Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of biphenyldimethyldicarboxylate (DDB), a synthetic compound, in use for the treatment of chronic hepatitis was studied on hepatic injury caused in rats by administration of carbon tetrachloride (CCl4). Starting at time of administration of the first dose of CCl4, rats received DDB at four dose levels (3, 15, 75 or 375 mg/kg), silymarin (22 mg/kg), a combination of DDB (75 mg/kg) and silymarin (22 mg/kg) or saline (control) once orally daily for 30 days. The administration of DDB in CCl4-treated rats at 75 or 375 mg/kg resulted in 61.2-76.2% decrease in alanine aminotransferase (ALT) and 46.9-60.8% decrease in aspartate aminotransferase (AST), respectively compared with the CCl4 control group. Silymarin treatment resulted in 34.6 and 30% decrease in ALT and AST, while DDB (75 mg/kg) combined with silymarin (22 mg/kg) resulted in 58.2 and 31% decrease in ALT and AST, respectively. Serum creatinine increased by 50% by DDB at 375 mg/kg. After treatment with DDB at 75 or 375 mg/kg or DDB combined with silymarin, the development of liver necrosis and fibrosis caused by CCl4 was markedly reduced, while after DDB combined with silymarin no DNA aneuploid cells could be observed. The decrease in glycogen and protein contents in hepatocytes caused by CCl4 was markedly prevented by co-treatment with DDB at 75 or 375 mg/kg or DDB combined with silymarin. It is concluded that in the model of hepatic injury caused by chronic administration of CCl4 in rats, the synthetic compound DDB, limits hepatocellular injury and exerts antifibrotic effect. Better improvement in protein, DNA, mucopolysaccharide content was seen after both DDB and silymarin compared to DDB alone. It is suggested, therefore, that DDB alone or in combination with silymarin might prove of benefit in the therapy of chronic liver disease. Monitoring of kidney functions in patients taking DDB is warranted.
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PMID:Effects of biphenyldimethyl-dicarboxylate administration alone or combined with silymarin in the CCL4 model of liver fibrosis in rats. 1772 39

Clinical manifestations of liver involvement in multiple myeloma (MM) are uncommon. Rare cases of MM present as acute liver disease. We report a case of a 55-year-old woman with MM who presented with painless jaundice, mild pruritus, and abnormal liver function tests resembling acute cholestatic hepatitis without the stigmata of chronic liver disease. Initial laboratories included elevated liver function tests (aspartate aminotransferase 74 U/L and alanine aminotransferase 45 U/L) and an elevated white blood cell count of 19,600 cells/microL with 33% circulating plasma cells. Myeloma parameters demonstrated an immunoglobulin G lambda monoclonal protein with lambda light-chain Bence-Jones proteinuria. Bone marrow was hypercellular with 70% plasmacytosis. A liver biopsy revealed a diffuse portal and sinusoidal infiltration of plasma cells with lambda light-chain restriction. In this report, we review the literature of liver involvement in MM.
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PMID:Liver involvement in multiple myeloma. 1802 72

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that manifests as pulmonary emphysema, liver cirrhosis and, rarely, as the skin disease panniculitis, and is characterized by low serum levels of AAT, the main protease inhibitor (PI) in human serum. The prevalence in Western Europe and in the USA is estimated at approximately 1 in 2,500 and 1 : 5,000 newborns, and is highly dependent on the Scandinavian descent within the population. The most common deficiency alleles in North Europe are PI Z and PI S, and the majority of individuals with severe AATD are PI type ZZ. The clinical manifestations may widely vary between patients, ranging from asymptomatic in some to fatal liver or lung disease in others. Type ZZ and SZ AATD are risk factors for the development of respiratory symptoms (dyspnoea, coughing), early onset emphysema, and airflow obstruction early in adult life. Environmental factors such as cigarette smoking, and dust exposure are additional risk factors and have been linked to an accelerated progression of this condition. Type ZZ AATD may also lead to the development of acute or chronic liver disease in childhood or adulthood: prolonged jaundice after birth with conjugated hyperbilirubinemia and abnormal liver enzymes are characteristic clinical signs. Cirrhotic liver failure may occur around age 50. In very rare cases, necrotizing panniculitis and secondary vasculitis may occur. AATD is caused by mutations in the SERPINA1 gene encoding AAT, and is inherited as an autosomal recessive trait. The diagnosis can be established by detection of low serum levels of AAT and isoelectric focusing. Differential diagnoses should exclude bleeding disorders or jaundice, viral infection, hemochromatosis, Wilson's disease and autoimmune hepatitis. For treatment of lung disease, intravenous alpha-1-antitrypsin augmentation therapy, annual flu vaccination and a pneumococcal vaccine every 5 years are recommended. Relief of breathlessness may be obtained with long-acting bronchodilators and inhaled corticosteroids. The end-stage liver and lung disease can be treated by organ transplantation. In AATD patients with cirrhosis, prognosis is generally grave.
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PMID:Hereditary alpha-1-antitrypsin deficiency and its clinical consequences. 1856 11

