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

---

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

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.
...
PMID:Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase. 611 67

Non-sulphated conjugates of cholic (C) and chenodeoxycholic (CDC) acids in serum and total conjugates in urine were determined by radioimmunoassay during drainage of extrahepatic cholestasis in twelve patients studied under three different situations: without refeeding of bile, with refeeding after a delay of one to eight days, and with immediate refeeding. The changes in the serum concentrations and renal excretion of C and CDC varied considerably between patients, but the following general features could be discerned: In patients without bile refeeding but with external drainage, the serum concentrations and renal excretion of C and CDC decreased rapidly. In patients with delayed bile refeeding during drainage, the serum concentrations of C and CDC increased when refeeding of bile was begun but only slightly and temporarily, and no influence on renal excretion could be observed. In patients with immediate bile refeeding through an internal drainage the serum concentrations decreased slowly and renal excretion increased during the first week. These differences in the pattern of serum bile acid concentrations were not reflected in the serum concentrations of bilirubin, alkaline phosphatase, alanine aminotransferase or gamma glutamyltransferase.
...
PMID:Cholic and chenodeoxycholic acids during drainage of cholestasis in man with and without bile refeeding. Determination of serum and urinary concentrations by radioimmunoassay. 613 7

In an attempt to study the diagnostic value of alpha-fetoprotein (AFP), serum AFP concentrations were measured by radioimmunoassay in 34 neonates and infants with obstructive hepatobiliary diseases and the results were compared with the normal ranges of AFP at this age. Eighteen of 24 infants with biliary atresia and four of six infants with neonatal hepatitis had raised AFP values. In only one of four infants with choledochal cyst, did the AFP value exceed the normal range. In 10 older children with this lesion, AFP was normal. Serum AFP concentrations in biliary atresia did not correlate with the serum bilirubin, s-GOT, s-GPT, anatomic type of the lesion or postoperative bile flow. From these observations, it would appear that the elevation of AFP in infantile cholestasis is unrelated to underlying diseases except in case of alpha 1-antitrypsin deficiency. Serum AFP concentrations in neonates with physiological jaundice, were seldom elevated, and showed a good correlation with serum levels of total bilirubin. Possible mechanisms causing this elevation of AFP may be different from those involved in infantile cholestasis.
...
PMID:Alpha-fetoprotein in infantile obstructive jaundice in comparison with the normal ranges. 616 59

Thirteen breast-fed one-month-old infants with prolonged jaundice not due to known causes were included in this study. All infants were investigated at one and twelve months of age. Serum concentrations of total (TB) and conjugated bilirubin (CB), aspartate (ASAT) and alanine aminotransferase (ALAT), alkaline phosphatase (AP), alpha-1-antitrypsin (alpha-1-AT), alpha-1-fetoprotein (AFP) and the two primary bile acids; cholic (CA) and chenodeoxycholic acid (CDCA) were determined at both ages. The Pi-phenotype of alpha-1-AT was determined at the age of twelve months. The serum concentrations of TB, CB, AP and AFP were elevated at the age of one month but were normal at the age of twelve months. No changes in the serum concentrations of ASAT or ALAT were observed between one and twelve months of age, and the values were within the reference ranges. The serum concentrations of alpha-1-AT were within the reference range at both ages. Two infants were heterozygous for MZ, and they had normal serum alpha-1-AT concentrations. The serum concentrations of CA and CDCA were elevated at the age of one month and were still significantly elevated at the age of twelve months indicating that the infants had slight cholestasis at the age of one month, and that the cholestasis had largely subsided by the end of the first year of life.
...
PMID:Cholic acid, chenodeoxycholic acid, alpha-1-fetoprotein and alpha-1-antitrypsin serum concentrations in breast-fed infants with prolonged jaundice. 617 51

