to the presence of 10 predefined criteria. Of 53 patients with one or more risk factors (group 2), 26 harbored CBD calculi; none of 35 patients with no risk factors (group 1) had CBD stones. Jaundice correlated best, with a sensitivity of 69%; and pancreatitis had the lowest sensitivity (12%). Elevated serum bilirubin and alkaline phosphatase levels correlated better than liver enzymes and serum amylase. The sensitivity and negative predictive value of cholescintigraphy scanning for diagnosing CBD calculi were better than those of ultrasonography, the sensitivity being 84% versus 50% and the negative predictive value 95% versus 82%. Endoscopic retrograde cholangiopancreaticography was successful in 94% of the patients, and CBD calculi were diagnosed in 74%. Moreover, peroperative cholangiography was 100% sensitive with no false-positive results. Ultimately, a palpable stone at surgery was the best predictor. When all the criteria were analyzed, it was found that as the number of criteria increased so did the percentage of patients harboring CBD calculi.
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PMID:Evaluation of the predictors of choledocholithiasis: comparative analysis of clinical, biochemical, radiological, radionuclear, and intraoperative parameters. 1634 96

In the first part of our review, we discussed the general evaluation and clinical presentation of the various hepatic infections occurring in patients with AIDS. In addition, we focused on specific hepatic parenchymal infections. In this article, we will discuss the major clinical syndromes arising from opportunistic infections affecting the gallbladder (acalculous cholecystitis), biliary tree (AIDS-cholangiopathy), and pancreas (pancreatitis). Acalculous cholecystitis can develop in patients with AIDS who have not experienced the severe precipitating physiologic stresses normally required in patients without AIDS. The most common presentation is with right upper quadrant (RUQ) pain and tenderness. The diagnosis is a clinical one since there is no standard test, other than surgery. Cholecystectomy is the treatment of choice. The most common AIDS-associated infective complication of the biliary tree is AIDS-cholangiopathy. This is best viewed as a form of secondary sclerosing cholangitis resulting from a variety of opportunistic infections within the biliary tree. Affected persons present with RUQ pain and have marked elevations in the canalicular enzymes, alkaline phosphatase, and gamma-glutamyl transferase. Morphologic abnormalities are identified by endoscopic retrograde cholangiopancreatography. These include stricturing, dilatation, and beading of the biliary tract. Endoscopic sphincterotomy of the papilla of Vater may provide symptomatic relief for patients with papillary stenosis. Opportunistic infections within the pancreas gland have been documented in both pre- and postmortem studies. However, the true incidence of pancreatitis related to infections is unknown. The presentation is similar to that of pancreatitis from other causes. A computerized tomogram of the abdomen is the investigation of choice. Tissue aspiration or biopsy of the pancreas is required to demonstrate the presence of an opportunistic infection. The management is usually supportive, as it is rare that a specific infection is identified and treated.
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PMID:Hepatobiliary and pancreatic infections in AIDS: Part II. 1136 92


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