Ganciclovir treatment in children with cytomegalovirus (CMV) infection is still controversial and only indicated in selected cases. The aim of thi study was to evaluate clinical and demographic features of CMV hepatitis in immunocompetent children and to determine the effect of ganciclovir treatment in these patients retrospectively. The study was carried out in a group o 29 children with CMV hepatitis. All the patients were investigated for signs of infection, inborn errors of metabolism, genetic diseases, extrahepatic biliary atresia and other causes of hepatitis. Two patients with congenital CMV infection and two patients with biliary atresia were excluded from the study group. The patients included in the study were divided into two groups: non-cholestatic hepatitis (n=16) as Group I and cholestatic hepatitis (n=9) as Group II. Four (25%) patients in the non-cholestatic group and four (44.4 in the cholestatic group were treated with ganciclovir for a median of 21 days. The mean age was 9.6+/- 10.9 months (median age 6 months) in Group I, while cholestatic hepatitis patients in Group II were significantly younger, with a mean age of 2.7+/-0.9 months (p<0.01). The most prominent symptoms at admission were diarrhea and vomiting (25%) in Group I. In Group I, all cases (100%) and in Group II, three of four cases (75%) treated with ganciclovir had recovery from acute CMV hepatitis. In the non-cholestatic group, no relapses were observed while one patient in the cholestatic group relapsed and progressed into chronic liver disease. Patients who received supportive treatment showed a marked decrease in GGT, ALT, AST and bilirubin levels spontaneously and no relapses of hepatitis were observed in at least one year of follow-up. Although ganciclovir therapy is not indicated particularly in immunocompetent cases, since most were self-limited infections, in case of progressive and persistent hepatitis, such as in our cases, ganciclovir was a treatment option; no side effect due to ganciclovir therapy was observed in our cases. Although ganciclovir seems to be effective in progressive CMV hepatitis, multicenter randomized studies in a large study group are necessar to determine the efficacy and indications for ganciclovir treatment.
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PMID:Cytomegalovirus hepatitis and ganciclovir treatment in immunocompetent children. 1877 67

A 66-year-old female presented with acute illness of severe hepatic dysfunction. She had a past history of chronic hepatitis of low disease activity. After admission and clinical investigation including liver biopsy, it showed an underlying chronic liver disease suggestive of autoimmune hepatitis (AIH) with early liver cirrhosis. Together with other clinical features, this patient was diagnosed as definite AIH type 1 by using the IAIHG (International Autoimmune Hepatitis Group) criteria. During this episode, superinfection by Epstein-Barr virus (EBV) was evidenced by positive PCR (polymerase chain reaction) test, and serial changes of EBV VCA IgM and IgG tests. Severe hepatic impairment was evidenced by markedly elevated AST level 3090 IU/L, high bilirubin level 26.4 mg/dL, and presence of ascites. The patient gradually recovered and liver function improved in agreement with the decline of EBV VCA titers. Immunosuppressive therapy resulted in further improvement of the aminotransferases levels. This is an unusual case of EBV superinfection on pre-existing AIH with early cirrhosis, which caused enhancement of the autoimmune disease process and resulted in severe hepatic decompensation and jaundice. We herein describe the case and briefly review the literature.
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PMID:Chronic autoimmune hepatitis with Epstein-Barr virus superinfection: a case report and review of literature. 1910 93

To optimize management of chronic liver disease (CLD), a simple and noninvasive test to determine oesophageal varices (EV) and liver fibrosis is necessary. We performed a cohort study in a single tertiary care centre in order to devise a simple index reflecting EV and liver fibrosis. We derived an index reflecting EV which resulted from portal hypertension (the first part) and evaluated the index's ability to detect liver fibrosis which resulted in portal hypertension (the second part). Five hundred fifty-six patients (the first part, n = 409, mean age = 55.4 years, EV prevalence = 34.0%; the second part, n = 147, mean age = 48.8 years, cirrhosis prevalence = 12.9%) with virus-related CLD were included. P2/MS [(platelet count [10(9)/L])(2)/(monocyte fraction [%] x segmented neutrophil fraction [%])] was derived to detect EV. The area under the receiver-operating characteristic curve (AUROC) of P2/MS was 0.916 (95% confidence interval, 0.879-0.954) for detecting EV, and 0.905 (0.862-0.947) for detecting high-risk EV (grade >or= II or with red colour signs). P2/MS had AUROCs of 0.952 (0.904-0.999) and 0.873 (0.792-0.955) for histological cirrhosis (METAVIR F4) and significant fibrosis (METAVIR F2-F4), respectively, which were significantly greater than those of AST-to-platelet count ratio index (0.658, P < 0.001; 0.644, P = 0.003) and FIB-4 (0.776, P = 0.031; 0.707, P = 0.026). The predictive values of P2/MS were maintained at similar accuracy in subsequent validation sets. Our study suggests that P2/MS comprising only the complete blood count results is an efficient and noninvasive marker reflecting the presence of EV and the grade of liver fibrosis in patients with virus-related CLD. An independent external validation of P2/MS is required.
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PMID:Complete blood count reflects the degree of oesophageal varices and liver fibrosis in virus-related chronic liver disease patients. 1920 Jan 33

