Twenty three patients (first group) who were newly diagnosed to have various neurological disease, 42 patients (second group) with seizure disorder receiving chronic therapy(more than 1 year) with diphenylhydantoin or diphenylhydantoin with phenobarbital, and 42 controls were studied to determine the effect of diphenylhydantoin on the metabolism of vitamin D.
Comparing the blood levels before treatment with those 3 weeks after treatment in the first group, there were no significant decreases in serum calcium (from 9.38±0.50 to 9.05± 72 mg/dl; P<0. 05), significant decreases in serum inorganic phosphorus (from 4.83±0.60 to 4.38±0.33 mg/dl;
P<0.001), and significant inreases in serum alkaline phosphatase(from 103.08±85.59 to 192.30±36.30 I.U; P<0.001)
Chronic therapy (second group) was associated with the significant decreases in serum calcium (8.96±0.41 vs. 9, 60±0.41 mg/dl in controls; P< 0. 001), serum inorganic phosphorus (2.86±0.48 vs. 4.05±0.51 mg/dl in controls; P<0.001), and the significant increases in serum alkaline phosphatase (218.59±120.14 vs. 56.00±28.63 I.U. in controls; P<0, 001).
We can speculate that in the early stage of diphenylhydantooin therapy, the expected deficiency of vitamin D seemed to elevate the levels of parathyroid hormone, which caused accelerated demineralization of the bone as a compensatory mechanism, and in the later stage this compensatory mechanism seemed to be break down accompanied by hypocalcemia. Thus vitamin D. supplementation appears indicated in the patients on chronic anticonvulsant therapy.
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