Hepatic Gamma-Glutamyl Transferase and Hepatic Fibrosis in
Patients with Alcoholic Liver Disease

Yamauchi, Masato; Kimura, Kazuhide; Kawase, Hitoshi; Watanabe, Yuri; Kitahara, T; Ogura, K.; Fujisawa, Kiyoshi; Kameda, Haruo

doi:10.1159/000469460

Cited by 7 publications

(1 citation statement)

References 15 publications

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“…Enhanced potential for increased GSH consumption and ROS generation have also recently been reported in children given CBZ, DPH, or PB (Aycicek and Iscan 2007). Notably in human alcoholics, the increases in serum or plasma GGT activity have been consistently associated with much less of a change in hepatic tissue GGT activity (Ishii et al 1986; Ivanov et al 1980; Selinger et al 1982; Teschke et al 1983; Yamauchi et al 1984). This result is presumed partly due to the specific hepatic tissue components analyzed, and contributions from extrahepatic tissues to blood GGT activity (Ikeda and Taniguchi 2005; Whitfield 2001).…”

Section: Hepatic Metabolic Enzyme Induction and Associated Clinical Pmentioning

confidence: 99%

Effects of Hepatic Drug-metabolizing Enzyme Induction on Clinical Pathology Parameters in Animals and Man

et al. 2010

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Hepatic drug-metabolizing enzyme (DME) induction is an adaptive response associated with changes in preclinical species; this response can include increases in liver weight, hepatocellular hyperplasia and hypertrophy, and upregulated tissue expression of DMEs. Effects of DME induction on clinical pathology markers of hepatobiliary injury and function in animals as well as humans are not well established. This component of a multipart review of the comparative pathology of xenobiotically mediated induction of hepatic metabolizing enzymes reviews pertinent data from retrospective and prospective preclinical and clinical studies. Particular attention is given to studies with confirmation of DME induction and concurrent evaluation of liver and/or serum hepatobiliary marker enzyme activities and histopathology. These results collectively indicate that in the rat, when histologic findings are limited to hepatocellular hypertrophy, DME induction is not expected to be associated with consistent or substantive changes in serum or plasma activity of hepatobiliary marker enzymes such as alanine aminotransferase, alkaline phosphatase, and gamma glutamyltransferase. In the dog and the monkey, published studies also do not demonstrate a consistent relationship across DME-inducing agents and changes in these clinical pathology parameters. However, increased liver alkaline phosphatase or gamma glutamyltransferase activity in dogs treated with phenobarbital or corticosteroids suggests that direct or indirect induction of select hepatobiliary injury markers can occur both in the absence of liver injury and independently of induction of DME activity. Although correlations between tissue and serum levels of these hepatobiliary markers are limited and inconsistent, increases in serum/plasma activities that are substantial or involve changes in other markers generally reflect hepatobiliary insult rather than DME induction. Extrahepatic effects, including disruption of the hypothalamic-pituitary-thyroid axis, can also occur as a direct outcome of hepatic DME induction in humans and animals. Importantly, hepatic DME induction and associated changes in preclinical species are not necessarily predictive of the occurrence, magnitude, or enzyme induction profile in humans.

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