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)

Seven men and three women (mean age, 31.2 years; range, 20-45 years) received a strictly controlled regular diet during a 2-week control period, followed by the regular diet supplemented with daily consumption of 1.2 g/kg body weight honey dissolved in 250 ml of water during a 2-week test period. At the end of each period, overnight fasting blood samples were withdrawn for assays of blood glucose, blood minerals, vitamin C, beta-carotene, uric acid, glutathione reductase, immunoglobulin E, hemoglobin, blood indices and cells, serum ferritin, serum iron, and iron-binding capacity. Results showed that honey increased antioxidant agents. It increased blood vitamin C concentration by 47%, beta-carotene by 3%, uric acid by 12%, and glutathione reductase by 7%. Honey increased serum iron by 20% and decreased plasma ferritin by 11%. It increased the percentage of monocytes by 50%, and increased lymphocyte and eosinophil percentages slightly. Honey reduced serum immunoglobulin E by 34% and increased serum copper by 33%. It decreased aspartate transaminase by 22% and alanine transaminase by 18%. Honey markedly reduced lactic acid dehydrogenase by 41%, decreased creatinine kinase by 33%, and reduced fasting blood sugar by 5%. It caused slight elevations in blood zinc and magnesium, hemoglobin, and packed cell volume. It may be concluded that honey increased antioxidant agents, serum iron and blood indices, and trace elements and decreased immunoglobulin E, liver and muscle enzymes, and fasting blood sugar in healthy subjects.
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PMID:Effects of daily consumption of honey solution on hematological indices and blood levels of minerals and enzymes in normal individuals. 1293 25

Non-A-E hepatitis and acute cryptogenic hepatitis are the names given to the disease of patients with clinical hepatitis, but in whom serologic evidence of A-E hepatitis has not been found. Over a period of 8 years, we evaluated in Brazil 32 patients who fulfilled the criteria for this diagnosis in order to determine patterns of the clinical illness, laboratory parameters, or histologic features. Each patient was subjected to virologic tests to exclude A-E hepatitis and cytomegalovirus/Epstein-Barr virus infection. Drug-induced hepatitis and autoimmune disease were also excluded. Wilson's disease was excluded in young patients. The course of the disease was clinical/biochemical recovery in 3 months in 25 patients and persistent alanine aminotransferase (ALT) elevation in 7 patients. Three of these had chronic hepatitis, and one had severe fibrosis on liver biopsy. During the acute illness, mean peak ALT was 1267 IU/L, bilirubin was 4.0 mg/dL, and ferritin was 1393 IU/mL. GB virus type C (GBV-C) was found in six patients, and TT virus (TTV) in five patients. We conclude that, in Brazil, non-A-E hepatitis probably originates from still unidentified viruses. The course of the disease and the histologic patterns are similar to those recorded for known viruses. Continuous survey for the specific etiologic agents is needed.
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PMID:Clinical, histologic and serologic evaluation of patients with acute non-A-E hepatitis in north-eastern Brazil: is it an infectious disease? 1456 27

Ferritin is an indispensable parameter in the diagnosis of latent iron deficiency anemia or siderosis. In this study, we evaluated the utility of a reagent for ferritin measurement in a latex agglutination (LA) test, using general chemistry analyzers. The intraassay coefficient of variation (CV) was 0.8-3.4% and the interassay CV was 0.0-0.7%. Linearity was observed up to 1100 ng/mL. The effective sensitivity value was 4.0 ng/mL. In addition, good results were obtained with the prozone test, the effects of interferences, correlation with the enzyme immunoassay (EIA) method, and functional assay sensitivity. A significant positive correlation with C-reactive protein (r=0.586, P<0.001) was found. When compared with liver-related biochemical parameters (asparate aminotransferase (AST) and alanine aminotransferase (ALT)) in patients with impaired liver function, ferritin varied in parallel with the liver-related parameters. This assay system was able to measure ferritin accurately over a wide range, and thus could be used to diagnose cancer, siderosis, and iron deficiency anemia. The LA assay system can be employed for measurement with general chemistry analyzers, with rapid and convenient execution. In addition, the LA test allows the simultaneous measurement of other markers of iron deficiency anemia, so clinicians can rapidly obtain examination results.
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PMID:Latex agglutination test for ferritin measurement. 1461 45

