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)

Serum total lipids, lipoprotein cholesterol, apolipoprotein A (Apo A), and liver function tests have been investigated in patients with acute viral hepatitis and chronic liver disease. Hypertriglyceridaemia, absence of alpha and pre beta bands on the lipoprotein electrophoresis pattern, low level of Apo A, and presence of abnormal lipoproteins (beta-VLDL and beta2-LP) were observed in the early phase of acute hepatitis. A positive correlation was found between Apo A and high-density lipoprotein cholesterol, and a negative one between Apo A and triglyceride, bile acids, total bilirubin, and serum alanine aminotransferase. Lipoprotein abnormalities found in the early phase of acute hepatitis are probably due to low lecithin-cholesterol acyltransferase activity. The reappearance of alpha lipoprotein and the increase of Apo A are sensitive indices of improvement of liver function. In chronic liver disease low levels of cholesterol and Apo A indicate the severity of liver cell injury.
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PMID:Serum total lipids, lipoprotein cholesterol, and apolipoprotein A in acute viral hepatitis and chronic liver disease. 69 Feb 42

The authors administered lovastatin (Mevacor, MSD) to 18 patients with primary hyperlipoproteinaemia (familial and non-familial) with a lipoprotein pattern type IIa and IIb. During treatment a marked reduction of atherogenic indicators of the lipid metabolism occurred, i.e. a decline of total cholesterol (-28.6%), LDL-cholesterol -39%), apolipoprotein B (-18.6%), the index of total cholesterol/HDL-cholesterol (-44.6%) and the index LDL-cholesterol/HDL-cholesterol (-48.2%). At the same time a favourable effect on indicators of the lipid metabolism to which a protective action is ascribed was recorded: a rise of HDL-cholesterol (+13.6%) and apolipoprotein AI (+13%) and AII (+13%). An excellent effect was observed also in four heterozygotes with familial hypercholesterolaemia which is usually rather resistant to other types of hypolipidaemic treatment. The drug was very well tolerated and subjective side-effects of treatment were minimal. Despite the fact that a number of laboratory indicators was followed up, the authors did not observe any undesirable side-effects, only a transient and marginal rise of ALT in one patient. Lovastatin is, due to its potent hypolipidaemic effect, a new hope in the treatment of hypercholesterolaemia. Its usefulness in the prevention of ischaemic heart disease, as well as its safety during prolonged administration are tested at present in long-term investigations.
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PMID:[Personal experience with lovastatin, a HMG-CoA reductase inhibitor (Mevacor, MSD) in the treatment of hypercholesterolemia]. 184 44

This study compared the effects of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, fish oil, and placebo on plasma lipids and lipoproteins in patients with mixed hyperlipidemia. After an initial run-in phase, 32 patients were randomized for 6 weeks to either (1) pravastatin 40 mg/d, n = 10; (2) fish oil (himega 6 g/d, equivalent to 3 g omega-3 fatty acids/d), n = 10; or (3) placebo. After single drug therapy, in the pravastatin group mean total plasma cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (apo) B fell significantly by 23% (P < .001), 30% (p < .001), and 26% (P < .01), respectively. LDL Stokes' diameter did not change. In the fish oil group mean plasma triglycerides (TG) fell 30% (P < .05), LDL Stokes' diameter increased from 25.0 to 25.9 nm (P < .05), and there was a nonsignificant increase in LDL-C. There were no changes in the placebo group. To assess the effect of the combination of pravastatin plus fish oil therapy, all patients, except one woman from the placebo group who developed nausea on fish oil, then took combined therapy of pravastatin 40 mg/d plus fish oil 6 g/d for an additional 12 weeks. In each case, there were no clinically significant episodes of muscle tenderness or elevation of creatine phosphokinase or alanine aminotransferase. After 12 weeks of combined therapy of pravastatin plus fish oil, there were significant reductions in the mean TC, TG, LDL-C, and apoB in the three groups compared with baseline levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of pravastatin and omega-3 fatty acids on plasma lipids and lipoproteins in patients with combined hyperlipidemia. 824 Oct 95

