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Clinical Chemistry 28: 1367-1370, 1982;
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Clinical Chemistry, Vol 28, 1367-1370, Copyright © 1982 by American Association for Clinical Chemistry

Serum copper concentration and hepatic enzyme induction during long- term therapy with anticonvulsants

JC Tutor, MP Fernandez and JM Paz

We evaluated hepatic enzyme induction by measuring urinary D-glucaric acid and serum gamma-glutamyltransferase in a group of 40 adult epileptics of both sexes who were receiving long-term treatment with phenobarbital and (or) phenytoin. Total concentrations of copper and ceruloplasmin in their serum and the oxidase activity of ceruloplasmin were significantly greater than in the control group. However, non- ceruloplasmin copper and specific oxidase activity of the ceruloplasmin (activity per gram) were unchanged. A highly significant relationship was found between gamma-glutamyltransferase and (a) copper (r = 0.682, p less than 0.001), (b) ceruloplasmin (r = 0.523, p congruent to 0.001), and (c) the oxidase activity of the ceruloplasmin (r = 0.598, p less than 0.001). There is also a significant correlation of hemopexin with ceruloplasmin (r = 0.531, p congruent to 0.001) and the oxidase activity of the ceruloplasmin (r = 0.598, p less than 0.001). These results suggest that hypercupremia in patients undergoing long-term anticonvulsant therapy is a direct result of hepatic enzyme induction caused by the drugs that induce synthesis of ceruloplasmin.


The following articles in journals at HighWire Press have cited this article:


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 Hum Exp ToxicolHome page
C.-S. Liu, H.-M. Wu, S.-H. Kao, and Y.-H. Wei
Phenytoin-mediated oxidative stress in serum of female epileptics: A possible pathogenesis in the fetal hydantoin syndrome
Human and Experimental Toxicology, March 1, 1997; 16(3): 177 - 181.
[Abstract] [PDF]

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K. Ghose and A. Taylor
Hypercupraemia Induced by Antiepileptic Drugs
Human and Experimental Toxicology, January 1, 1983; 2(3): 519 - 529.
[Abstract] [PDF]


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Copyright © 1982 by the American Association for Clinical Chemistry.