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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients, both women aged 31 and 73 years, were admitted with chest pain and coma, respectively. They had very high aspartate aminotransferase levels, accompanied by relatively low alanine aminotransferase levels. The second patient had developed acute liver failure and hepatic encephalopathy. Both patients were chronic alcohol abusers and had taken therapeutic doses of acetaminophen for a couple of days. The marked elevation of the aminotransferase levels and the rapid decline of these levels after discontinuing the use of acetaminophen and alcohol led to the diagnosis of acetaminophen hepatotoxicity. In chronic alcohol abusers, cytochrome P450 2E1 is induced and the amount of glutathione is depleted. This combination causes the formation of a relatively large amount of the radical N-acetyl-p-benzoquinone imine and a low potential to detoxify this metabolite, so that even small amounts of acetaminophen may cause liver damage. It is recommended that chronic alcohol abusers (more than four alcoholic beverages per day) use no more than 2 g acetaminophen per day.
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PMID:[Acetaminophen use by chronic alcohol abusers: a therapeutic dose may be too much for the liver]. 1192 19

Hepatocellular carcinoma is a primary tumor complicating liver disease, associated with cirrhosis in 80-90% of the cases. A kidney transplant recipient with chronic B and C viral hepatitis was admitted because of general malaise, renal function impairment and positive AST, ALT and alkaline phosphatase tests, and very high alpha-fetoprotein levels. Ascites, spontaneous bacterial peritonitis and renal failure developed. A CT showed multiple liver masses. Renal failure required hemodialysis. The patient died 17 days after the initial symptoms with hepatic encephalopathy. A postmortem liver biopsy confirmed the diagnosis of cirrhosis and hepatocellular carcinoma (HCC). This report, as well as a few others, shows the accelerated evolution of chronic viral hepatitis in kidney transplant patients and questions the convenience of kidney transplantation and the adequate follow up in chronic viral hepatitis.
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PMID:[Fatal acute hepatic failure with hepatocarcinoma presentation in a patient with renal transplant with asymptomatic chronic B and C hepatitis]. 1172 27

Hepatic encephalopathy and elevated serum ammonia levels occur commonly after portacaval shunt and are hypothesized to be, in part, due to decreased hepatic blood flow. Prior work has demonstrated increased blood flow to the liver following hepatic periarterial neurectomy. In this experimental study, we investigated the functional, hemodynamic, and histopathological changes in the liver and kidney occurring after the addition of hepatic periarterial neurectomy to side-to-side portacaval shunt in dogs. It is our hypothesis that the addition of hepatic periarterial neurectomy to portacaval shunt will decrease postshunt ammonia levels. Side-to-side portacaval shunt was performed in 12 dogs (group I). Hepatic periarterial neurectomy was added to portacaval shunt in 9 dogs (group II). Serum levels of ammonia, urea, creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, albumin, and bilirubin together with hepatic blood flow were determined in both groups preoperatively and on postoperative day 21. The pre- and postoperative histopathologic changes of the liver and kidney were evaluated. There was significantly less postoperative elevation of serum ammonia and aspartate aminotransferase when hepatic periarterial neurectomy was added to the portacaval shunt procedure. Hemodynamic studies of hepatic artery and hepatic tissue indicated better blood flow in group II. The histopathologic evaluation of group II showed expansion of sinusoids, portal vessels, and portal areas and increased portal fibrosis as compared to group I. The results of this experimental study show that adding hepatic periarterial neurectomy to the portacaval shunt procedure improves postoperative serum levels of ammonia and aspartate aminotransferase and hepatic artery and tissue blood flow.
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PMID:An attempt to decrease ammonia levels after portacaval anastomosis in dogs: hepatic periarterial neurectomy. 1235 34

For the development of an artificial liver support system, a clinically relevant large-animal model of fulminant hepatic failure (FHF) is indispensable. Although several large-animal models have been reported so far, they have not been entirely satisfactory. Recently, we have developed a new porcine model of FHF by means of intraportal administration of 0.1 mg/kg of alpha-amanitin and 1 microg/kg of lipopolysaccharide (LPS). This model has the following superior features: 100% mortality within 5 days along with a marked elevation of aspartate transaminase (AST) levels to around 10,000 IU/l, and severe metabolic disorders such as serum lactate accumulation, hypoglycemia, coagulopathy, plasma amino acid imbalance, and hyperammonemia; an onset of hepatic encephalopathy and a significant increase in intracranial pressure immediately before death; a reversal of FHF by orthotopic liver transplantation, proving that the toxicity is liver-specific and that the graft liver is unaffected; and the capability of the damaged liver to recover and achieve both morphological and functional regeneration in 1 week if supported by an efficient auxiliary graft. Because this porcine model satisfies many of the required criteria of an optimal FHF model, it is expected to provide a useful tool for the study of FHF and the development of new therapies.
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PMID:Large-animal models of fulminant hepatic failure. 1459 18