Persistent nephrotic syndrome is frequently accompanied by severe hyperlipidemia, and this may pose a substantial risk for cardiovascular disease. Lipid-lowering drugs are prescribed by many nephrologists for adult patients but rarely for nephrotic children. The present investigation was designed to evaluate the safety and efficacy of gemfibrozil in nephrotic children. Eight girls and four boys aged from 5 to 17 years were enrolled in this study. They were all steroid and immunosuppressive resistant patients with nephrotic range proteinuria. Placebo was administered to five patients and gemfibrozil was administered to seven patients for four months. Blood samples were taken for the determination of cholesterol, triglyceride, low-density lipoprotein (LDL), high-density lipoprotein (HDL), BUN, serum creatinine (Scr), ALT, AST, CPK, apolipoprotein A (apo A), apoliporotein B (apo B), and serum albumin levels during the initial and subsequent examinations. At the end of the fourth month, gemfibrozil reduced total cholesterol by 34%, LDL by 30%, apo B by 21% and triglycerides by 53% (p < 0.05). HDL cholesterol and apo A levels were not significantly altered. Renal function and urine protein excretion were not affected by gemfibrozil. In this study gemfibrozil therapy had no side effects and had favorable effects on the lipoprotein profile of nephrotic patients.
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PMID:The effects of gemfibrozil on hyperlipidemia in children with persistent nephrotic syndrome. 1185 78

Familial hypobetalipoproteinemia (FHBL) is a rare codominant disorder of lipoprotein metabolism characterized by low levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B. Heterozygotes for FHBL have less-than-half normal LDL-cholesterol and apoB concentrations, whereas homozygotes have extremely low or undetectable LDL-cholesterol and apoB levels. These reductions in LDL-cholesterol and apoB have been suggested to provide FHBL subjects with resistance to atherosclerosis. FHBL can be caused by mutations in the APOB gene on chromosome 2. We present four novel mutations and one previously described mutation in APOB causing FHBL in five families. Immunoblotting and DNA sequencing were used to characterize the novel mutation apoB-40.3 (c.5564_5565insC) and the previously reported mutation apoB-80.5 (c.11040T>G). The apoB-6.9 (c.1018_1025del) and apoB-25.8 (c.3600T>A) mutations were identified by DNA sequence analysis, as variants shorter than apoB-31 are not detectable in plasma. A fifth mutation, the splice variant c.82+1G>A, was identified by sequencing and was found in a homozygous subject. In approximately 50% of the FHBL subjects, plasma alanine aminotransferase concentrations were mildly increased, suggestive of fatty liver. All affected FHBL subjects had low to low-normal serum vitamin E concentrations, highlighting the important and recognized relationship between lipid and vitamin E concentrations.
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PMID:Four novel mutations in APOB causing heterozygous and homozygous familial hypobetalipoproteinemia. 1287 64

Combinations of tests comprising alpha2-macroglobulin, haptoglobin, apolipoprotein Al, gamma-glutamyltransferase, total bilirubin (Fibrotest) and alanine aminotransferase (Actitest) are being developed as alternatives to liver biopsy in patients with chronic hepatitis C. The aim of this study was to assess in the same laboratory the impact of parameter assay variations on Fibrotest and Actitest results and intra-patient reproducibility of the two tests. The stability of the samples for each test was studied after storage at -80 degrees C and -20 degrees C. Within-run, between-run and total imprecision for each parameter assay, and for Fibrotest and Actitest results, were determined. Transferability of assay results between different analyzers was studied. Intra-patient reproducibility was assessed in 55 hospitalized patients. Fibrotest and Actitest reference ranges were determined in 300 blood donors (reference group). The stability of the parameters was affected by serum storage at -20 degrees C only. The impact of parameter analytical variability on Fibrotest and Actitest results was less than 10% and intra-patient reproducibility was acceptable (p > 0.05). The transferability between different analyzers of results of assays performed under the same standardized and calibration conditions was excellent. Fibrotest and Actitest reference ranges in blood donors were (mean+/-SE) 0.075+/-0.004 and 0.068+/-0.004, respectively. The low intra-laboratory and intra-patient variability in Fibrotest and Actitest results confirm Fibrotest and Actitest reliability.
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PMID:Intra-laboratory analytical variability of biochemical markers of fibrosis (Fibrotest) and activity (Actitest) and reference ranges in healthy blood donors. 1508 May 67

A 32-year-old man presented with increases in serum alanine aminotransferase activity, iron concentration, and transferrin saturation, suggestive of hepatic dysfunction and iron overload. In addition, he had unusually low plasma concentrations of LDL-cholesterol and apolipoprotein (apo) B. Hepatic ultrasonography was consistent with fatty liver. On liver biopsy, marked steatosis and moderate to marked iron deposition were observed. The patient was found to carry the HFE C282Y and H63D mutations, which are associated with hereditary hemochromatosis, and the alpha(1)-antitrypsin PiZ variant. An immunoblot of plasma for apoB showed the presence of a truncated apoB species, indicative of familial hypobetalipoproteinemia. DNA sequence analysis revealed that the patient was heterozygous for the apoB-80.5 (c.11040T>G) mutation. This unique case shows an unusual combination of underlying disorders that could all be contributing to liver dysfunction and fatty liver.
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PMID:Liver dysfunction and steatosis in familial hypobetalipoproteinemia. 1551 99

