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Alanine aminotransferase ALT

L-alanine + a-ketoglutaric acid------ L-glutamic acid + pyruvic acid [Pg.28]

DAOS = 3,5-dimethoxy-iV-ethyl-Ar-(2-hydroxy-3-sulfopropyl)-aniUne sodium salt [Pg.28]

Storage The strips should be stored between 2-25°C. After opening the aluminium foil the strip should be used immediately. [Pg.29]

Sample material Serum, heparin plasma, EDTA plasma or fluoride plasma. [Pg.29]


The nurse immediately reportsany elevated alanine aminotransferase (ALT) level to the primary health care provider. The primary health care provider may want to continue monitoring the ALT level or discontinue use of the drug because of the danger of hepatotoxidty. However, abrupt discontinuation may cause a decline in cognitive functioning. [Pg.308]

The choice of IFN-a as a potential treatment for chronic hepatitis C in 1986 was empirical (Hoofnagle et al. 1986). At this time, the causative agent of chronic non-A, non-B hepatitis had not yet been identified, and there was no way of evaluating HCV replication or, thus, the antiviral activity of a drug. In the first cohort of 10 patients with chronic non-A, non-B hepatitis treated with IFN-a, a significant decline in alanine aminotransferase (ALT) levels was observed in 8 patients, and liver histology had improved at the end of therapy in the three patients who were biopsied (Hoofnagle et al. 1986). Ten years later, 5 of the 10 patients were free of infection (Lau et al. 1998). [Pg.214]

Ribavirin is a guanosine analog synthesized more than 35 years ago, which possesses broad-spectrum antiviral activity against several RNA and DNA viruses in vitro (Sidwell et al. 1972). When administered as monotherapy in patients with chronic hepatitis C, ribavirin induces a decline of serum alanine aminotransferase (ALT) levels while no effect on sustained virologic response is detectable (Di Bisceglie et al. 1992). [Pg.327]

Use of the plasma enzyme alanine aminotransferase (ALT) in monitoring the progress of infectious hepatitis. [Pg.3]

Hepatocellular damage manifests as elevated serum aminotransferases [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)]. The degree of transaminase elevation does not correlate with the remaining functional metabolic capacity of the liver. An AST level two-fold higher than ALT is indicative of alcoholic liver damage. [Pg.328]

A few cases of hepatotoxicity have been reported with rosiglitazone and pioglitazone, but no serious complications have been reported, and symptoms typically reverse within several weeks of discontinuing therapy. Therefore, periodic liver function tests should be performed at baseline and during thiazolidinedione therapy. Patients with a baseline alanine aminotransferase (ALT) level greater than 2.5 times the upper limit of normal should not receive a TZD. If ALT levels rise to greater than 3 times the upper limit of normal in patients receiving a TZD, the medication should be discontinued. [Pg.657]

Activated partial thromboplatin time (aPTT) Adrenocorticotropic hormone (ACTH) Alanine aminotransferase (ALT, SGPT) Albumin... [Pg.1545]

The practicing clinician has a number of different tests available to aid in the evaluation of patients with suspected hepatitis C. These include measurement of alanine aminotransferase (ALT) levels, liver biopsy, serological tests (ELISA and recombinant immunoblot assay), and molecular methods for detection and quantitation of HCV RNA. [Pg.220]

Several case reports of hepatotoxicity with pioglitazone or rosiglitazone have been reported, but improvement in alanine aminotransferase (ALT) was consistently observed upon drug discontinuation. Baseline ALT should be obtained prior to therapy and then periodically thereafter at the practitioner s discretion. Neither drug should be started if the baseline ALT exceeds 2.5 times the upper limit of normal. The drugs should be discontinued if the ALT is more than 3 times the upper limit of normal. [Pg.232]

Laboratory evaluation frequently shows leukocytosis, increases in creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and myoglobinuria. [Pg.823]

Primates offer all of the possible dosing routes available in humans, but body size often limits dosing volumes. If volumes for subcutaneous or intramuscular injections exceed those suggested above, enzyme elevations [particularly alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] are frequently observed (unpublished results). Continuous infusion techniques in alert animals are available in some laboratories either through use of programmable backpack pumps or jacket-and-tether systems (Perkin and Stejskal, 1994). [Pg.618]

Glutamate pyruvate transaminase (SGPT), now frequently referred to as alanine aminotransferase (ALT)... [Pg.803]

Serum chemistry markers play an important role in hepatotoxicity evaluation in human and animal safety studies. The classic markers of hepatotoxicity are alanine aminotransferase (ALT), aspartate aminotrasnferase (AST) and alkaline phosphatase (ALP) [124—127]. Drug-induced hepatotoxicity can be difficult to assess in some circumstances. Hepatotoxic responses can be intrinsic (predictable, dose-related) or idiosyncratic (unpredictable, non-dose-related). ALT, AST and ALP are generally not useful for predicting idiosyncratic responses. The administration of some drugs, such as isoniazid, can lead to a high incidence of ALT elevation, but are tolerated by most patients without severe hepatotoxicity. Adverse drug reactions can be masked... [Pg.369]

The reactions catalyzed by two of the most important of these enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are shown below. [Pg.123]

