ABSTRACT
In recent years, it has become apparent that chronic treatment with anticonvulsant drugs can result in a variety of disorders of vitamin D, mineral, and bone metabolism. Among the most commonly observed clinical abnormalities are hypocalcemia, increased serum alkaline phosphatase concentration, reduced serum of 25-hydroxyvitamin D (25OHD) levels, mild increase in serum immunoreactive parathyroid hormone (iPTH) concentration, radiological evidence of decreased bone mass, increased incidence of bone fractures, and histologic evidence of osteomalacia. Drug-induced alterations in the hepatic and renal metabolism of vitamin D, and direct inhibitory effects of certain drugs on transmembrane mineral transport mechanisms, appear to be the basis of most of these clinical manifestations. This group of drug-induced mineral disorders is frequently referred to as "anticonvulsant osteomalacia."
