Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.
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PMID:Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy. 1103 77

Chemoactivation of the neutrophil (PMN) via the complement system has been observed in many inflammatory conditions and is thought to play a pathogenic role in acute pancreatitis. This study examined the effects of PMN depletion in experimental hemorrhagic pancreatitis and tested the role played by complement. Severe pancreatitis was induced by a choline-deficient, 0.5% ethionine-supplemented diet in female Institute of Cancer Research (ICR) mice weighing 11-13 g. Neutropenia was induced by an antibody injection. Total complement depletion was achieved by tail vein injections of cobra venom factor (CVF). Serum amylase levels and local pancreatic injury were not significantly modulated by either PMN or complement depletion at 72 hours. Systemic and remote organ injury, assessed by the formation of ascites, hematocrit, and serum alanine aminotransferase levels, was significantly reduced in neutropenic mice but failed to be moderated by complement depletion. In addition, liver and lung myeloperoxidase activity was independent of complement depletion. At 5 days, mortality was zero in PMN-depleted mice. There was no improvement in survival in the CVF-treated group. Neutrophils are important in the systemic injury and mortality of severe pancreatitis. PMN chemoactivation involves mechanisms other than complement.
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PMID:Neutrophils, not complement, mediate the mortality of experimental hemorrhagic pancreatitis. 1113 69

Liver injury is a manifestation of the systemic inflammatory response during acute pancreatitis. We have demonstrated that elastase induces macrophage tumor necrosis factor (TNF) production in distant organs, thus mimicking pancreatitis-associated organ injury. The aim of this study was to determine the mechanism by which elastase induces hepatic cytokine production. Rat livers (n = 40) were perfused with elastase +/- gadolinium (Gd) to inhibit Kupffer cells. Liver parenchymal enzymes and TNF were measured in the effluent. In vitro, rat hepatocytes or Kupffer cells were treated with elastase (1 U/ml) +/- Gd (0.5 mg/ml) or pyrrolidine dithiocarbamate (PDTC; 0.5 mg/ml). TNF protein, TNF messenger RNA, and NF-kappa B activation were determined. In vivo, Gd blunted the elastase-induced TNF production and decreased AST, ALT, LDH, and nonviable cells (propidium iodide) (P < or= 0.03 vs. elastase). In vitro, elastase induced TNF production from Kupffer cells (P < 0.001 vs. control) but not from hepatocytes. Gd or PDTC significantly attenuated the elastase-induced TNF production (P < 0.001). Elastase-induced overexpression of TNF messengerRNA and activation of NF-kappa B was attenuated by Gd. Pancreatic elastase induces a pattern of liver injury similar to that seen during acute pancreatitis by activating cytokine production and gene expression within Kupffer cells via NF-kappa B. Gd exhibits a protective effect against elastase-induced liver injury by inhibiting activation of NF-kappa B.
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PMID:Pancreatic elastase induces liver injury by activating cytokine production within Kupffer cells via nuclear factor-Kappa B. 1202 2

BACKGROUND: The routine use of serum elastase-1 in patients, pre- and post-endoscopic retrograde cholangiopancreatography (ERCP), has been strongly supported but not sufficiently correlated with diagnosis, patient outcome/prognosis, or routine markers such as serum amylase. The value of serum elastase-1 post-ERCP, as far as clinical diagnosis and prognosis is concerned, was tested and compared with serum amylase in terms of sensitivity, specificity, positive prognostic value (PPV), and negative prognostic value (NPV). METHODS: In a prospective study of 38 consecutive patients undergoing ERCP, we assessed the following biochemical parameters 24 h before ERCP and 2 and 18 h after ERCP: alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (gamma-GT), alkaline phosphatase (ALP), amylase (AMS), lactate dehydrogenase (LDH), and pancreatic elastase-1. RESULTS: Statistically significant changes were found between pre-ERCP and 18-h post-ERCP in elastase-1 (P=0.009), amylase (P=0.016), gamma-GT (P=0.04), and ALP (P=0.04). Changes between 2-h and 18-h post-ERCP in all parameters tested were not statistically significant. No statistical significance was found between any biochemical parameter and specific ERCP diagnosis. CONCLUSIONS: This study showed that 2-h post-ERCP serum elastase-1 was 100% specific for post-ERCP pancreatitis or other underlying severe pathology while, at the same time, amylase was only 50% specific. The specificity of serum elastase-1 still remained high (87.5%) 18-h post-ERCP, while amylase only had a specificity of 25% at that time. In contrast, amylase had a sensitivity of 83.3 and 90% in the 2-h and 18-h post-ERCP serum samples, while elastase-1 only had a sensitivity of 56.7 and 73.3%, respectively.
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PMID:The true value of serum elastase-1 in endoscopic retrograde cholangiopancreatography (ERCP). 1214 13

