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)

Fulminant hepatic failure (FHF) is a severe, life-threatening disorder. Previous studies have suggested that intravenous prostaglandin treatment may improve survival in FHF. The present study was performed to further investigate the possible benefit of intravenous prostaglandin E1 (PGE1) for patients with FHF. A total of 18 patients, all excluded as candidates for hepatic transplantation, were studied. Thirteen of 18 participated in a randomized, double-blind, placebo-controlled trial. PGE1 was administered by continuous infusion at a dose of 10 to 40 microg/h as tolerated. After 48 hours of blinded treatment, 3 of 7 patients randomized to placebo were converted to open-label PGE1 for lack of biochemical and/or clinical improvement. Mean values for alanine transaminase, aspartate transaminase, total bilirubin, prothrombin time, factor V percent, factor VII percent, hepatic encephalopathy score, days from onset of symptoms to initiation of treatment, and cause of FHF were similar between treatment groups. Ten of 18 patients (55%) enrolled in this trial survived. However, survival was not different between PGE1-(60%) and placebo (50%) treated patients. The greatest predictor of survival was the number of days from onset of symptoms to hospitalization, which was significantly (P = .002) shorter for survivors (3.3 v 12.4 days), regardless of PGE1 treatment. Six of 8 patients (75%) who began PGE1 therapy and 4 of 5 placebo-treated patients (80%) hospitalized within 10 days of onset of symptoms survived. By contrast, all 5 patients who were hospitalized and subsequently began PGE1 treatment 10 days or longer after the onset of symptoms died. We conclude that early recognition and hospitalization is the most important factor in reduction of mortality from FHF. It is unclear whether PGE1 treatment is beneficial when administered during this period. However, it is apparent that PGE1 was not effective for treatment of FHF if treatment started more than 10 days after onset of this clinical syndrome.
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PMID:Treatment of fulminant hepatic failure with intravenous prostaglandin E1. 972 81

In fulminant hepatic failure (FHF), the development of hepatic encephalopathy is associated with grossly abnormal concentrations of plasma amino acids (PAA). Normalization of the ratio of branched-chain amino acids to aromatic amino acids (Fischer's ratio) correlates with clinical improvement. This study evaluated changes in PAA metabolism during 4 h of isolated, normothermic extracorporeal liver perfusion using a newly designed system containing human blood and a rhesus monkey liver. Bile and urea production were within the physiological range. Release of the transaminases AST, ALT and LDH were minimal. The ratio of branched (valine, leucine, isoleucine) to aromatic (tyrosine, phenylalanine) amino acids increased significantly. These results indicate that a xenogeneic extracorporeal liver perfusion system is capable of significantly increasing Fischer's ratio and may play a role in treating and bridging patients in FHF in the future.
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PMID:Xenogeneic, extracorporeal liver perfusion in primates improves the ratio of branched-chain amino acids to aromatic amino acids (Fischer's ratio). 1035 51

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

When a patient with acetaminophen overdose arrives in the emergency room more than 14 hours after ingestion, the value of N-acetylcysteine is unproven and patient mortality is at least 10%. Anecdotal case reports have indicated benefit of extracorporeal detoxification of these late-arriving patients with acetaminophen overdose. We identified 10 patients with serious acetaminophen overdose, 8 that arrived in the emergency room 16 to 44 hours after acetaminophen overdose with plasma levels predicting severe hepatic toxicity, and 2 that arrived in the emergency room 8 to 12 hours after overdose but with exceedingly high levels. All patients developed severe hepatitis (mean peak alanine aminotransferase, 4,052; mean peak protime, 25 seconds). At 16 to 68 hours after overdose, the patients were treated for 4 to 6 hours with the Liver Dialysis System (Hemocleanse Inc, W. Lafayette, IN), a single-access hemodiabsorption system indicated for treatment of serious drug overdose and for treatment of hepatic encephalopathy. Acetaminophen levels fell an average of 73% during treatment. Treatment was repeated 24 or 48 hours later if acetaminophen was still measurable in plasma. All 10 patients recovered intrinsic liver function and general health, with liver enzymes starting to normalize 24 hours after treatment, and were discharged 3 to 7 days after overdose. No patient required liver transplant. Because market introduction of Liver Dialysis, there have been 40 more patients with acetaminophen-induced hepatotoxicity treated with Liver Dialysis. All have recovered liver function without long-term sequelae. Though most of these patients with already established hepatic toxicity from acetaminophen would recover without extracorporeal blood therapy, treatment with the Liver Dialysis System should assure recovery from acute hepatic failure, and may shorten the clinical course of the illness.
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PMID:Treatment of acetaminophen-induced hepatitis and fulminant hepatic failure with extracorporeal sorbent-based devices. 1192 6

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

Patients with chronic hepatitis B (CHB) may develop severe disease exacerbations (flare) with jaundice, and some may progress to fulminant hepatic failure. Whether early administration of lamivudine can prevent liver failure and mortality is uncertain. We investigated the role of lamivudine treatment in severe hepatitis B virus (HBV) exacerbations. Consecutive patients presented with severe flare-up of HBV (new onset of jaundice plus alanine aminotransferase greater than five times upper limit of normal) treated with lamivudine and historical controls who did not receive lamivudine were studied. All patients had no hepatic encephalopathy on admission. Univariate analysis and multivariate logistic regression were performed on various clinical and laboratory factors for the prediction of mortality. Twenty-eight patients treated with lamivudine and 18 controls were identified. Overall, nine patients died and two other received liver transplants for fulminant hepatic failure. Six of 28 (21.4%) lamivudine-treated patients vs five of 18 (27.8%) controls died or received a liver transplant (P = 0.62). On multivariate analysis, platelet < or = 143 x 10E9/L (odds ratio 22.4, 95% CI 1.8-281.6) and bilirubin > 172 micromol/L (odds ratio 18.4, 95% CI 1.5-228.5) were independent predictors of liver-related mortality. The mortality of patients who had thrombocytopenia and high bilirubin, thrombocytopenia, high bilirubin, and no risk factor were 69.2%, 11.1%, 12.5% and 0% respectively. Hence lamivudine confers no survival benefit to conventional treatment in severe exacerbations of CHB. Patients with thrombocytopenia and high bilirubin should be considered for liver transplantation.
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PMID:The role of lamivudine and predictors of mortality in severe flare-up of chronic hepatitis B with jaundice. 1243 Dec 4

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

The present study was designed to examine the effects of the donor of nitric oxide (NO), NaNO(2) and the inhibitor of NO synthase, N(omega)-nitro-L-arginine (L-NNA), on the development of dimethylnitrosamine (DMNA)-induced chronic hepatitis in rats. L-NNA decreased rat survival and enhanced the severity of hepatic encephalopathy in the DMNA-treated animals. The aggravation of the morphological signs of hepatitis, the activation of serum alanine aminotransferase and cytosolic superoxide dismutase activities and the increase in the liver malondialdehyde content were observed in this group. The treatment with NaNO(2) improved liver morphology, decreased serum marker enzyme activities, lowered the activities of alpha-D-mannosidase and N-acetyl-beta-D-glucosaminidase compared to the DMNA-treated group. The results of the morphological and biochemical studies suggest that L-NNA increased DMNA-induced liver damage, whereas NaNO(2) partially prevented the development of chronic hepatitis. It is proposed that the opposite effects of L-NNA and NaNO(2) are partially explained by a modulation of the free radical-dependent processes in the liver.
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PMID:Effect of the nitric oxide donor and the nitric oxide synthase inhibitor on the liver of rats with chronic hepatitis induced by dimethylnitrosamine. 1559 49


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