Hepatitis C virus (HCV) infection is a common cause of liver disease in thalassemia major patients in Western, especially Mediterranean, countries. Its significance in thalassemic patients from Southeast Asia has not been critically evaluated. In this report, we describe our study of the prevalence of HCV infection among Thai patients with thalassemia. The relationships of the infection to blood transfusion and the infection's effects on liver function have also been determined. Of the 104 patients studied, 21 (20.2%) tested positively by enzyme immunoassay for anti-HCV antibody, whereas only 2 patients (2%) had the hepatitis B surface antigen. There was no significant relationship between the presence of anti-HCV antibodies and the number and frequency of blood transfusions. In fact, 2 patients (10%) who tested positive for anti-HCV antibodies had never received transfusions. Patients with anti-HCV antibodies had significantly abnormal liver functions, such as higher levels of serum aspartate aminotransferase (SGOT) and alanine aminotransferase (SGPT) and lower levels of serum albumin, compared with patients without anti-HCV antibodies (P = .021, .017, and .004, respectively). However, there were also significant correlations between iron status as indicated by transferrin saturation or serum ferritin levels and SGOT, SGPT, and gamma-glutamyltransferase (GGT) levels. Moreover, abnormal liver function as represented by elevated levels of SGOT, SGPT, GGT, and serum alkaline phosphatase was observed more frequently in patients with iron overload than in patients with a lower degree of iron burden. The presence of HCV did not alter the effects of iron overload on liver function. The findings suggest that both HCV and iron overload are the main causes of abnormal liver function in Thai patients with thalassemia. The treatment of both problems, if coexisting in patients with thalassemia, is required to prevent progression to chronic liver disease.
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PMID:Prevalence and clinical significance of hepatitis C virus infection in Thai patients with thalassemia. 1468 98

The mechanism(s) determining the progression from fatty liver to steatohepatitis is currently unknown. Our goal was to define the relative impact of iron overload, genetic mutations of HFE, and insulin resistance on the severity of liver fibrosis in a population of subjects with nonalcoholic fatty liver disease (NAFLD) who had low prevalence of obesity and no overt symptoms of diabetes. In a cohort of 263 prospectively enrolled patients with NAFLD, 7.4% of patients had signs of peripheral iron overload and 9% had signs of hepatic iron overload, but 21.1% had hyperferritinemia. The prevalence of C282Y and H63D HFE mutations was similar to the general population and mutations were not associated with iron overload. Although subjects were on average only moderately overweight, insulin sensitivity, measured both in the fasting state and in response to oral glucose, was lower. Univariate analysis demonstrated that the presence of severe fibrosis was independently associated with older age, female sex, overweight, aspartate/alanine aminotransferase ratio, serum ferritin level, fasting glucose and insulin levels, decreased insulin sensitivity, and with histologic features (degree of necroinflammation and steatosis). After adjustment for body mass index (BMI), age, sex, and degree of steatosis, ferritin levels (odds ratio [OR] = 1.77; 95% CI = 1.21- 2.58; P =.0032) and the oral glucose insulin sensitivity (OR = 0.53; CI = 0.33-0.87; P =.0113) were independent predictors of severe fibrosis. In conclusion, the current study indicates that insulin resistance is a major, independent risk factor for advanced fibrosis in patients with NAFLD. Increased ferritin levels are markers of severe histologic damage, but not of iron overload. Iron burden and HFE mutations do not contribute significantly to hepatic fibrosis in the majority of patients with NAFLD.
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PMID:Relative contribution of iron burden, HFE mutations, and insulin resistance to fibrosis in nonalcoholic fatty liver. 1518 21

Hepatitis C virus (HCV) infection is common in patients with end-stage renal disease. The severity of liver damage, including fibrosis, in these cases varies widely. Although many investigators have searched for noninvasive alternatives to liver biopsy for evaluating the extent of liver fibrosis, no useful noninvasive predictors have been found. Currently, liver biopsy is essential to assess the degree of fibrosis. The aim of this retrospective study was to investigate a range of clinical and laboratory parameters in HCV-infected hemodialysis (HD) patients and identify possible predictors of fibrosis. Ninety-five consecutive HD patients with HCV infection underwent liver biopsy. Each specimen was evaluated for fibrosis stage. Correlations were sought between the degree of fibrosis and the age, HD duration, time since first possible HCV exposure, body mass index, HCV RNA titer, serum ferritin level, and serum alanine aminotransferase (ALT) level. The analysis revealed no significant correlations between fibrosis stage and the parameters investigated (mean age: r =.017, P =.89; mean HD duration: r =.066, P =.576; body mass index r =.231, P =.152; HCV RNA titer: r =.015, P =.091; serum ferritin: r =.134, P =.32; serum ALT r =.108, P =.927). Links with serum ALT were reevaluated with upper normal levels arbitrarily set at 30 IU/L and 20 IU/L, but these analyses also revealed no correlations between fibrosis stage and ALT level (P =.98 and P =.449, respectively). Therefore liver biopsy is still essential for accurate assessment of liver pathology in HD patients with HCV.
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PMID:Investigation of possible clinical and laboratory predictors of liver fibrosis in hemodialysis patients infected with hepatitis C virus. 1501 98