The main biochemical indices of hepatic functions (the activities of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, alpha-amylase, choline esterase and the concentrations of total bilirubin, cholesterol, and glucose) were studied in the sera of 256 patients with chronic opisthorchiasis. It was found that with diseases manifested in different clinical forms (cholangitis, cholecystitis, cholangiocholecystitis, cholangiohepatitis, cholecystitis in combination with pancreatitis), most study indices are within the normal ranges, but significantly differ from the means in a group of apparently healthy individuals. The findings suggest that such clinical forms of opisthorchiais as cholangiocholecystitis and cholangiohepatitis are characterized by manifestations of cytolysis and cholestasis, as cholecystitis is manifested by cytolysis, as cholecystitis in combination with pancreatitis, by cholestasis, and as cholangitis, by cholestasis and hepatic cell insufficiency. It is possible that further studies will provide evidence for how to correct detected disorders during pathogenetic therapy.
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PMID:[Biochemical characteristics of hepatic functions in different clinical forms of chronic opisthorchiasis]. 1222 56

We have demonstrated that pancreatitis-associated ascitic fluid contributes to hepatocyte injury during acute pancreatitis; a phenomenon independent of ascites' enzymatic content and Kupffer cell-derived cytokines. Our aim is to characterize the mechanisms of pancreatitis-associated ascitic fluid induced hepatocyte death. NIH mice were injected intraperitoneally with pathogen-free pancreatitis-associated ascitic fluid. Twenty-four hours later, serum AST, ALT, LDH, and hepatocyte apoptosis (TUNEL) were measured. Human hepatocytes (CCL-13) were treated with pancreatitis-associated ascitic fluid +/-SB203580 or caspase-3 inhibitor-II. Mitochondrial membrane integrity was determined by DiOC6 staining. Apoptosis was measured by TUNEL staining and flow cytometry after dual labeling with Annexin-V/7-AAD. Data are mean +/- SEM of triplicates. Pancreatitis-associated ascitic fluid increased serum AST, ALT, LDH, and apoptotic cells in the mouse liver (all P < 0.03 vs. sham). In CCL-13 cells, pancreatitis-associated ascitic fluid induced a time and dose-dependent increase in apoptosis, in addition to p38-MAPK phosphorylation (P = 0.02 vs. control), caspase-3 cleavage (P < 0.03 vs. control) and decreased DiOC6 mitochondrial staining (P < 0.01 vs. control). Both caspase-3 inhibitor-II and SB203580 decreased apoptosis, but the former had no effect on DiOC6 staining. Pancreatitis-associated ascitic fluid induces liver injury and hepatocyte apoptosis by activating p38-MAPK and caspase-3 dependent pro-apoptotic pathways.
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PMID:Liver injury during acute pancreatitis: the role of pancreatitis-associated ascitic fluid (PAAF), p38-MAPK, and caspase-3 in inducing hepatocyte apoptosis. 1260 Apr 44

Laparoscopic cholecystectomy has become the treatment of choice for patients with symptomatic cholelithiasis. About 10-20% of patients with gallbladder stones may also present associated common bile duct stones. The management of the latter remains controversial because many different surgical strategies are available: laparoscopic treatment (laparoscopic common bile duct exploration), sequential endoscopic and laparoscopic treatment (endoscopic retrograde cholangiopancreatography/endoscopic sphincterotomy [ERCP/ES] prior to laparoscopic cholecystectomy), inverted sequential endoscopic-laparoscopic treatment (laparoscopic cholecystectomy followed by ERCP/ES), and combined endoscopic-laparoscopic treatment (laparoscopic cholecystectomy with intraoperative ERCP/ES). The aim of this study was to evaluate the efficacy and safety of sequential endoscopic-laparoscopic treatment in patients with cholecystocholedocholithiasis. We retrospectively analyzed the clinical, biochemical and radiological features of 552 patients operated on for cholelithiasis from 1991 to 2001. Common bile duct stones were suspected on the basis of increased serum levels of bilirubin, GOT, GPT, GGT, alkaline phosphatase; presence of jaundice; history of pancreatitis or cholangitis; dilated common bile duct (diameter > 8 mm) or common bile duct stones at hepatobiliary ultrasonography; presence of common bile duct stones at MR-cholangiography or at i.v. cholangiography. In patients with suspected common bile duct stones, preoperative ERCP was performed; if common bile duct stones were confirmed, ES was performed. When common bile duct stones were not suspected preoperatively, laparoscopic cholecystectomy was performed directly. Overall morbidity, mortality and conversion rates in the two groups were evaluated. Of 552 patients admitted for cholelithiasis, 62 (11.3%) underwent preoperative ERCP for suspected common bile duct stones. In 41 patients (66.1%) common bile duct stones were identified and ES with common bile duct stone extraction was performed in 40 patients (clearance: 97.5%). The overall morbidity was 16% (10 cases of post-ERCP acute pancreatitis); no mortality occurred. The conversion rate during subsequent laparoscopic cholecystectomy was 4.8%. In the group of patients with no suspicion of common bile duct stones, the conversion rate was 4.9%. Sequential treatment cannot be considered the best approach for patients with cholecystocholedocholithiasis because of its morbidity rate and the high rate of negative preoperative ERCP findings. Combined endoscopic-laparoscopic treatment seems to present more advantages, especially in term of morbidity, hospital stay and patient compliance and may, in future, be considered the treatment of choice for patients with cholecystocholedocholithiasis.
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PMID:["Sequential" treatment: is it the best alternative in cholecysto-choledochal lithiasis?]. 1261 26

