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)

Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47.5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu,Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.
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PMID:Excess dietary histidine decreases the liver copper level and serum alanine aminotransferase activity in Long-Evans Cinnamon rats. 1312 63

In normal mice, plasma histamine levels were 29.4+/-10.1 pmol/ml. When 0.1 microg of lipopolysaccharide (LPS) was intravenously injected into Propionibacterium acnes (P. acnes)-primed ICR mice, histamine levels increased remarkably to 61.2+/-15.9 pmol/ml (p<0.001). An increase was also observed in liver tissues. Oral administration of histidine at 200 mg/kg once daily for 5 d before intravenous LPS injection increased the plasma alanine aminotransferase (ALT) activity to 2936.5+/-356.3 IU/l, a significant change compared with the controls (2244.8+/-425.5 IU/l, p<0.05). The 24 h survival rate after LPS injection was 72.7% in the mice treated with 50 mg/kg of ranitidine, in contrast with 50% in the control group although the treatment did not significantly decrease the plasma ALT activity. On the other hand, 50 mg/kg of pyrilamine significantly reduced plasma ALT activity (p<0.001). The results suggested that histamine levels are related to hepatic damage in the P. acnes plus LPS induction of liver injury.
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PMID:Influence of histamine in a liver injury model induced by Propionibacterium acnes and lipopolysaccharide. 1451 42

We recently treated a patient with severe aplastic anaemia (SAA) who also had chronic hepatitis B virus (HBV) infection. The HBV serological status at the time of diagnosis of SAA was HBsAg(+) and HBeAg(+). Subsequent analysis of the precore region of HBV DNA showed wild-type. He received anti-thymocyte globulin (ATG) and cyclosporin A (CsA) therapy twice. After each course of ATG infusion and during CsA therapy he developed lymphopenia for 1 and 2.5 months, respectively. His serum alanine aminotransferase (ALT) became normalized during the period of lymphopenia, but the serum HBV viral load increased. When his peripheral lymphocytes count recovered, his ALT became elevated again. Lamivudine was effective to normalize his elevated ALT and suppress viral replication. The phenomenon observed in this case supports the prevailing notion that hepatitis B flare-up in HBV carriers after chemotherapy is caused by an immune-mediated mechanism. Meanwhile, this is the first documented case of SAA who developed HBV reactivation upon recovery of lymphopenia after immunosuppressive therapy. This also highlights the necessity of pre-emptive therapy with lamivudine in SAA/HBsAg(+) patients to receive immunosuppressive therapy with ATG/CsA.
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PMID:Restoration of immunity and reactivation of hepatitis B virus after immunosuppressive therapy in a patient with severe aplastic anaemia. 1511 33

Fenofibrate-induced acute or chronic hepatitis is rare, and only 11 reports from French, Italian or Spanish literature have been published up to date. We report a case of fenofibrate-induced acute cholestatic hepatitis. To the best of our knowledge, this is the first one reported in Taiwan. A 61-year-old man developed acute cholestatic hepatitis after taking fenofibrate 100 mg tid for 10 days. Laboratory profile on admission showed serum total bilirubin 9.3 mg/dL, direct bilirubin 2.7 mg/dL, alanine aminotransferase 249 IU/L, aspartate aminotransferase 259 IU/L, alkaline phosphatase 259 IU/L, and gamma-glutamyl transpeptidase 1014 IU/L. Pathology proved hepatocanalicular cholestasis in liver. Fenofibrate was discontinued immediately. His clinical manifestations and liver function tests improved gradually and returned to nearly normal in 2 months. We suggest that liver function tests, including total bilirubin, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase, be checked at least 2 weeks after taking the drug and that serum aminotransferase be monitored every 3 months during the first 12 months of therapy. Treatment should be discontinued if alanine aminotransferase values increase by more than 100 IU/L.
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PMID:Fenofibrate-induced acute cholestatic hepatitis. 1535 12

