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A prospective study of folate metabolism has been conducted in outpatient anticonvulsant-treated epileptics on 68 occasions. An attempt was made to compare the relative sensitivities of serum and red cell measurements of folic acid, lactic dehydrogenase (LD), and 2 hydroxybutyric dehydrogenase (2HBD). The most sensitive indices of folate deficiency appeared to be serum folate, red cell LD, red cell folate, and red cell 2HBD, respectively. The correlation between these measurements was not close, except in comparisons of red cell and serum folate. No easily performed screening test for folate deficiency emerged. Serial changes in these measurements were carried out on 15 patients during an interval of 18 months. No progressive signs of folate depletion appeared during this time. The significance of these findings is discussed.

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.