To evaluate the potential role of taurine deficiency in the pathogenesis of parenteral nutrition-induced cholestasis, 20 premature (less than 34 weeks AGA) infants were randomized to receive parenteral nutrition with and without taurine (10.8 mg/kg/day) during the first 10 days of life. Birth weight, gestational age, and protein and caloric intake were similar in both groups. Plasma taurine levels and hepatic function were assessed before the study began (3 +/- 1 days of age), at 5 +/- 1 days of age, and at 9 +/- 1 days of age. Although plasma taurine levels were significantly greater at 5 +/- 1 and 9 +/- 1 days of age (p = 0.009) in the group receiving supplementation, no differential effect on hepatocellular function could be detected during this short period of time. A decrease in plasma ammonia (p = 0.001), alanine aminotransferase (ALT) (p = 0.036), gamma-glutamyltranspeptidase (GGTP) (p = 0.05), 5'-nucleotidase (5'N) (p = 0.001), and bile salt concentrations was noted in both groups, indicating the rapid maturation of hepatic function even in the presence of parenteral nutrition during the first 10 days of life.
...
PMID:Effect of taurine supplementation on hepatic function during short-term parenteral nutrition in the premature infant. 642 96

The gamma-GT/ASAT (aspartate aminotransferase) and gamma-GT/ALAT (alanine aminotransferase) ratios were examined in 6 children with neonatal hepatitis (NH), 14 children with extrahepatic biliary atresia (EHBA), and 8 children with intrahepatic cholestasis (IHC) (of which 3 with the Aagenaes syndrome). A ratio above 1 is suggestive of EHBA. Both ratios differentiate very well between NH and EHBA, but there is considerable overlap in the enzyme ratios between the EHBA and the IHC groups. Gamma-GT/transaminase ratios may prove to be a useful indicator in the diagnostic work-up of children with liver and biliary tract disease, allowing for early surgery in patients with EHBA, and with a low risk of subjecting NH patients to unnecessary surgery. In our cases the gamma-GT/ALAT ratio separated better between EHBA and IHC than the gamma-GT/ASAT ratio. Furthermore, the case histories made EHBA seem unlikely in two out of three IHC patients with a gamma-GT/ALAT ratio above 1.
...
PMID:Liver enzyme ratios in neonatal liver disease. 652 89

Bile duct obstruction was induced in 6 cats by surgical ligation and transection of the common bile duct. Clinical and laboratory changes were monitored weekly for 25 to 54 days. Clinical signs of obstruction were similar in all cats and included anorexia, pyrexia, lethargy, intermittent vomiting, weight loss, palpable gallbladder, hepatomegaly, and bleeding tendencies. Tissue jaundice and acholic feces were evident grossly as early as postsurgical day (PSD) 4 with a mean onset of jaundice at PSD 5.3 +/- 0.4. Hematologic changes were initially characterized by a mild neutrophilic leukocytosis that increased with the chronicity of bile duct obstruction. Regenerative anemia developed in 4 cats associated with gastrointestinal blood loss. Acute serum biochemical changes were characterized by a marked increase in the mean values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and copper. Comparatively, only moderate increases in mean serum alkaline phosphatase activity were observed. Mean total bilirubin values increased remarkably at postsurgical week (PSW) 1, reaching a maximal value of 23.1 +/- 4.4 mg/dl at PSW 3 with 71.6 +/- 2.7% direct bilirubin. With chronicity of bile duct obstruction ranging from PSW 3 to PSW 7, the mean serum values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, serum alkaline phosphatase, and total and direct bilirubin stabilized and then declined, whereas the increased mean serum copper values persisted. At PSD 25 to 54, hepatic copper values and serum bile acids were markedly increased. Seemingly, clinicopathologic changes of induced cholestatic hepatic injury depended largely on the duration of biliary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Hematologic and biochemical abnormalities associated with induced extrahepatic bile duct obstruction in the cat. 663 41

