Influence of Diphenylhydantoin and Phenobarbital on Intestinal Calcium Transport in the Rat*

Koch, H. U.; Kraft, D; Herrath, D. von; Schaefer, K.

doi:10.1111/j.1528-1157.1972.tb05167.x

Cited by 97 publications

(46 citation statements)

References 19 publications

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“…In the present study however, the reduction found was 0.3mg/dl, which is the lower limit of this variation and was not enough to increase the PTH serum levels and was not associated with the metabolism of vitamin D. This reduction in the calcium serum levels could be attributed to the direct action of the anticonvulsants in the cells (intestine and bone) as shown in the case of phenobarbital and phenytoin but this has not yet been proven. However, in the case of carbamazepine, this asumption was in agreement with normal levels of serum 25-hydroxycholecalciferol that were found 3,10,11 . The mean total alkaline phosphatase serum levels were significantly higher in the patients than in the control group.…”

Section: Discussionsupporting

confidence: 66%

Bone mineral density, vitamin D and anticonvulsant therapy

Filardi

Guerreiro

Magna

et al. 2000

Arq. Neuro-Psiquiatr.

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-The aim of this study was to assess bone mineral density and vitamin D metabolism in patients on chronic anticonvulsant therapy. Methods: Sixty-nine men, outpatients on chronic anticonvulsant therapy, who had been treated for at least 5 years, were studied, comparing them to thirty healthy controls. Bone mineral density was measured as well as serum levels of calcium, ionized calcium, alkaline phosphatase, PTH, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. Results: No differences in bone mineral density, serum levels of vitamin D and intact-PTH were observed between patients and controls. Bone mineral density was not associated with chronic anticonvulsant therapy. Conclusion: Those adult patients who were on chronic anticonvulsant therapy and who lived in low latitude regions had normal bone mineral density as well as vitamin D serum levels.KEY WORDS: vitamin D, calcium, anticonvulsant, bone mineral density. Densidade mineral óssea, vitamina D e terapia anticonvulsivanteRESUMO -O objetivo deste estudo foi avaliar a densidade mineral óssea e o metabolismo da vitamina D em usuários crônicos de anticonvulsivantes. Métodos: Foram estudados 69 pacientes ambulatoriais, masculinos, usuários crônicos de anticonvulsivantes por período mínimo de 5 anos e comparados a 30 controles normais. Foram efetuadas as medidas da densidade mineral óssea e dos níveis plasmáticos do cálcio, cálcio iônico, fosfatase alcalina, paratormônio, 25-hidroxi-colecalciferol e 1,25-di-hidroxi-colecalciferol. Resultados: Nenhuma diferença na densidade mineral óssea e nos níveis plasmáticos da vitamina D e paratormônio foram observadas entre os pacientes e os controles. A densidade mineral óssea não se mostrou associada ao uso crônico de anticonvulsivantes. Conclusões: Pacientes adultos, do sexo masculino, usuários crônicos de anticonvulsivantes, residentes em regiões ensolaradas, têm densidade mineral óssea e níveis plasmáticos de vitamina D normais. PALAVRAS-CHAVE: vitamina D, cálcio, anticonvulsivante, densidade mineral óssea.Alterations in calcium, vitamin D and bone tissue metabolism have been associated with the following drugs: phenobarbital, phenytoin, primidone and carbamazepine 1,2 . Alterations in the metabolism of calcium are generally very slight and subclinical, but clear cases of hypocalcemia could occur in 4% to 30% of individuals. The intensity of the clinical symptoms depends on many factors, such as: intake of vitamin D, exposure to the sun, physical activity, other diseases that interfere in vitamin D metabolism, the positive correlation of these manifestations with the type of drug, individual drug dosage, and period of exposure, as well as polytherapy 3,6 .This study, which was conducted to assess bone mineral density and vitamin D metabolism in a sample of the Brazilian epileptic population on chronic anticonvulsant therapy, was motivated by the fact that the intensity of alterations of vitamin D metabolism and bone mass was related not only to the chronic use of anticonvulsants but also to other vari...

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Section: Discussionsupporting

confidence: 66%

Bone mineral density, vitamin D and anticonvulsant therapy

Filardi

Guerreiro

Magna

et al. 2000

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

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“…With regard to calcium metabolism, clinical studies have shown that the use of antiepileptic agents was frequently associated with the development of hypocalcemia, and there is a finding that antiepileptic agents decrease intestinal transport of calcium (8,9). However, the hypocalcemia which usually leads to bone fracture was not observed when the treatment with zonisamide at 80 mg / kg for 5 weeks significantly decreased the BMD in tibial bones measured in this experiment.…”

Section: Discussionmentioning

confidence: 60%

Effects of Chronic Administration of Zonisamide, an Antiepileptic Drug, on Bone Mineral Density and Their Prevention With Alfacalcidol in Growing Rats

et al. 2003

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Abstract. We investigated the effects of chronic administration of zonisamide, an antiepileptic agent, on bone metabolism in growing rats. Administration of zonisamide at a dose of 80 mg / kg per day, s.c. for 5 weeks significantly decreased bone mineral density (BMD) at the tibial metaphysis and the diaphysis. The percent rate of decrease in BMD at the tibial metaphysis and the tibial diaphysis was 9.2% and 5.0%, respectively. There was no significant difference between these groups in the growth of the rats. Treatment with zonisamide at a dose of 80 mg / kg increased serum pyridinoline level, a marker of bone resorption, while it does not affect the serum intact osteocalcin level, a marker of bone formation. Combined administration of alfacalcidol, an active vitamin D 3 metabolite, at a dose of 0.1 mg / kg per day with zonisamide prevented a decrease in BMD and showed an increase of serum pyridinoline levels. These results suggest that zonisamide may cause bone loss by accelerating bone resorption rather than inhibiting bone formation. Moreover, the bone loss induced by zonisamide could be prevented by combining zonisamide with alfacalcidol.

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“…Because there is evidence that transmembrane movement of sodium ion plays an important role in the cellular transport of calcium ion in both intestine and bone (33)(34)(35), it could well be that DPH inhibition of membrane permeability to sodium reduces transmembrane calcium transport in these tissues as well. In support of this view, DPH has been shown to directly inhibit intestinal calcium transport in vivo under conditions in which vitamin D metabolism is apparently not altered (12). Thus, the effect of DPH on PTH-induced cAMP generation could well occur via inhibitory effects on PTH-induced changes in intracellular calcium ion concentration.…”

Section: Effects Of Diphenylhydantoin and Phenobarbital On Bone Resormentioning

confidence: 63%

“…In addition, there is experimental evidence which suggests that anticonvulsant drugs may indeed have direct effects on mineral metabolism. Koch et al (12) have reported that DPH appears to directly inhibit intestinal calcium transport in the rat and Harris et al (9) have demonstrated that DPH can inhibit parathyroid extract-induced 45Ca release from mouse calvaria in vitro.…”

Section: Introductionmentioning

confidence: 99%