Trimethoprim-sulfamethoxazole (TMP-SMZ) is one of the most commonly used antibiotics. Although many of its adverse effects are well recognized, TMP-SMZ related hepatotoxicity is considered rare and is usually characterized by cholestasis or mixed hepatocellular-holestatic reactions. In this study, we describe the case of a previously healthy young man with acute fulminant liver failure caused by TMP-SMZ. The patient presented with complaints of 'flu-like' symptoms with myalgia and fever after taking TMP-SMZ for 7 d for otitis externa. The patient subsequently developed fever, worsening jaundice, and a rash on his neck and chest. Liver enzymes peaked on day 3 with alanine aminotransferase (ALT) 11,549, aspartate aminotransferase (AST) 23,289, alkaline phosphatase 245, and total bilirubin 10.3 mg/dL, with a conjugated bilirubin of 8.3 mg/dL, prothrombin time (PT) 60.5 s, partial normalized ratio (PTT) 49 s, and international normalized ratio (INR) 7.5. Of note, acetaminophen level on admission was undetectable. Serology for hepatitis A, B, C, cytomegalovirus, HIV, toxoplasmosis, and blood cultures were all negative. The patient developed hepatic encephalopathy with hallucination on day 4. Laboratory tests revealed a serum ammonia level of 190 U, serum creatinine kinase (CK) 10,466 (42 on admission), serum creatinine 8.2 mg/dL (1.2 on admission), and significant metabolic acidosis. Renal ultrasound was unremarkable. The patient was started on hemodialysis for acute renal failure. Meanwhile, liver transplantation assessment was also initiated. On day 8 post-admission (15 d after taking TMP-SMZ), the patient received a successful orthotopic liver transplant.
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PMID:Successful orthotopic liver transplantation after trimethoprim-sulfamethoxazole associated fulminant liver failure. 1470 31

As a somatic evaluation by outpatient psychotherapy service for alcoholics is being done very rarely the patients are not informed about health harm related to alcohol having the "false feeling of safety". The aim of the study was to evaluate a functional and morphological liver state of patients served by such a service for minimum 5 years who were sent do the Department of Clinical Toxicology via intervention medicine. The changes in the central nervous system were also considered. The West Haven criteria of altered mental state in hepatic encephalopathy were applied. The Number Connection Test, part A and B, and "100-7" test were used to psychometric evaluation. A significantly higher serum ammonia concentration (p<0.02), AST, ALT and GTP enzymes activity, bilirubin (p<0.02), iron (p=0.005) concentration and significantly lower prothrombin index and albumin concentration were found in the group of ethanol dependent patients as compared to the reference group. A significantly lower RBC and platelets number, lower Ht and significantly elevated MCV compared to the control group were also found. The relationship between West Haven criteria and results of laboratory testing was shown: a worse West Haven criteria a worse metabolic disorders. The pathologic changes in the liver ultrasonography and scintigraphy were significantly higher in the group of ethanol dependent patients. The presented observations indicate on necessity of close co-operation between psychologists, therapeutics and clinical toxicologists in early diagnosing and treatment the organ injury in alcohol addicted patients.
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PMID:[Difficulties in diagnosis of hepatic encephalopathy in ethanol dependent patients]. 1552 71

Recently, continuous venovenous hemodiafiltration (CVVHDF) and plasmapheresis (PF) were suggested as supportive therapy options in combination with standard treatment in advanced liver failure. The aim of this study was to analyze the effects of supportive extracorporeal treatment (SET) in a group of patients with advanced hepatic failure. A total of 25 patients (7 women, 18 men; mean age, 39.3+/-15.4 years; 13 were transplant recipients [6 women, 7 men; mean age, 37.7+/-16.9 years]) were included. All patients were in hepatic coma and receiving standard coma and liver failure management when they received SET. Number of SET sessions; levels of serum blood urea nitrogen, creatinine, albumin, calcium, phosphorus, ammonia, alanine and aspartate aminotransferase, and total/conjugated bilirubin; and prothrombin times (PTT) before and after SET were recorded retrospectively. 7.7+/-7.9 SET sessions were performed. Thirteen liver transplant recipients required SET for an average of 9.7+/-8.3 days after transplantation. Serum ammonia and bilirubin levels were lower after termination of supportive therapy when compared with initial levels (p<0.0001 and p<0.005 respectively). During follow-up, hepatic encephalopathy and liver failure resolved in 11 patients, while 14 patients (7 transplant recipients) died. There was no significant difference between patients in either group except that PTT was shorter in patients who survived (p<0.01). Further analyses revealed that in surviving patients, ammonia clearance was higher (p<0.01). In patients with advanced liver failure, or liver transplants, CVVHDF and/or PF could be supportive options combined with standard treatment.
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PMID:Effect of supportive extracorporeal treatment in liver transplantation recipients and advanced liver failure patients. 1702 48

