Age and Ageing (1977), 6, 228 ANTICONVULSANT-INDUCED OSTEOMALACIA

Four cases of osteomalacia associated with the long term consumption of phenytoin (Dilantin) were admitted to a geriatric unit in a two-month period. No other cause for their disease was found. The diagnosis was made on biochemical data and no bone biopsy was obtained. Radiographic evidence was found in two cases only. Osteomalacia as a consequence of long-term anticonvulsant therapy has been recognized for ten years. Initial observations were made at the Chalfont Centre for Epilepsy, Buck-inghamshire by Wright (1965). It was found that 20 % of patients treated with phene-turide plus phenytoin plus phenobarbitone had a raised serum alkaline phosphatase, and that 16 % of control patients treated with only phenytoin and phenobarbitone also had a raised value. Subsequent studies (Richens & Rowe 1970) made on young epileptics resident in epileptic colonies, consuming a diet adequate in vitamin D, have shown the development of osteomalacia with long-term therapy. Dent et al. (1970) showed that phenobarbitone and its derivatives, e.g. phenytoin, are responsible for enzyme induction leading to increased break-down of active forms of vitamin D to inactive forms. This problem has a particular relevance to the production of osteomalacia in the elderly and the consequent morbidity from fractures and myopathy. This report of four cases admitted to the Wellington Hospital Geriatric Unit within a two-month period highlights the problem