Seven children who were suffered from rickets during administration of anti-convulsants were studied. In this study, the effects of anticonvulsants on liver and bone metabolism were discussed. The serum levels of 25-hydroxycholecalciferol were measured in all cases, and in three cases, serum parathyroid hormone le-vels were also measured.
In six of seven patients, the serum levels of 25-hydroxycholecalciferol were subnormal or markedly low. And the serum levels of parathyroid hormone were markedly elevated in two of three patients.
In all seven cases, serum alkaline phosphatase levels were markedly elevated. And in three of these patients, serum γ-glutamyl transpeptidase levels were also elevated without the increase of serum GPT or GOT.
Though serum calcium levels were not always decreased, serum inorganic phosphorus levels were markedly low in all seven cases.
All these patients were administered phenobarbital and acetazolamide. In six of them, metabolic acidosis was observed, and after elimination of acetazolamide, metabolic acidosis was corrected in five patients. And in two of them, the improvement of rachitic change occurred only after elimination of acetazolamide. These findings suggest the important role of acetazolamide in the development of rickets.
Since the anticonvulsants such as phenobarbital and diphenylhydantoin accelerate the inactivation of vitamin D activity, the administration of these anticonvulsants seems to increase the requirement of vitamin D.
