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)

For the evaluation of certain differences in the diminution of export proteins of the liver we examined some exactly defined groups of liver diseases with the aim of further differentiation of the pathogenetic mechanisms. We measured the activity of glutamate-oxalacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, lactate dehydrogenase, alkaline phosphatase, cholinesterase and lecithin-cholesterol acyltransferase, the Quick value, the coagulation factors I, II, V, VII, VIII, IX and X. Clotting factors were determined by a Schnitger-Gross Coagulometer. Prothrombin, antithrombin III, plasminogen, factor VIII associated antigen and activated factor XIII were measured by immunoelectrophoresis according to Laurell. Lipoprotein electrophoresis in agarose gel was performed to evaluate changes in lecithin-cholesterol acyltransferase activity. Except of the rising diminution of export proteins in the course of liver disease from acute hepatitis to cirrhosis we found also specific changes of the patterns of the plasma specific enzymes. These proteins were diminished dependent on their half life time and the inflammatory activity--measured as the height of the transaminases. Lecithin cholesterol acyltransferase and factor VIII did not participate in the general diminution of the most export proteins; some details were found to explain this differing behaviour. Results are critically discussed with regard to new aspects in the biochemistry of the damaged liver cell.
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PMID:[Correlations between the diminished secretion of export proteins from the liver and the plasmatic activity of liver cell enzymes (author's transl)]. 42 91

Fasting serum bile acid (SBA) was measured by the enzymic fluorimetric method coupled with the NAD-resazurin system in 23 controls, 35 asymptomatic carriers of HIs antigen including 4 e antigen carriers and 91 patients with various liver diseases. All GHBs and e antigen carriers showed SBA within the normal range. SBA was most significantly correlated with serum bilirubin (gamma=0.74) and was a more sensitive index for impaired liver function than bilirubin or alkaline phosphatase in 164 radomly chosen samples from the liver disease group. In serial determinations of SBA with reference to GOT, GPT, changing patterns of these two parameters were classified into the parallel type and the discrepant type. Thirty two out of 40 cases with chronic liver disease belonged to the parallel type. SBA remained abnormal even after the normalization of transaminase in 12 out of 20 resolving episodes in cases of the parallel type, regardless of diagnosis. Since SBA changes according to the stage of the disease activity, serial and simultaneous estimation of SBA and GOT, GPT was found to be helpful in the observation of liver diseases. Maximum values of SBA elevation in an endogenous bile acid tolerance test after eating two egg yolks were higher than controls in 4 out of 7 cases with liver disease, who were associated with normal fasting SBA.
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PMID:Evaluation of fluorimetrically estimated serum bile acid in liver disease. 84 3

The plasma half lives of antipyrine, paracetamol, and lignocaine given by mouth were measured in 23 patients with stable chronic liver diseases of varying severity. Fifteen patients received all three drugs and 19 at least two. The half life of paracetamol was abnormally prolonged in nine out of 17 patients (mean 2-9 hours, normal 2-0 hours), of antipyrine in 10 out of 19 patients (mean 30-4 hours, normal 12-0 hours), and of lignocaine in 19 out of 21 patients (mean 6-6 hours, normal 1-4 hours). Prolongation of the half lives of all three drugs was significantly correlated with an increase of the vitamin-K1-corrected prothrombin time ratio and a reduction in serum albumin concentration. There was no correlation with serum bilirubin concentration or serum alanine aminotransferase activity. This suggests that impaired drug elimination was related to depressed hepatic protein synthesis. Considerable prolongation of the half life of one drug was invariably associated with delayed elimination of the others. The half life of lignocaine, however, was always the most prolonged and was a highly sensitive indicator of hepatic dysfunction. The pharmacokinetic characteristics of a drug as well as the severity of liver disease should be taken into account when considering drug dosage in patients with chronic liver disease.
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PMID:Antipyrine, paracetamol, and lignocaine elimination in chronic liver disease. 86 46

