Abnormal bone mineral metabolism after long-term anticonvulsant treatment.
OBJECTIVE
To present a case of anticonvulsant-induced disturbances of bone mineral metabolism associated with long-term phenytoin treatment.


METHODS
An 87-year-old woman was hospitalized with generalized acroparesthesia. Her medical history was significant for grand mal epilepsy, which had been treated with phenytoin for more than ten years. On admission she was found to be hypocalcemic, and her alkaline phosphatase concentration was markedly elevated.


CONCLUSIONS
Further investigations revealed that the patient's serum concentration of 25-hydroxycalciferol was well below the expected range. Phenytoin treatment was withdrawn, and calcitriol supplementation commenced. Ten weeks later she was normocalcemic, and the calcitriol dosage was reduced. Radiologic investigations at this time revealed an ununited hip fracture, as well as widespread evidence of bone demineralization.


CONCLUSIONS
Minor elevations of liver enzymes observed in association with anticonvulsant treatment may reflect hepatic microsomal enzyme induction. Marked elevation of serum alkaline phosphatase, particularly when seen in concert with hypocalcemia, may be markers of anticonvulsant-induced bone disease. Under these circumstances, further radiologic investigations and measurement of the vitamin D serum concentration should be undertaken.
Alderman
C P
CP
Repatriation General Hospital, Daw Park, South Australia.
Hill
C L
CL
D000368:Aged; D000369:Aged, 80 and over; D015519:Bone Density; D002112:Calcifediol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D004830:Epilepsy, Tonic-Clonic / Q000188:drug therapy; D005260:Female; D006801:Humans; D006996:Hypocalcemia / Q000139:chemically induced*; D010672:Phenytoin / Q000009:adverse effects* / Q000627:therapeutic use; D013997:Time Factors; D014807:Vitamin D / Q000097:blood
D014807:Vitamin D; D010672:Phenytoin; D002112:Calcifediol