The most common adverse effects of lamivudine seen at doses used to treat HBV are mild they include headache, malaise, fatigue, fever, insomnia, diarrhea, and upper respiratory infections. Elevated alanine aminotransferase (ALT), serum lipase, and creatine kinase may also occur. The safety and efficacy of lamivudine in patients with decompensated liver disease have not been established. Dosage adjustment is required in individuals with renal impairment. Coadministration of trimethoprim-sulfamethoxazole decreases the renal clearance of lamivudine. [Pg.581]

Liver dysfunction. In a 4-year study in 1221 liver dysfunction-free (serum aspartate aminotransferase [AST] and alanine aminotransferase [ALT] <39 lU/L and no medical care for or no past history of liver disease) males aged 35-56 years, was investigated for the association of coffee consumption with the development of increased serum AST and/or ALT activities. From the analysis using the Kaplan-Meier method, the estimated incidence of serum AST and/ or ALT > 40 lU/L, > 50 lU/L, and > 60 lU/ L decreased with an increase in coffee consumption. From the Cox proportional haz-... [Pg.175]

Hepatotoxicity. Duloxetine is rarely associated with increases in serum transaminase levels, typically in the first 2 months of treatment. In controlled trials in major depressive disorder, elevations of alanine aminotransferase (ALT) to greater than three times the upper limit of normal occurred in 0.9% (8 of 930) of the duloxetine-treated patients and in 0.3% (2 of 652) of the placebo-treated patients. Current product labeling contains a caution regarding the use of duloxetine in patients with significant alcohol use or chronic liver disease. Postmarketing reports have indicated that increases in transaminases have occurred in some patients with chronic liver disease (Cymbalta 2005). [Pg.33]

Because of the potential for hematological and hepatic toxicity, carbamazepine should not be administered to patients with liver disease or thrombocytopenia or to those at risk for agranulocytosis. For this reason, carbamazepine is strictly contraindicated in patients receiving clozapine. Because of reports of teratogenicity, including increased risks of spina bifida (Rosa 1991), microcephaly (Bertol-lini et al. 1987), and craniofacial defects (Jones et al. 1989), carbamazepine is relatively contraindicated in pregnant women. Pretreatment evaluation should include a complete blood count and determination of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. [Pg.153]

B. Indications and nse Infergen is indicated for treating chronic hepatitis C virus (HCV) infection in adults with compensated liver disease who have anti-HCV serum antibodies and/or the presence of HCV RNA. It is also effective in the subsequent treatment of patients who did not respond or relapsed after initial interferon therapy. In some patients with chronic HCV infection, Infergen normalizes serum alanine aminotransferase (ALT) concentrations, reduces serum HCV RNA concentrations to undetectable quantities (<100 copies/ml), and improves liver histology. [Pg.188]

E. Therapeutic response Efficacy of Infergen therapy was determined by measurement of serum alanine aminotransferase (ALT) concentrations at the end of therapy (24 weeks) and following 24 weeks of observation after the end of treatment of adults with chronic HCV infection. Serum HCV RNA was also assessed using a quantitative reverse transcriptase polymerase chain reaction (RT-PCR). At the end of 24 weeks of treatment, ALT normalization was observed in 39% of patients on Infergen and in 35% of patients on interferon alfa-2b Intron A). Only 17% of patients in each group... [Pg.189]

E. Therapeutic response A randomized trial compared treatment with PEG-Intron, once weekly, to treatment with Intron A (interferon alfa-2b), three times weekly, in 1219 previously untreated adults with chronic hepatitis from HCV infection. Patients were treated for 48 weeks. Response to treatment was defined as undetectable HCV RNA (less than 100 copies per ml) and normalization of the liver enzyme alanine aminotransferase (ALT) at 24 weeks post-treatment. Response rates to the l.Opg/kg PEG-Intron doses and to Intron A were 24% and 12%. Patients receiving PEG-Intron with viral genotype 1 had a response rate of 14%, while patients with other viral genotypes had a 45% response rate. [Pg.206]

Some enzymes show relatively high activity in only one or a few tissues. The presence of increased levels of these enzymes in plasma thus reflects damage to the corresponding tissue. For example, the enzyme alanine aminotransferase ALT, see p. 248) is abundant in the liver. The appearance of elevated levels of ALTin plasma signals possible damage to hepatic tissue. Increases in plasma levels of enzymes with a wide tissue distribution provide a less specific indication of the site of cellular injury. This lack of tissue specificity limits the diagnostic value of many plasma enzymes. [Pg.65]

Pattern of serum alanine aminotransferase (ALT) and bilirubin in the plasma, following poisoning with the toxic mushroom Amanita phalloides. [Pg.249]


See other pages where Alanine aminotransferase ALT is mentioned: [Pg.23]    [Pg.333]    [Pg.340]    [Pg.83]    [Pg.669]    [Pg.353]    [Pg.544]    [Pg.1507]    [Pg.1509]    [Pg.180]    [Pg.69]    [Pg.196]    [Pg.85]    [Pg.305]    [Pg.54]    [Pg.83]    [Pg.85]    [Pg.102]    [Pg.136]    [Pg.138]    [Pg.180]    [Pg.664]    [Pg.248]   


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