A 56-year-old man was admitted to our hospital with a diagnosis of hilar bile duct cancer. Abdominal ultrasonography, computed tomography and endoscopic retrograde cholangiopancreatography showed no other concomitant disease. Biochemical data showed 0.6 mg/dL of total bilirubin, 104 IU/L of alanine aminotransferase and 469 mg/dL of alkaline phosphatase. Carbohydrate antigen 19-9 was elevated as 112.1 U/mL. Operative findings included a resectable left hilar bile duct cancer and grayish-white nodules 0.3-0.5cm in diameter on the surface of segments 6 and 4 of the liver. Although intrahepatic metastasis of the bile duct cancer was highly suspected under intraoperative US, frozen section was reported to show the small nodules containing multiple biliary hamartomas, so-called von Meyenburg complex. Therefore, a left hepatic lobectomy together with resection of the extrahepatic bile duct followed by a Roux-en-Y hepaticojejunostomy was the procedure of choice. His postoperative course was uneventful. The intraoperative findings could have been misdiagnosed due to their similarity to intrahepatic metastasis and intraoperative histology is indispensable to differentiate von Meyenburg complex in this case. The possibility of a preoperative imaging diagnosis for von Meyenburg complex seems to depend on the size of the bile duct structure in each hamartoma. To the best of our knowledge, this is the fourteenth case of bile duct cancer associated with von Meyenburg complex reported in the literature. The following case is being reported because of the rarity of the disease and to stress the importance of intraoperative histology to avoid misdiagnosis as the disseminated disease, particularly when malignant neoplasia is surgically treated.
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PMID:Hilar bile duct cancer associated with preoperatively undetectable von Meyenburg complex--report of a case. 1536 38

A 65-year-old woman died three days after being involved in a traffic accident, following an episode of ventricular fibrillation. She was diagnosed as having suffered cardiac contusion, liver contusion, mediastinal hematoma and rib fracture on admission. Her electrocardiogram showed complete right bundle branch block, complete atrioventricular block, and right axis deviation. Aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and creatine kinase-MB were found to be elevated on biochemical blood analysis. These findings recovered and her condition appeared to improve daily. At autopsy, epicardial and intramyocardial haemorrhage were macroscopically seen in the posterior wall of the bilateral ventricles. On microscopic examination, there was evidence of fresh haemorrhage and coagulative necrosis with inflammatory reaction in the ordinary myocardium and adipose tissue around the atrioventricular node, which had spread to the proximal portion of the His' bundle. It is considered that these findings caused ventricular fibrillation to occur, and that the cause of death in this case was myocardial contusion due to blunt thoracic injury. This case would indicate that myocardium nearby atrioventricular junction is vulnerable to external force. Moreover, it would seem that fatal arrhythmia occasionally occurs during the follow-up stage, despite the lack of any significant clinical findings.
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PMID:Case reports. 1. An autopsy case of fatal arrhythmia induced by injuries of the atrioventricular conduction system: a case report. 1557 75

Aspirin is commonly used as an anti-inflammatory therapy for Kawasaki syndrome. Early initiation with high dose aspirin (80 to > 100 mg/kg per day), followed by low-dose therapy at the afebrile stage, has been often used to reduce morbidity and mortality in coronary complications. We report a 10-month-old infant who was diagnosed with Kawasaki syndrome. Sudden onset of poor activity, poor appetite, lethargy, tachycardia, tachypnea, hepatomegaly, increased AST/ALT, coagulopathy and hyperammonemia developed 3 days after the high-dose aspirin therapy. His histopathological and ultrastructural findings from the liver biopsy were compatible with Reye's syndrome. He recovered completely, and there was no recurrence.
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PMID:Reye's syndrome developing in an infant on treatment of Kawasaki syndrome. 1595 35

The authors conducted a prospective, open-label, pilot trial of the effects of the antidiabetic thiazolidinedione (TZD) rosiglitazone in two patients with moderate to severe plaque psoriasis. Case 1: A lean, euglycemic 43-year-old nondiabetic man with a 2-year history of plaque psoriasis presented with lesions involving 10% of his body surface (Figures 1A, 1B, 1C). He had no other chronic or acute medical problems. He had previously been managed sporadically with topical triamcinolone acetonide, an intermediate-strength glucocorticoid, and was off antipsoriatic medication for 5 months. He was started on rosiglitazone p.o., 8 mg q.d. After 10 weeks on rosiglitazone, the lesions developed increased erythema, spreading, and shedding of scale (Figures 2A, 2B, 2C). After an additional 26 weeks, the lesions had largely disappeared (Figures 3A, 3B, 3C). The patient remained euglycemic throughout the study. His liver function enzymes (alanine transferase [ALT] and aspartate transferase [AST]) remained normal throughout the study: ALT, 23 IU/L; AST, 47 IU/L before treatment; ALT, 25 IU/L; AST, 33 IU/L after treatment. There were no adverse events. Case 2: An overweight 68-year-old woman (body mass index, 29 kg/m2; with a 12-year history of type 2 diabetes and 5-year history of psoriasis presented with generalized plaque psoriasis over 20% of her body, including two large, thick, silvery plaques with the texture of leather over the lower part of the back (Figure 4A). She was given rosiglitazone p.o., 4 mg b.i.d. for 24 weeks, which resulted in significant improvement in psoriasis (Figure 4B). After an additional 26 weeks on rosiglitazone, the plaques had cleared on her back (Figure 4C) and over her entire body, including scalp, ears, and posterior forearms (not shown). Her glycemic control improved (hemoglobin A1c decreased from 7.7% to 7.2%) and liver function remained normal throughout the study (ALT, 24 IU/L; AST, 14 IU/L before treatment; and ALT, 26 IU/L; AST, 15 IU/L after treatment). There were no adverse events.
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PMID:Improvement in psoriasis with rosiglitazone in a diabetic and a nondiabetic patient. 1627 61