We conducted a study to assess the effect of phenobarbital, carbamazepine, and valproate on serum lipid profiles and lipoprotein (a) in 64 children with epilepsy (aged between 1 and 15 years) admitted to the child neurology outpatient clinic between July 2000 and July 2002. The children were separated as group 1 (18 children), treated with phenobarbital, 5 mg/kg/day; group 2 (22 children), treated with carbamazepine, 10 to 15 mg/kg/day; and group 3 (24 children), treated with sodium valproate, 20 mg/kg/day. Plasma lipoprotein (a), total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein A and apolipoprotein B levels, and liver enzymes alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyltransferase were determined before the initiation of the treatment and at 3, 6, and 12 months of the treatment period. The mean age of children in group 1 was significantly low compared with those in groups 2 and 3 (P <.05). The mean pretreatment lipid levels among the groups were not significantly increased. The mean lipoprotein (a) levels were significantly increased in all groups at 3, 6, and 12 months of the treatment period (P <.05). The increase in alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol at 3, 6, and 12 months was statistically significant in group 1 (P <.05). The higher levels in lipoprotein (a) (mean > 30 mg/dL) were observed only in carbamazepine-treated patients at 6 and 12 months. The percentage of children with lipoprotein (a) levels over 30 mg/dL was 44%, 63%, and 33% in the phenobarbital-, carbamazepine-, and valproate-treated children, respectively. Antiepileptic drugs significantly increase the level of lipoprotein (a), which is a major risk factor for atherosclerosis, and also have variable effects on other lipid parameters. Lipoprotein (a) levels should be closely followed in patients receiving antiepileptic drugs. (J Child Neurol 2006;21:70-74).
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PMID:Effect of antiepileptic drugs on plasma lipids, lipoprotein (a), and liver enzymes. 1655 57

The aim of this study was to evaluate the relationship between apolipoprotein E gene polymorphism and nonalcoholic fatty liver disease. The study group consisted of 237 nonalcoholic fatty liver disease patients who were detected by ultrasonography and 201 controls with ultrasonographically normal livers. DNA amplifications were performed by polymerase chain reaction technique and apolipoprotein E genotypes were evaluated after digestion with CfoI restriction enzyme. Serum levels of glucose, lipids, lipoproteins, and apolipoproteins were measured in all subjects. Additionally, viral hepatitis markers, liver enzymes, and body mass index were assessed. Patients were found to have significantly higher triglyceride, glucose, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase levels and lower high-density lipoprotein cholesterol and apolipoprotein (a) levels than controls (P<0.05). There were no statistically significant differences in genotypes and allele frequencies between all patients and controls. Comparing nonobese patients with controls, the frequencies of allele epsilon2 and genotype epsilon2epsilon3 were statistically significantly different in the controls (P=0.04 and P=0.01, respectively). In conclusion, occurrence of the epsilon2 allele and epsilon2epsilon3 genotype may be protective against development of nonalcoholic fatty liver disease.
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PMID:Apolipoprotein E gene polymorphism in nonalcoholic fatty liver disease. 1743 74

The effect of the anti-hypertensive drug eprosartan on metabolic parameters is currently not extensively documented. We evaluated the effect of eprosartan on parameters involved in atherogenesis, oxidative stress and clotting activity. This open-label unblinded intervention study included 40 adult patients with essential hypertension taking eprosartan. Eprosartan significantly reduced by 8% (p<0.001) the systolic and by 13% (p<.001) the diastolic blood pressure, and in-creased by 24% the time needed to produce oxidative by-products (p=0.001), a marker of oxidative stress. In contrast, ep-rosartan did not alter 8-isoprostane (8-epiPGF2a) levels, another marker of oxidative stress. Additionally, eprosartan re-duced by 14% aspartate aminotransferase and by 21% then alanine aminotransferase activity, while it had a neutral effect on the lipid profile and apolipoprotein levels and did not influence glucose homeostasis, creatinine and uric acid levels. Eprosartan did not affect the clotting/fibrinolytic status (estimated by plasminogen activator inhibitor 1, tissue plasmino-gen activator and a2 antiplasmin levels), or the enzymatic activity of the lipoprotein associated phospholipase A2 (Lp-PLA2) and paraoxonase 1 (PON1). In conclusion, eprosartan should be mainly considered as an anti-hypertensive agent with neutral effects on most of the metabolic parameters in hypertensive patients.
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PMID:Effects of eprosartan on serum metabolic parameters in patients with essential hypertension. 1894 87


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