Fulminant hepatic failure (FHF) is a condition with a sudden onset of necrosis followed by degeneration of hepatocytes, without any previously established liver disease, generally occurring within hours or days. FHF is associated with a wide spectrum of neuropsychiatric alterations ranging from stupor to coma, culminating in death. In the present study FHF was induced in rats by the administration of thioacetamide (TAA). Oxidative stress is thought to play a prominent role in the pathophysiology of cerebral changes during FHF leading to the assumption that antioxidants might offer protection. Hence, in the present study the protective effect of C-Phycocyanin (C-PC), a natural antioxidant, was evaluated on TAA-induced tissue damage. C-Phycocyanin was administered intraperitoneally twice at 24 h interval (50 mg/kg body weight) along with the hepatotoxin TAA (300 mg/kg body weight). The animals were sacrificed 18 h after the second injection of TAA treatment and various biochemical parameters were analysed in liver, serum and brain tissues. These studies revealed significant prevention of TAA-induced liver damage by C-PC, as evidenced by a) increase in survival rate; b) the prevention of leakage of liver enzymes (AAT and AST) and ammonia into serum; c) increase in prothrombin time and d) liver histopathology. Ultrastructural studies of astrocytes of different regions of brain clearly showed a decrease in edema after C-PC treatment. TAA-induced histopathological lesions in different regions of the brain namely cerebral cortex, cerebellum and pons medulla were significantly reduced by the co-administration of C-PC with TAA. Further C-PC treatment resulted in a) decrease in the levels of tryptophan and markers of lipid peroxidation and b) elevation in the activity levels of catalase, glutathione peroxidase in different regions of brain. These studies reveal the potential of C-PC in ameliorating TAA-induced hepatic encephalopathy by improving antioxidant defenses.
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PMID:Co-administration of C-Phycocyanin ameliorates thioacetamide-induced hepatic encephalopathy in Wistar rats. 1716 76

Minimal hepatic encephalopathy (MHE) is characterized by disturbance of mental state and neuromuscular function. To assess the clinical efficacy of acetyl-L: -carnitine (ALC) in the treatment of MHE, we performed a randomized, double-blind, placebo-controlled study administering ALC in cirrhotic patients with this disease and evaluating their cognitive functions. One hundred and twenty-five cirrhotic patients, of whom 21 were infected by hepatitis B virus, 75 by hepatitis C virus and 29 with cryptogenic cirrhosis, were enrolled in our study. Patients were randomly divided into two groups, and using double-blind administration, group A was treated with ALC and group B with placebo for 90 days. The two groups were similar in demographic characteristics, aetiology of cirrhosis, duration and Child-Pugh grade. Minimal hepatic encephalopathy was diagnosed with the Trail Making Test (TMT), Symbol Digit Modalities Test (SDMT) and Auditory Verbal Learning Test (AVL) and cognitive function with the Mini Mental State Examination (MMSE). After 90 days in group A treated with ALC, we observed a significant decrease in prothrombin time (P < 0.001), bilirubin serum levels (P < 0.01), AST (P < 0.001), fasting NH(4) serum levels (P < 0.001), Trail Making Test-A (P < 0.001) and Trail Making Test-B (P < 0.001), and a significant increase in albumin serum levels (P < 0.005), MMSE test (P < 0.001), Symbol Digit Modalities Test (P < 0.001), BDT (P < 0.001), AVL long-term test (P < 0.001) and AVL total test (P < 0.001). No significant differences were observed in EEG in either group of patients treated with ALC or placebo. The benefits of ALC in comparison with placebo are demonstrated in greater reductions in serum ammonia levels, as well as in improvements of neuropsychological functioning.
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PMID:Acetyl-L-carnitine treatment in minimal hepatic encephalopathy. 1835 30

Hepatic encephalopathy (HE) is a common reversible neuropsychiatric syndrome associated with chronic and acute liver dysfunction and significant morbidity and mortality. Although a clear pathogenesis is yet to be determined, elevated ammonia in the serum and central nervous system are the mainstay for pathogenesis and treatment. Management includes early diagnosis and prompt treatment of precipitating factors (infection, gastrointestinal bleeding, electrolyte disturbances, hepatocellular carcinoma, dehydration, hypotension, and use of benzodiazepines, psychoactive drugs, and/or alcohol). Clinical trials have established the efficacy of lactulose and lactitol enemas in the treatment of acute hepatic encephalopathy. Extensive clinical experience has demonstrated the efficacy of oral lactulose and lactitol with the goal of two to three soft bowel movements a day for the treatment of chronic HE. However, lactulose and lactitol have significant gastrointestinal side effects. For patients unable to tolerate lactulose or lactitol or who still have persistent chronic HE with lactulose or lactitol, neomycin, metronidazole and rifaximin are second-line agents. More recent data supports the benefits of rifaximin used solely and as an additional agent with fewer side effects than neomycin or metronidazole. Newer therapies being investigated in humans with clinical promise include nitazoxanide, the molecular adsorbent recirculating system (MARS), L-ornithine phenylacetate, sodium benzoate, and/or sodium phenylacetate and Kremezin((R)) (AST-120).
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PMID:Current trends in the treatment of hepatic encephalopathy. 1970 77


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