Antiepileptic Drugs and Vitamin D Supplementation

Offermann, G.; Pinto, Vânia Lopes; Kruse, Rolf

doi:10.1111/j.1528-1157.1979.tb04771.x

Cited by 53 publications

(46 citation statements)

References 37 publications

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“…In accordance with other reports on calcium-phosphate metabolism in anticonvulsant treated patients (Bonfils et al, 1976;Christiansen et al, 1974;Hahn, 1976;Offermann et al, 1979) our patients demonstrated significant elevations of serum alkaline phosphatase and iPTH, hypocalciuria, hypomagnesemia and a reduced calcium-phosphate product in serum.…”

Section: Discussionsupporting

confidence: 95%

Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs

et al. 1980

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Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.

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Section: Discussionsupporting

confidence: 95%

Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs

et al. 1980

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“…Effects of epilepsy treatment on vitamin D status in children More than three decades ago, Offerman et al [52] first reported the high prevalence of low vitamin D status among children with epilepsy. Since then, extensive research on vitamin D deficiency associated with anticonvulsant drugs in pediatric patients has been conducted [53][54][55][56][57][58][59][60].…”

Section: Vitamin D Deficiencymentioning

confidence: 99%

Epilepsy treatment by sacrificing vitamin D

Cebeci¹,

Ekici²

2014

Expert Review of Neurotherapeutics

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Epilepsy is one of the most common neurologic disorders in childhood that often requires long term treatment with antiepileptic drugs. Both antiepileptic treatment and the comorbidities associated with epilepsy have a negative impact on bone health in growing children. Given the fact that vitamin D deficiency is a major public health problem worldwide, clinicians caring for children with chronic diseases should be aware of effects of the medication on the bone metabolism. Yet, vitamin D deficiency due to antiepileptic treatment is an overlooked issue among neurologists. In this review, we briefly describe vitamin D metabolism and the effect of vitamin D in the brain. We also discuss the literature in terms of vitamin D deficiency and antiepileptic treatment in the pediatric population.

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“…2 AED medication, particularly long-term therapy or polytherapy, is recognized to be associated with hypovitaminosis D. [3][4][5] Adults with epilepsy are known to be at considerably increased risk for bone fractures compared with the general population, and increasing age and duration of AED treatment are significant risk factors. [6][7][8] In 1979, Offerman et al 9 documented that 72% of 83 children aged 10 to 16 years with epilepsy and 50% of 16 control patients exhibited 25-hydroxy vitamin D (25OHD) <15 ng/mL. Since then, several cross-sectional studies evaluated the prevalence of hypovitaminosis D in pediatric epilepsy.…”

Section: Introductionmentioning

confidence: 98%