Treatment of anticonvulsant osteomalacia with 1 chydroxycholecalciferol Anticonvulsants cause osteomalacia,' possibly by the induction of an altered vitamin-D metabolism in the liver leading to a lack of 25- hydroxycholecalciferol (25-HCC).2We describe the short-term treat- ment of a patient with anticonvulsant osteomalacia with small amounts of 1-HCC, a vitarnin-D analogue that has been used in renal osteo- dystrophy3 and other metabolic bone diseases. Case historyA 5 1-year-old woman with an infantile spastic paresis on the right, and epi- lepsy treated for 30 years with phenobarbital 50 mg and phenytoin 75 mg three times a day was seen because of fatigue and increasing pains in the trunk and legs.She had had little exposure to sunshine for six years and her diet was deficient in vitamin D. The whole thorax and vertebral column were extremely painful on palpation and percussion.Pelvic side-pressure evoked pain in the pubic region.She had spastic paresis of the right arm and leg.Relevant laboratory data were: serum Ca 2 01 mmol/l (8 04 mg/ 100 ml) and P 0-52 mmol/l (1 6 mg/ 1OOml), total protein 73 g l1(7-3 g! 100 ml), albumin 55 g I (5-5 g/100 ml), alkaline phosphatase 112 IU/l (normal < 45),
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Bull et al. (1977) studied this question.