Extrahepatic manifestations of chronic hepatitis C virus (HCV) infection have been well described. However, hyperlipasemia and/or pancreatitis have not been reported. Following the observation that several HCV patients had elevated lipase levels, this retrospective study was conducted to assess the association between hyperlipasemia and/or pancreatitis with hepatitis C infection. Of 204 subjects who underwent evaluation for hepatitis C, 103 had lipase levels determined at baseline. The control group consisted of 41 nonHCV subjects with a variety of gastrointestinal diseases including 18 with nonalcoholic liver disease. Twenty-five percent of HCV patients had elevated lipase at baseline as compared to 10% of controls (P = 0.04; OR = 3.1; 95% CI: 1.02-9.60). Mean lipase levels were 253 +/- 72 units/liter (normal range 114-286 units/liter and 210 +/- 42 units/liter for the HCV and control groups, respectively (P = 0.002). No significant difference in amylase was found between the groups. There was a significant association between ALT (> 1.5 times the upper limit of normal) and lipase (P = 0.02; OR = 3.0; 95% CI: 1.1-7.5). Among 30 patients who received interferon-based therapy +/- ribavirin, 11 had elevated lipase at baseline. Six of these patients responded to therapy and demonstrated normalization of lipase levels. In contrast, all nonresponders with baseline hyperlipasemia continued to have high lipase levels (P = 0.17; OR = 4.0; 95% CI: 0.6-28.4). Furthermore, only 3 of 8 (37.5%) patients with normal lipase responded to treatment as compared to 6 of 10 (60%) of hyperlipasemic patients (P = 0.36; OR = 2.5; 95% CI: 0.4-16.9). In conclusion, hyperlipasemia and/or subclinical pancreatitis may represent extrahepatic manifestations of HCV infection and should not preclude treatment.
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PMID:Hyperlipasemia associated with hepatitis C virus. 1292 63

The purpose of this study was to summarize the clinical findings in 40 dogs with systemic hypersensitivity reactions associated with the administration of potentiated sulfonamides. Dogs ranged from 6 months to 14 years of age, with a mean of 5.7 +/- 3.2 years. Spayed female dogs were overrepresented (24 of 40, or 60% of the dogs), as were Samoyeds (3 of 40; 8%) and Miniature Schnauzers (5 of 40; 13%). Mean dosages of potentiated sulfonamides were 47.0 +/- 14.9 mg/kg/d (range, 23.4-81.4 mg/kg/d). The time from the 1st administration of the drug to the onset of the clinical signs of hypersensitivity ranged from 5 to 36 days, with a mean of 12.1 +/- 5.9 days. There was no relationship between either the dosage or type of sulfonamide given and the time to the onset of the clinical signs. Fever was the most common clinical sign observed (55% of the dogs); thrombocytopenia was 2nd (54%), and hepatopathy (28%) was 3rd. Neutropenia, keratoconjunctivitis sicca (KCS), hemolytic anemia. arthropathy, uveitis, skin and mucocutaneous lesions, proteinuria, facial palsy, suspected meningitis, hypothyroidism, pancreatitis, facial edema, and pneumonitis were also observed in some patients. Of 39 dogs with adequate follow-up, 30 (77%) recovered, whereas 8 (21%) either died or were euthanized, and 1 recovered clinically but had persistent increases in alanine aminotransferase (ALT) activity. Dogs with hepatopathy generally had a poorer prognosis (46% recovery) than dogs without hepatopathy (89% recovery; P = .0035). Sixty-three percent of the dogs with thrombocytopenia recovered, compared to 90% of the dogs without thrombocytopenia (P = .042). Recovery was not associated with sex, age, breed, or type of sulfonamide administered.
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PMID:Clinical findings in 40 dogs with hypersensitivity associated with administration of potentiated sulfonamides. 1452 30

We report on a 68-year-old female patient who was admitted with abdominal pain. Elevated lipase and CRP caused us to suspect pancreatitis. Because an enlarged pancreas head was found on ultrasound, an endoscopic retrograde cholangio- and pancreaticography was performed with a pethidine-containing premedication. Thereafter, bilirubin, gamma-glutamyl transpeptidase and alkaline phosphatase increased dramatically. There was also a moderate elevation of aspartate aminotransferase and alanine aminotransferase. A second endoscopic retrograde cholangio- and pancreaticography with the same premedication was performed in order to exclude an undetected concretion. This led to a further increase of bilirubin. An association with the drugs given as premedication was therefore suspected, and in fact, a hypersensitivity reaction towards pethidine was confirmed by the lymphocyte transformation test. We thus conclude that pethidine caused an immunologically mediated hepatic injury.
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PMID:Dramatic increase in bilirubin after ERCP - pethidine as a possible cause of drug-induced hepatitis. 1466 Nov 25


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