Potential risk factors for vitamin D levels in medium- and long-term use of antiepileptic drugs in childhood

Yıldız, Edibe Pempegül; Poyrazoğlu, Şükran; Bektaş, Gonca; Kardelen, Aslı Derya; Aydınli̇, Nur

doi:10.1007/s13760-017-0775-x

Cited by 24 publications

(19 citation statements)

References 19 publications

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“…This study established that vitamin D deficiency or insufficiency is common in children with epilepsy on ASMs in this region of sub-Saharan Africa, occurring in 60.3% of the study group. Similar results were found in other studies undertaken in Australia, USA, Denmark, Spain, Turkey, Israel, Iran, Egypt, and Korea where the prevalence of vitamin D deficiency or insufficiency in children with epilepsy ranged between 50-66% [20][21][22][23][24]26,32,34,37]. As demonstrated since vitamin D deficiency is common in children with epilepsy, where there is capacity, all patients on ASMs should be investigated for vitamin D deficiency and supplemented accordingly.…”

Section: Discussionsupporting

confidence: 85%

“…This is the first study to report that children on enzyme-inducing ASMs have lower levels of 25(OH)D 2 and 24,25(OH) 2 D 3 levels probably as result of increased destruction of vitamin D. The median duration of ASMs was five and a half years so the group had established time period of epilepsy and prolonged time period of prescribed ASMs. However, this study did not show difference in the number of ASMs used between children with vitamin D deficiency and those without, compared to other studies which have shown polytherapy to be associated with lower vitamin D levels [19,21,22,27,28,40,42,43]. Our cohort was recruited from a tertiary center which manages a greater proportion of children with severe forms of epilepsy requiring multiple ASMs.…”

Section: Discussioncontrasting

confidence: 54%

“…Conflicting study methodologies have challenged comparison across studies such that meta-analyses conclude that ASMs may be associated with decreased bone mineral density (BMD) in children with epilepsy [16,17]. But studies have also reported no ASM effect on BMD or vitamin D levels [12,18,19], and others found no variance in the effect of enzyme-inducing ASMs compared to non-inducing ASMs on BMD [20][21][22]. Some specifically highlight the increased impact from monotherapy with sodium valproate, carbamazepine and levetiracetam [23][24][25][26].…”

Section: Retrospective Longitudinal 172mentioning

confidence: 99%

“…Some specifically highlight the increased impact from monotherapy with sodium valproate, carbamazepine and levetiracetam [23][24][25][26]. Other studies conclude that the key risks are polypharmacy and chronic ASM use [21,22,27]. Table 1 summaries some of the key cohort studies illustrating the variation in findings.…”

Section: Retrospective Longitudinal 172mentioning

confidence: 99%

“…Association of vit D levels in children on monotherapy Risk greatest with use of VPA and CBZ Yildz et al Turkey [22] (2017) III VPA, CBZ, LEV, PB…”

Section: Introductionmentioning

confidence: 99%

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Vitamin D abnormalities and bone turn over analysis in children with epilepsy in the Western Cape of South Africa.

Kija

Gidal

Shapson-Coe

et al. 2019

Seizure

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A B S T R A C TPurpose: The effects of antiseizure medications (ASMs) on bone metabolism is inconsistent. Most studies are in high income settings and none from sub-Saharan Africa.Methods: A hospital based cross-sectional study in a paediatric epilepsy service with a comparison group assessed vitamin D metabolism.Results: Seventy-five children with epilepsy and 75 comparison group were recruited. Median age for children with epilepsy was 9 years (range 1-17 years) and controls 3 years (range 1-12 years). Vitamin D deficiency occurred in 11(16.2%) children with epilepsy versus 6 (8.8%) control group (p = 0.29). Vitamin D insufficiency occurred in 30 (44.1%) children with epilepsy compared to 27(39.7%) control group. Children on ASMs had lower mean vitamin D levels than the control group (p = 0.02). Children on enzyme-inducing ASMs had lower mean vitamin D levels (p = 0.08), vitaminD 2 (p = 0.0018), vitaminD 3 (p = 0.004), serum phosphate levels (p = 0.000), and higher mean parathyroid hormone levels (p = 0.03) compared to controls. There was no difference in dietary intake and ancestry, although the dietary content of both groups was low in vitamin D products.Conclusions: Low vitamin D levels were common in children from both groups, but statistically lower for the children on ASMs. Children on enzyme-inducing ASMs need screening for vitamin D deficiency. The literature supports extending this for all children on ASMs. This is the first study to report that children on enzymeinducing ASMs have lower levels of Vitamin D 2 and D 3 levels, probably as result of increased destruction of vitamin D. Improved vitamin D intake for children in vulnerable settings is important.in the liver to form 25-hydroxyvitamin D 3 and subsequently 1α hydroxylation in the kidneys to form 1α, 25 dihydroxy-vitamin D 3 . The degradation of Vitamin D 3 in the kidneys occurs through an enzyme CYP24 to form the metabolites 24, 25 dihydroxy-vitamin D 3 and 1α, 24, 25 trihydroxy-vitamin D 3 [6,7]. In vitro studies support that CYP3A4 catalyzes the hydroxylation of 125 dihydroxy vitamin D 3 into inactive metabolites in the liver and small intestines, where CYP24A1 is nearly absent, which results in decreased intestinal calcium uptake. Notably, CYP3A4 also contributes to the catabolism of 25 hydroxy vitamin D 3 by catalyzing its hydroxylation into 425 dihydroxy vitamin D 3 [8].ASMs induce hepatic cytochrome P450 enzymes, especially https://doi.

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