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Biomedical subjects

J Hunter

Publications and source records attributed to J Hunter.

At least 217 records · Page 12Linked to original sources
PubMed1972

Folate deficiency after anticonvulsant drugs: an effect of hepatic enzyme induction?

Serum and red cell folate levels were reduced in 59% and 58% respectively of 75 children with epilepsy attending a residential school. The degree of folate deficiency was significantly related to increased hepatic microsomal enzyme activity, assessed from increased urinary excretion of D-glucaric acid and also correlated with the daily dose of anticonvulsant taken. Anticonvulsant drugs are known to have inducing properties, and since folate is required as a cofactor in drug hydroxylations it is suggested that folate depletion results from increased demand for the cofactor after induction of drug-metabolizing enzymes. As folate deficiency may ultimately limit drug metabolism this hypothesis would explain why blood phenytoin levels decrease and fit control may worsen after correction of folate deficiency in epileptic patients.

Adipates↗
PubMed1971

Altered calcium metabolism in epileptic children on anticonvulsants.

A survey of 105 epileptic children aged 10-16 years at a residential school who were taking anticonvulsant drugs showed reduced serum calcium levels in 30% and a raised serum alkaline phosphatase in 24%. Urinary D-glucaric acid excretion, a quantitative index of hepatic enzyme induction, was raised in 94% of the children, and statistical analysis showed a significant inverse correlation with the level of serum calcium. These findings give further support for the view that an important factor in the development of the hypocalcaemia and occasional clinical osteomalacia in epileptics on anticonvulsant drugs is an alteration of vitamin-D metabolism in the liver as a result of microsomal enzyme induction. As a consequence there is an increased requirement for vitamin D which may not be met by average intakes in Britain.

Adipates↗
PubMed1971

Controlled trial of phetharbital, a non-hypnotic barbiturate, in unconugated hyperbilirubinaemia.

Eleven patients with mild unconjugated hyperbilirubinaemia (Gilbert's syndrome) took part in a double-blind cross-over trial of phenobarbitone and phetharbital, a non-hypnotic barbiturate. Significant reductions in plasma bilirubin were observed with both drugs, but six patients complained of sleepiness on phenobarbitone, and phetharbital was preferred by most patients. Phetharbital was also effective in the rare severe unconjugated hyperbilirubinaemia of the Crigler-Najjar syndrome (Type 2). Symptoms attributed to Gilbert's syndrome, including nausea and abdominal pain, were less consistently relieved.

Abdomen↗