An enzymatic-fluorimetric method using a highly purified 3alpha-hydroxysteroid dehydrogenase (Sterognost-3alpha, Nyco) was used to determine fasting serum bile acid concentrations on 49 occasions in 43 patients with various liver diseases. A two-hour postprandial bile acid determination was carried out on 29 occasions in 27 of the patients. Fasting bile acid concentration correlated significantly both in cholestatic hepatobiliary and in parenchymatous liver disease to serum bilirubin and aspartate aminotransferase (ASAT) but not to alanine aminotransferase (ALAT), alkaline phosphatase, or albumin. The two-hour postprandial bile acid concentration was above normal in all patients with biochemical and/or histological signs of hepatobiliary disease, also when fasting concentration was within normal limits. In parenchymatous liver disease correlations existed between the two-hour postprandial bile acid concentration and bilirubin, ASAT, and ALAT. The sensitivity of serum bile acid estimation was compared to other liver function tests. Both the fasting and the postprandial serum bile acid concentrations tended to be more sensitive tests of hepatobiliary disease than bilirubin, ASAT and ALAT.
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PMID:Serum bile acid concentrations in patients with liver disease. 95 69

In olfacto-odorimetrical examinations of 32 patients with chronic liver diseases (18 female and 14 male patients at the age of 23 to 77 years) 13 patients with a disturbed olfactory function were found. With one exclusion these patients suffered from liver cirrhosis. On the basis of the anamnesis in 10 of these patients a causal connection between disturbance of smelling and liver disease could be assumed. Out of this group with chronic active hepatitis of 10 patients only 1 patient had a disturbed olfactory function. In 8 patients with disturbed olfactory function suffering from liver cirrhosis a comparison of the olfactometrical findings with activity of GOT and GPT in the serum and the serum bilirubin content showed a correlation between possibilitiy of smelling and serum bilirubin level. Possible causes of appearing olfactory disturbances are demonstrated in short.
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PMID:[Functional study on the sense of smell in patients with chronic liver disease]. 102 Mar 83

Two hundred and forty-three patients receiving renal replacement therapy (RRT) and 20 renal unit staff were tested for antibodies to hepatitis C (HCV). Three patients (1.2%) were positive by the first generation test kit, the lowest rate in patients receiving RRT reported in the literature to date. These three, and eight other patients tested positive by the second generation kit, a prevalence rate of 4.5%. Anti-HCV antibody positivity was associated with higher mean serum alanine aminotransferase (p = 0.0003) and aspartate aminotransferase (p = 0.018) levels. However, only one of the 11 anti-HCV positive patients had liver transaminase levels more than twice the upper limit of the laboratory reference range. Anti-HCV positivity was associated with a higher mean number of units of blood transfused (p = 0.035). None of 20 staff were anti-HCV positive. Twenty-five of 212 (11.7%) patients reported a history of liver disease; none of these were anti-HCV positive. Hepatitis B surface antigen was detected in eight of 215 (3.7%) patients, of which three were e antigen positive. There was evidence of past hepatitis B infection in 53 of 215 (24.7%) patients, more frequently in Maoris (p = 0.001). Overall, significantly raised liver transaminases were present in three of 198 (1.5%) patients and in no staff. This unit has a remarkably low prevalence of antibodies to HCV, an observation supported by the low rate of abnormal serum liver enzymes.
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PMID:Prevalence of antibodies to hepatitis C virus in patients receiving renal replacement therapy, and in the staff caring for them. 128 95