Hepatitis B virus (HBV) and hepatitis C virus (HCV) often cause chronic liver disease. We hypothesized that environmental factors adversely impact the liver function in workers with these types of hepatitis. We used liver function tests including aspartate aminotransferase, alanine aminotransferase, and g -glutamyltransferase to evaluate whether hazardous work conditions increase the incidence of chronic liver disease among HBV and HCV infected workers. Organic solvent, night work, visual display terminals, dust, lead, vibrations, and ionizing radiation all led to increased impairment of liver function in patients with hepatitis as compared to the control group that were not exposed to such agents. Therefore, hazardous working conditions have to be carefully considered in the progress of chronic liver disease in workers infected with HBV and HCV.
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PMID:Hazardous environmental factors enhance impairment of liver function in HBV and HCV hepatitis. 1927 35

Combinations of noninvasive markers may improve discrimination of chronic liver disease severity. The aims of this study were to compare four validated serum and ultrasound-based markers of hepatic disease severity head-to-head with liver biopsy and to assess optimal combinations with consideration of cost. A total of 67 patients with biopsy-proven chronic hepatitis C underwent all four techniques on the same visit [aspartate aminotransferase (AST) to platelet ratio index (APRI); Enhanced Liver Fibrosis (ELF) panel; transient elastography (TE) and ultrasound microbubble hepatic transit times (HTT)]. Markers were combined according to increasing financial cost and ordinal regression used to determine contributions. APRI, ELF, TE and HTT predicted cirrhosis with diagnostic accuracy of 86%, 91%, 90% and 83% respectively. ELF and TE were the most reliable tests with an intra-class correlation of 0.94 each. Either ELF or TE significantly enhanced the prediction of fibrosis stage when combined with APRI, but when combined together, did not improve the model further. Addition of third or fourth markers did not significantly improve prediction of fibrosis. Combination of APRI with either ELF or TE effectively predicts fibrosis stage, but combinations of three or more tests lead to redundancy of information and increased cost.
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PMID:Optimal combinations of ultrasound-based and serum markers of disease severity in patients with chronic hepatitis C. 1980 1

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease that is strongly associated with insulin resistance. Myotonic dystrophy (DM1) is the most common form of adult-onset muscular dystrophy, and there is a high frequency of insulin resistance due to insulin receptor mRNA splicing defects in muscle tissue. The frequency and predictors of NAFLD in this population have not been described. Thirty-six patients with DM1 were prospectively assessed for the presence of NAFLD and insulin resistance. NAFLD was defined by abnormal liver chemistry tests with ultrasound or pathologic evidence of steatosis in the absence of other liver disease. Abnormal liver chemistry tests were found in 44% of DM1 patients (mean ALT 73 +/- 21 U/L, AST 53 +/- 15 U/L), and 87% were attributable to NAFLD. Clinical predictors of NAFLD included increased insulin resistance by the homeostasis model assessment (HOMA) method (9.5 vs. 4.0 U, P = 0.03), elevated fasting insulin (40.4 vs. 16.1 microIU/ml, P = 0.03), abdominal obesity (98.6 vs. 90.8 cm, P = 0.03), elevated triglycerides (195.7 vs. 136.8 mg/dl, P = 0.02), and elevated total cholesterol (213.6 vs. 180.6 mg/dl, P = 0.02). NAFLD is very common and should be considered in the management of DM1. It is strongly associated with markers of insulin resistance and features of the metabolic syndrome. These findings support the role of peripheral insulin resistance in the pathogenesis of NAFLD.
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PMID:Frequency and predictors of nonalcoholic fatty liver disease in myotonic dystrophy. 1981 85

Elevated serum amino-transferase levels may be associated with liver injury. Testing for aspartate aminotransferase (AST) or alanine aminotransferase (ALT) is part of many routine screening approaches. The aim of this manuscript was to scrutinize the evidence for using ALT testing as a primary screening parameter for liver diseases. We conclude that (i) elevated serum ALT levels indicate a high specificity and a reasonable sensitivity liver injury, (ii) 10 - 25 % of German adults have elevated ALT levels, (iii) ALT values are increased in the majority but not all patients with acute and chronic liver disease (iv) elevated ALT-values are associated with an increased risk of liver-specific mortality, (v) elevated ALT values are also a risk factor for non-hepatic diseases including diabetes mellitus type 2, metabolic syndrome, cardiovascular diseases and malignancies, (vi) many liver diseases identified by an ALT screening can be treated successfully including prevention of development of clinical endpoints, (vii) an ALT-screening is very likely to be cost-effective although studies are needed for Germany to support this conclusion.
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PMID:[ALT screening for chronic liver diseases: scrutinizing the evidence]. 2007 96


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