Liver function tests in persons receiving anticonvulsant medications

Wall, Margaret; Baird-Lambert, J.; Buchanan, N.; Farrell, Geoffrey C.

doi:10.1016/1059-1311(92)90024-u

Cited by 19 publications

(10 citation statements)

References 9 publications

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“…Elevated plasma AHSG levels, as the cause of the higher CSF levels in the glioma group, could result from several mechanisms. For Ribom/Westman-Brinkmalm/Smits/ Davidsson example, anti-epileptic drugs are known to cause liver enzyme induction and changes in the hepatic ultra structure [28,29], and it is possible that they also influence the AHSG production in the liver. A blood-brain barrier disruption demonstrated by contrast enhancement might also affect the AHSG levels in CSF.…”

Section: Discussionmentioning

confidence: 99%

Elevated Levels of alpha-2-Heremans-Schmid Glycoprotein in CSF of Patients with Low-Grade Gliomas

Ribom¹,

Westman‐Brinkmalm²,

Smits³

et al. 2003

Tumor Biol

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Little is known about the expression of mitogens and other tumour-related substances in the cerebrospinal fluid (CSF) of glioma patients. The aim of the current study was to determine the presence of aberrant proteins in the CSF of patients with low-grade gliomas. Lumbar puncture was performed in 8 adult patients with supratentorial low-grade gliomas at the time of diagnosis and in 7 controls. Two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionisation time of flight mass spectrometry were used to detect and quantify deviant proteins in the CSF. Two isoforms of α₂-Heremans-Schmid glycoprotein (AHSG) were identified and demonstrated in higher levels in patients with low-grade gliomas compared with the control group consisting of patients with mixed neurological diagnoses (p = 0.001 and p = 0.04, respectively). In 1 patient, the level of AHSG was significantly reduced after gross total resection of the tumour. AHSG appears in the present proteome screening as a novel substance in glioma research. This glycoprotein is expressed in the fetal human brain and is believed to be involved in the embryonic development of the neocortex. Further analyses are planned to determine the significance of the increased levels of AHSG in the CSF of patients with low-grade gliomas.

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Section: Discussionmentioning

confidence: 99%

Elevated Levels of alpha-2-Heremans-Schmid Glycoprotein in CSF of Patients with Low-Grade Gliomas

Ribom¹,

Westman‐Brinkmalm²,

Smits³

et al. 2003

Tumor Biol

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“…In a large, multicenter screening study for viral hepatitis, the prevalence of HBV or HCV infection was 24.8% 37 and asymptomatic liver chemistry abnormalities occurred in over three quarters of patients taking anticonvulsant medication. 38 Thus, a decision to observe an asymptomatic patient closely and repeat a liver chemistry test, versus proceeding with an additional evaluation, must be made in the context of the clinical scenario.…”

Section: Initial Approach To the Evaluation Of Abnormal Liver Chemistmentioning

confidence: 99%

AGA technical review on the evaluation of liver chemistry tests

2002

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“…Hepatic enzyme inducers, such as sodium phenobarbitone, have been reported to increase the serum enzyme levels in human patient populations, and elevations in ALT, AST, and gGT were seen in patients following treatment with several anticonvulsant drugs (Aiges et al 1980;Wall et al 1992). In a study of epileptic patients receiving drug therapy, elevations in gGT were seen in almost all individuals leading the authors of the study to conclude that this did not indicate hepatic damage, since none of the patients exhibited clinical symptoms.…”

Section: Serum Enzyme Activity Elevation In Human Studiesmentioning

confidence: 99%

Liver Hypertrophy

Elcombe²,

et al. 2012

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Preclinical toxicity studies have demonstrated that exposure of laboratory animals to liver enzyme inducers during preclinical safety assessment results in a signature of toxicological changes characterized by an increase in liver weight, hepatocellular hypertrophy, cell proliferation, and, frequently in long-term (life-time) studies, hepatocarcinogenesis. Recent advances over the last decade have revealed that for many xenobiotics, these changes may be induced through a common mechanism of action involving activation of the nuclear hormone receptors CAR, PXR, or PPARa. The generation of genetically engineered mice that express altered versions of these nuclear hormone receptors, together with other avenues of investigation, have now demonstrated that sensitivity to many of these effects is rodent-specific. These data are consistent with the available epidemiological and empirical human evidence and lend support to the scientific opinion that these changes have little relevance to man. The ESTP therefore convened an international panel of experts to debate the evidence in order to more clearly define for toxicologic pathologists what is considered adverse in the context of hepatocellular hypertrophy. The results of this workshop concluded that hepatomegaly as a consequence of hepatocellular hypertrophy without histologic or clinical pathology alterations indicative of liver toxicity was considered an adaptive and a non-adverse reaction. This conclusion should normally be reached by an integrative weight of evidence approach.

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Liver function tests in persons receiving anticonvulsant medications

Cited by 19 publications

References 9 publications

Elevated Levels of alpha-2-Heremans-Schmid Glycoprotein in CSF of Patients with Low-Grade Gliomas

Elevated Levels of alpha-2-Heremans-Schmid Glycoprotein in CSF of Patients with Low-Grade Gliomas

AGA technical review on the evaluation of liver chemistry tests

Liver Hypertrophy

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