Metabolic acidosis in patients receiving anticonvulsants

Nagai, Bunsaku; Matsuda, Ichiro; Kondo, Takahito; Taniguchi, Naoyuki; Arashima, Shinichiro; Mitsuyama, Takashi; Oka, Yogo; Honma, Motoyasu

doi:10.1007/bf00442432

Cited by 4 publications

(1 citation statement)

References 13 publications

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“…Prolonged use of anticonvulsant drugs results in several adverse effects, including vitamin D deficiency rickets, folic acid deficiency [1], systemic lupus erythematosus (SLE)-like syndrome [2], renal tubular acidosis [3] and vitamin E deficiency [4][5][6], In an early report [6], we described a vitamin E deficiency state accompanying hydrogen peroxide-induced hemolysis in anticonvulsant-treated children. Erythrocytes from vitamin E-deficient rats were extremely sensitive to extracellular zinc concentrations.…”

Section: Introductionmentioning

confidence: 99%

Serum Zinc and Vitamin E Concentrations in Handicapped Children Treated with Anticonvulsants

Higashi¹,

Ikeda²,

Matsukura³

et al. 1982

Dev Pharmacol Ther

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Serum zinc and vitamin E concentrations were measured in handicapped children aged 4-17 years, treated (n = 32) and untreated (n = 13) with phenytoin and phenobarbital. The mean serum zinc levels were 81 ± 16 and 82 ± 7 μg/dl in the treated and untreated children, respectively. The difference was not significant between these two groups. Hypozincnemia (below 70 μg/dl), however, was found in 7 of the 32 treated patients and in none of the 13 untreated children. The serum vitamin E level was 0.58 ± 0.18 mg/dl in the treated and 0.67 ± 0.17 mg/dl in the untreated children, indicating significantly lower levels in the treated patients (p < 0.005). A significant positive correlation was found between the serum zinc and vitamin E levels (r = 0.45, p < 0.005). Thus, long-term use of anticonvulsants results in a vitamin E and zinc deficiency, which may produce several unfavorable problems in children.

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Section: Introductionmentioning

confidence: 99%

Serum Zinc and Vitamin E Concentrations in Handicapped Children Treated with Anticonvulsants

Higashi¹,

Ikeda²,

Matsukura³

et al. 1982

Dev Pharmacol Ther

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Anticonvulsant-Induced Rickets Associated With Renal Tubular Acidosis and Normal Level of Serum 1,25-Dihydroxyvitamin D

Ishitsu¹,

Matsuda²,

Seino³

et al. 1981

Arch Pediatr Adolesc Med

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Pseudohypoparathyroidism type II and anticonvulsant rickets

et al. 1979

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A patient treated with anticonvulsants showed hypocalcemia and hyperphosphatemia in association with increased serum parathyroid hormone, reduced serum 25-hydroxy D3, diminished response in phosphorus excretion to exogenous parathyroid hormone and normal response in cyclic AMP excretion. Oral administration of Vitamin D3 resulted in normalization of serum 25-hydroxy D3, calcium, and phosphorus. At this stage, phosphorus excretion after parathyroid hormone returned to normal. These findings suggest that the patient had pseudohypoparathyroidism type II with anti-convulsant medication as a complicating factor.

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Metabolic acidosis in patients receiving anticonvulsants

Cited by 4 publications

References 13 publications

Serum Zinc and Vitamin E Concentrations in Handicapped Children Treated with Anticonvulsants

Serum Zinc and Vitamin E Concentrations in Handicapped Children Treated with Anticonvulsants

Anticonvulsant-Induced Rickets Associated With Renal Tubular Acidosis and Normal Level of Serum 1,25-Dihydroxyvitamin D

Pseudohypoparathyroidism type II and anticonvulsant rickets

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