Effectiveness of surgically induced acute hepatic failure in pig and most suitable time to apply artificial support in hepatic coma are evaluated in this work. Five male pigs weighing about 30-35 kg are employed. Latero-lateral porto-caval shunt was performed; the vascular disconnection of liver was obtained by ligature of blood vessels. Ligature was also placed on main biliary way after cholecistectomy. Blood samples were obtained (at 0, 1, 2, 6, 12, 18, 24 hours) to essay serum bilirubin, alkaline phosphatase and GOT-GPT levels as index of cholestasis and necrosis. Porto-caval encephalopathy was evaluated by means of serum ammonium levels, aminoacid pattern and E.E.G. Serum aminoacid pattern was carefully determined; its changes were found similar in man during coma. All pigs died 24-36 hours after surgery with liver ischemic and necrosis. Clinical and laboratory data obtained in experimental conditions were found similar to picture of acute hepatic failure in man, confirming validity of our model.
...
PMID:[Acute experimental hepatic insufficiency in pigs. Validity of a model with biohumoral and electroencephalographic monitoring]. 667 5

Concurrent treatments of cobalt chloride (CoCl2) and phenobarbital (PB), alone or in combination with lithocholic acid (LCA), were administered to rats for 7 days to assess whether or not a hypoactive hypertrophic smooth endoplasmic reticulum (HHSER) could be induced, as well as investigating the potential role of HHSER in the pathogenesis of cholestasis. LCA given alone slightly reduced hepatic triglycerides, significantly elevated plasma triglycerides and decreased microsomal glucose-6-phosphatase (G6P-ase) activity. PB administered alone significantly increased hepatic phospholipids and microsomal protein, phospholipid and cytochrome P-450 contents, as well as microsomal aminopyrine-N-demethylase (APDM-ase) activity. Functional indicators of liver impairment were associated primarily with CoCl2 treatment, whether given alone or in combination with PB + LCA. These signs included significantly reduced hepatic triglycerides, and increased plasma triglycerides associated with enhanced release of hepatic VLDL-triglycerides, as well as significantly decreased microsomal G6P-ase activity and/or reduced APDM-ase activity and cytochrome P-450 content. Elevated plasma bilirubin levels, and aspartate and alanine aminotransferase activities were also evident with concurrent CoCl2 + PB + LCA treatments. Combined CoCl2 + PB treatments, with or without LCA, caused significant increases in microsomal protein and phospholipid, and decreased activity of the rough endoplasmic reticulum (RER) marker G6P-ase, but no changes in cytochrome P-450 levels and no marked alterations in the activity of the SER marker APDM-ase. The data indicated that simultaneous CoCl2 and PB treatments, whether given alone or in combination with LCA, caused a functional impairment of the RER, and did not induce HHSER membranes.
...
PMID:Functional responses of the rat hepatic endoplasmic reticulum to treatment proposed as a model for cholestasis. 668 66

Hepatic dysfunction associated with parenteral nutrition (PN) is a well recognized occurrence. In order to define the temporal inter-relationships of direct bilirubin to other laboratory parameters, total and direct bilirubin, serum glutamic-pyruvic transaminase (SGPT), serum glutamic-oxaloacetic transaminase (SGOT), and alkaline phosphatase were measured prior to beginning PN and then weekly throughout the duration of PN in 60 consecutive neonates. Cholestatic jaundice (ChJ), defined as a direct bilirubin greater than or equal to 2.0 mg/dl, developed in 11 (33%) of 33 infants receiving PN for at least 2 weeks. Direct bilirubin was the most sensitive and earliest indicator of ChJ. SGOT and SGPT values in the ChJ group were not statistically different from the non-ChJ group until 2 weeks after the onset of cholestasis. Although there was a progressive increase in alkaline phosphatase during the course of PN, the increase was not greater in the ChJ group. In summary, direct bilirubin is the only laboratory indicator of hepatic status that need be determined serially in parenterally alimented infants. Although SGPT and SGOT may be helpful in characterizing hepatic dysfunction once ChJ has occurred, alkaline phosphatase levels do not reliably assess PN-associated liver injury.
...
PMID:Laboratory monitoring of parenteral nutrition-associated hepatic dysfunction in infants. 678 77


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---