Renal tubular acidosis and skeletal demineralization in patients on long-term anticonvulsant therapy

A new variant form of hepatic glycogenosis with acid maltase deficiency

“…Ammonium chloride and bicarbonate loading tests were performed by the method described previously (Matsuda et al, 1975).…”

Metabolic acidosis in patients receiving anticonvulsants

“…Serum calcium, phosphorus, and alkaline phosphatase, and blood pH, PCO2 and standard bicarbonate were measured by methods previously described (Matsuda et al, 1975). Serum immunoreactive parathyroid hormone (iPTH) was measured by the method of Saeki and Hayashi (1975).…”

“…Bone demineralization occuring in patients treated with long-term anticonvulsants is well known (McClaren and Lifshitz, 1973;Matsuda et al, 1975;Tolman et al, 1975). In order to explain this abnormality several surveys have been carried out on vitamin D metabolism and parathyroid hormone regulation (Ham et al, 1975;Tolman et al, 1975).…”

Alpha-tocopherol and fatty acid levels in red blood cells in patients treated with antiepileptic drugs.

“…The metabolic disturbances associated with therapy seem mainly to involve peroxidative damages relating to detoxification mechanisms including the mixed oxidase functions in liver microsomes (5,6). It also appears that this therapy may disturb metabolisms of vitamin E, as there have been a few reports that serum vitamin E levels were reduced in children receiving long-term antiepileptic treatment (7)(8)(9).…”

“…Given that the nutritional status of vitamin E has been reported to be reflected in RBC tocopherol levels in our previous studies (10,13,14), the finding of low RBC tocopherol levels in the children who were given AEDs in this study may be consistent with a hypothesis previously made on the basis of plasma tocopherol changes. That is, tocopherol exhaustion may occur in these children who were given drugs, because of increased peroxidation associated with an enhanced detoxification metabolism with NADPH-dependent electron transporting, as is known to occur in mixed oxidase functions in liver microsomes (5,6). This metabolism produces large numbers of oxygen radicals which may consume tocopherol in the associated membranes.…”