The coherence of carbohydrate-deficient transferrin (CDT) as a biomarker of alcohol abuse was investigated with 15 conventional laboratory parameters, with the self-reported medical history and with clinical findings, all previously reported to be associated with chronic alcohol intake. In total, 100 male persons who were at least suspected of abusing alcohol were assessed. Medical history, clinical picture and physical examination were taken, and laboratory parameters regarding blood count, liver enzymes, serum lipids, iron balance, Ig A and uric acid were determined. These data were correlated with the CDT values, the daily ethanol intakes reported, and several findings from medical history and clinical examination. The mean CDT level (mean+/-S.D.) of the entire group was 29.4+/-19.7 U/l. Eighty-one patients admitted a daily ethanol intake of 60 g or more. The ratio AST/ALT (de Ritis ratio) appeared as the best conventional parameter correlated with both CDT and ethanol intake. Mean corpuscular volume (MCV), serum iron, AST and red blood cell count also correlated significantly with CDT. CDT, AST and ferritin correlated significantly with the reported daily ethanol intake. It is concluded that CDT provides a reliable estimate of long-term alcohol intake.
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PMID:Carbohydrate-deficient transferrin (CDT) as a biomarker in persons suspected of alcohol abuse. 1517 58

Deferiprone (DFO) at the standard daily dose of 75 mg/kg was given to 13 transfusion-dependent patients with thalassemia in whom conventional desferrioxamine (DFX) therapy had proven ineffective and caused adverse side effects. In six patients, serum ferritin and alanine aminotransferase levels decreased significantly and urinary iron excretion increased. In seven patients in whom DFO administration alone was ineffectual, DFX was added at a daily dose of 40 to 50 mg/kg given subcutaneously for 7 to 10 days following transfusion. All patients exhibited a significant decrease in serum ferritin levels and an increase in urinary iron excretion, with alanine aminotransferase levels decreased in four patients. The combined DFX and DFO therapy could represent an effective alternative to conventional DFX therapy not only in nonresponding patients with thalassemia but also, by lowering to less than 25% the DFX dosage, in patients who exhibit important DFX-related side effects.
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PMID:Combined therapy with desferrioxamine and deferiprone: a new protocol for iron chelation in thalassemia. 1521 22

Although cardiac complications remain the main causes of death in thalassemic patients, right heart dysfunction has been little studied and the mechanism is still unclear. Echocardiography was performed in 39 patients with beta-thalassemia major and 35 aged-matched controls. The gender, age, heart rate, blood pressure, left ventricular ejection fraction (LVEF), acceleration time (AcT) of right ventricular outflow and right ventricular ejection time (RVET), AcT/RVET, and the presence of tricuspid regurgitation (TR) were compared between the two groups. We also compared the gender, age, age at first blood transfusion, serum ferritin level, alanine aminotransferase (ALT), the presence of antibodies to hepatitis C virus, liver fibrosis, splenectomy, platelet counts, diabetes mellitus, arrhythmia, cardiomegaly, LVEF, AcT, RVET, AcT/RVET, and signal intensity ratio (SIR) of myocardial magnetic resonance imaging (MRI) between thalassemic patients with and without TR. The incidence of TR in thalassemic patients was significantly higher than that in the control group (30.8 vs 11.4%, p=0.03). The incidences of splenectomy (p=0.03), platelet counts (p=0.01), and SIR of myocardial MRI (p=0.03) in thalassemic patients with TR were significantly higher than in those without TR. The AcT was shorter and the AcT/RVET ratio was smaller, suggesting higher pulmonary pressure in the thalassemic patients with TR. Occurrence of TR in patients with beta-thalassemia major may be a consequence of cardiac iron deposit, thrombocytosis, splenectomy, or pulmonary hypertension.
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PMID:Tricuspid regurgitation in patients with beta-thalassemia major. 1544 31

Twelve thalassaemia major patients have been given deferiprone 75 mg/kg body weight daily as iron chelation therapy for 5 years. Their ages ranged from 18 to 34 years (mean 24.2) at the end of the study. Two patients were hepatitis C virus (HCV) mRNA positive and a further 5 were positive for HCV antibody. The mean serum ferritin level fell significantly from 4,302 +/- 2,245 microg/l SD at baseline to 3,032 +/- 1,155 microg/l at 2 years (p = 0.037) and 2,229 +/- 1,070 microg/l (p = 0.007) at 5 years. At the end of the study, liver iron ranged from 3.59 to 23.7 mg/g dry weight (mean 11.9 +/- 5.4), 3 patients having levels >15 mg/g. There was no significant change in serum AST levels, but ALT levels fell significantly at 2 years (p = 0.019) and 5 years (p = 0.001). Liver biopsy at the end of the study showed no evidence of hepatic fibrosis caused by deferiprone. Cardiac studies showed no overall change in left ventricular ejection fraction but a significant improvement in isovolumic relaxation time (p = 0.045). We conclude that in this albeit small group of thalassaemia major patients, deferiprone was a safe long-term method of iron chelation. In a minority, higher doses of deferiprone or a combination with desferrioxamine would be needed to lower liver iron below 15 mg/g.
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PMID:Five-year trial of deferiprone chelation therapy in thalassaemia major patients. 1556 27


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