Liver Enzyme Induction by Anticonvulsant Drugs, and Its Relationship to Disturbed Calcium and Folic Acid Metabolism

Latham, A. N.; Millbank, L.; Richens, A.; Rowe, Dorothy J.

doi:10.1002/j.1552-4604.1973.tb00221.x

Cited by 19 publications

(13 citation statements)

References 12 publications

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“…Perhaps some surprising data relate to primidone with 7% of total anticonvulsant prescriptions but implicated in 7/43 (16%) pregnancies. Although there is a suggestion that primidone may be a more potent enzyme inducing agent, at least in the clinical doses used, than phenytoin or phenobarbitone (Latham et al, 1973) . In one clinical study involving nine women on long term OCS, cotrimoxazole failed to cause any decrease in circulating plasma steroid concentrations .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive‐drug interactions with anticonvulsants and antibiotics.

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Grimmer

Orme

et al. 1988

Brit J Clinical Pharma

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1. We have searched the adverse reactions register for the years 1968‐ 84 in an attempt to evaluate data relating to reported pregnancies in women on oral contraceptive steroids (OCS) who concurrently received either an antiepileptic drug or an antibiotic. 2. A total of 43 pregnancies were reported in women on OC therapy who concurrently received antiepileptic drugs and 63 pregnancies in women receiving antibiotics. In addition the number of prescriptions for both antiepileptics and antibiotics in England are reported for the years 1973‐84.

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Section: Introductionmentioning

confidence: 99%

Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive‐drug interactions with anticonvulsants and antibiotics.

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Grimmer

Orme

et al. 1988

Brit J Clinical Pharma

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“…, and a number of known enzyme inducers cause large increases in urinary D-glucaric acid excretion (Latham et al, 1973). While establishing an assay method for Dglucaric acid we have investigated the excretion of Dglucaric acid by users, and non-users of oral contraceptives.…”

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confidence: 99%

Urinary D‐glucaric acid and oral contraceptives.

Stevens¹,

Vose²,

Palmer³

1978

Brit J Clinical Pharma

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, 1973), and a number of known enzyme inducers cause large increases in urinary D-glucaric acid excretion (Latham et al., 1973). While establishing an assay method for Dglucaric acid we have investigated the excretion of Dglucaric acid by users, and non-users of oral contraceptives.Twenty None of these means were significantly different when compared by Student's t-test. Although some of the women taking oral contraceptives excreted more D-glucaric acid on day 20 than day 3 (Figure 1), the increases were much less than the five to ten fold increases in D-glucaric acid excretion caused by some drugs (Maxwell et al., 1972). In contrast to these results an earlier study (Mowat, 1968) provided evidence of an increased D-glucaric acid excretion by nine women taking oral contraceptives (four Ovulen, two Orthonovin, two Gynovlar, one Conovid E), when compared to non-users. A possible explanation for these differing results may be the higher doses of progestagen and oestrogen in most of the tablets used in Mowat's (1968) investigation. These generally contained 100 gg oestrogen with 2 or 3 mg progestagen, whereas the oral contraceptives used in the present study generally contained 30 or 50 g oestrogen with d-norgestrel (0.15 mg) or norethisterone (0.5 or 1 mg) as the progestagen.The results obtained in the present study appear to be compatible with observations of the lack of effect of oral contraceptives on the disposition of other drugs. Br.

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“…It has been shown that one ofthe aldehyde dehydrogenases induced in rat liver by administration of phenobarbital is sensitive to steroids (Koivula & Koivusalo, 1975) when oxidizing acetaldehyde and that the induced enzyme will oxidize glucuronolactone (Marselos & Hinninen, 1974). Since urinary excretion of glucaric acid (the dehydrogenation product of glucuronolactone) is increased in man after administration of various drugs (Latham et al, 1973), it is likely that this enzyme is inducible in humans, although the normal human liver aldehyde dehydrogenase is not sensitive to diethylstilboestrol (Kraemer & Deitrich, 1968).…”

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confidence: 99%

The action of progesterone and diethylstilboestrol on the dehydrogenase and esterase activities of a purified aldehyde dehydrogenase from rabbit liver

Julian¹

1977

Biochemical Journal

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A steroid-sensitive aldehyde dehydrogenase (EC 1.2.1.3) was purified from rabbit liver and is homogeneous by the criterion ofelectrophoresis in polyacrylamide gels with or without sodium dodecyl sulphate. The enzyme is tetrameric, of subunit mol.wt. 48 300, and contains no tightly bound zinc. The fluorescence ofthe protein is decreased in the presence of progesterone, which is inhibitory to the reactions catalysed by the enzyme. When NADH is bound to the enzyme, the fluorescence of the coenzyme is augmented to an extent independent of the presence of steroids or acetaldehyde. The purified enzyme catalyses the oxidation of acetaldehyde and glucuronolactone, and the hydrolysis of 4-nitrophenyl acetate. Each of these reactions is inhibited by progesterone in such a manner as to suggest the formation of a catalytically active enzyme-hormone complex. Diethylstilboestrol inhibits the hydrolysis ofesters by this enzyme, but stimulates the oxidation of aldehydes, except at low aldehyde concentrations; the ligand is then inhibitory. NADH inhibits the hydrolysis of 4-nitrophenyl acetate by the enzyme in a partially competitive fashion.

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Liver Enzyme Induction by Anticonvulsant Drugs, and Its Relationship to Disturbed Calcium and Folic Acid Metabolism

Cited by 19 publications

References 12 publications

Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive‐drug interactions with anticonvulsants and antibiotics.

Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive‐drug interactions with anticonvulsants and antibiotics.

Urinary D‐glucaric acid and oral contraceptives.

The action of progesterone and diethylstilboestrol on the dehydrogenase and esterase activities of a purified aldehyde dehydrogenase from rabbit liver

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