Histidine-tryptophan-ketoglutarate solution (HTK) and University of Wisconsin solution (UW) have been shown to have similar outcomes in cadaveric kidney, pancreas, and liver transplantation. Our institution changed from UW to HTK as the primary preservation solution for liver, kidney and pancreas transplantation. This study compares the perioperative and first year outcomes of liver transplantation using UW or HTK. Primary use of HTK began on May 1, 2003. We reviewed the records of all adult liver transplant recipients from July 1, 2002 to December 31, 2004. Recipients were compared based on organ preservation solution (UW n = 204, HTK n = 174). Outcomes included 1-, 6- and 12-month graft and patient survival and 1-, 7-, 14-, and 30-day liver function and serum creatinine. During the entire study period, the two groups were managed similarly in operative technique, immunosuppressive regimens, and donor liver criteria. Over 30 months, 378 adult patients underwent liver transplantation. There were no significant differences between UW and HTK in 1-, 6-, or 12-month graft or patient survival. The HTK group had a higher day 1 median AST, ALT, and total bilirubin, but the two groups were similar thereafter. An anticipated difference in infused volume between UW and HTK was demonstrated. In conclusion, to our knowledge, this is the first reported large case series from North America comparing HTK and UW in liver transplantation with 2- to 12-month follow-up. There were no significant differences between HTK and UW in this population when comparing 1 month graft function and first-year graft and patient survival.
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PMID:Comparison of histidine-tryptophan-ketoglutarate solution (HTK) and University of Wisconsin solution (UW) in adult liver transplantation. 1644 7

Alanine aminotransferase (ALT) is a pyridoxal enzyme found mainly in the liver and kidney, but also in small amounts in the heart, muscle, fat, and brain. Serum aminotransferase activities have been used broadly as surrogate markers for tissue injury and disease in human and veterinary clinical settings and in safety assessment of chemicals and pharmaceuticals. Because of its relative abundance in liver, increased serum ALT activity is generally considered indicative of liver damage. Two ALT isoenzymes, ALT1 and ALT2, are known and have been cloned and sequenced from human, rat, and mouse. In this study, we have cloned the complementary DNA encoding the canine orthologue of ALT1 (cALT1). The complete cDNA sequence comprised 1852 bases and contained a 1485-base open reading frame, which encodes a polypeptide of 494 amino acid residues. Canine ALT1 shares 87.7, 87.2, and 87.0% amino acid identity to its human, mouse, and rat orthologues, respectively. The cDNA was expressed in Escherichia coli, with a N-terminal His (6x) tag, and the recombinant enzyme was purified using immobilized metal-affinity chromatography. The final yield of the purified recombinant cALT1 was greater than 5mg/L culture. The alanine transaminase activity of purified cALT1 was 229.81U/mg protein, which is approximately 38-fold higher than that of total soluble recombinant E. coli cell lysate, confirming that the enzyme is a functional ALT. Evaluation of various canine tissues by RT-PCR revealed that the level of ALT1 expression is in the order of: heart>liver>fat approximately brain approximately gastrocnemius>kidney. The purified cALT1 will be helpful to develop isoenzyme-specific anti-bodies, which could further improve the diagnostic resolution of current ALT assays in drug safety studies.
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PMID:cDNA cloning, expression, purification, distribution, and characterization of biologically active canine alanine aminotransferase-1. 1649 81


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