We assessed the correlation between the positivity for serum IgM antibody to hepatitis C virus and the activity of liver disease in patients with chronic hepatitis C virus infection. Serum samples were taken from 10 antibody to hepatitis C virus-positive asymptomatic patients with normal serum ALT levels, from 14 untreated patients with clinically and histologically proven chronic hepatitis C and from 26 patients with clinically and histologically proven chronic hepatitis C assigned to receive recombinant interferon alpha-2a (6 million IU three times a week for 6 mo). Each serum specimen was tested for IgM antibody to hepatitis C virus-associated C100-3 antigen by enzyme-linked immunosorbent assay. Patients were observed for at least 12 mo. All 10 patients with normal ALT values tested negative for IgM antibody to hepatitis C virus. In contrast, 33 of 40 (82%) patients with chronic hepatitis C had IgM antibody to hepatitis C virus, and a positive correlation was seen between the ALT level and the level of IgM antibody to hepatitis C virus (r = 0.803, p less than 0.001). During interferon treatment, ALT levels declined into the normal range in 18 of 26 treated patients (69%) and remained normal after stopping treatment in 8 patients (31%). In untreated patients, in treated patients who did not respond to interferon treatment and in responder patients who relapsed, no significant changes in IgM antibody to hepatitis C virus levels were seen during the study period. In contrast, IgM antibody to hepatitis C virus became undetectable by the end of interferon treatment in seven of eight patients with a sustained response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of IgM antibody to hepatitis C virus in patients with chronic hepatitis C. 131 44

The development of a serologic assay to detect antibodies directed at an antigen (C-100-3) of the hepatitis C virus (anti-HCV) has been a major breakthrough in the long search for causative agents of non-A, non-B (NANB) hepatitis. The frequency of HCV in those who have end-stage liver disease is not known. Moreover, the rate of recurrence after liver transplantation (OLTx) and the rate of acquisition of new HCV infection as a result of the OLTx experience is as yet unknown. This study was performed in an attempt to answer these questions. The prevalence of HCV in 372 patients undergoing OLTx at the University of Pittsburgh was determined. Those transplanted for HBV-related liver disease with hepatoma had the highest rate of HCV antibody positivity (45.4%) followed by those with metabolic liver disease (42.5%), putative NANB liver disease (41.4%), and cryptogenic cirrhosis (20.9%); those with cholestatic liver disease exhibited the lowest rate (16.2%). HCV antibody was positive in only 26.3% of patients with hepatoma. Of those patients who were negative prior to transplantation, 12.2% acquired HCV antibody post-OLTx. In the putative NANB group, no difference was detected in the AST and ALT prior to transplantation in either the HCV antibody-positive or -negative patients. In patients with cryptogenic cirrhosis, those who were positive for HCV antibody had higher transaminase levels prior to transplantation than did those patients who were HCV antibody negative.
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PMID:Prevalence of hepatitis C virus antibody in a liver transplantation population. 131 88

We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 +/- 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p greater than 0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India.
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PMID:Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India. 132 39

The natural history of chronic hepatitis B patients who spontaneously cleared serum HBsAg was investigated. A total of 351 patients with chronic hepatitis B were observed in our hospital for at least 3 yr. Seven of these patients became HBsAg negative during the follow-up period. HBsAg disappeared within 6 mo (range = 11 to 169 days, mean = 70 days) after acute elevation of ALT. ALT levels as high as 500 IU were found in three patients, whereas such elevation was not demonstrated in the other four patients. After the disappearance of HBsAg, ALT levels returned to normal in all patients. With one exception, all patients seroconverted to antibody to HBsAg; however, hepatitis B virus DNA remained detectable in serum using the polymerase chain reaction in five patients. The titer of percent inhibition of antibody to HBcAg gradually decreased to less than 70% when a 1:200 dilution of the serum of six patients was used. Four of the patients had active liver disease develop: two had chronic active hepatitis and two had cirrhosis. Three of these four patients subsequently had hepatocellular carcinoma develop. These findings suggest that patients may suffer complications of chronic hepatitis even after normalization of transaminase activities and after the clearance of HBsAg. Thus hepatitis B virus should be considered as a possible factor associated with hepatocellular carcinoma even in the absence of HBsAg, particularly if serum hepatitis B virus DNA persists.
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PMID:Clearance of HBsAg in seven patients with chronic hepatitis B. 133 20


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