Effects of phenytoin and/or vitamin K2 (menatetrenone) on bone mineral density in the tibiae of growing rats

Onodera, Kenji; Takahashi, Atsushi; Sakurada, Shinobu; Okano, Yoshiro

doi:10.1016/s0024-3205(01)01522-3

Cited by 40 publications

(16 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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. This result is consistent with our previous finding that the administration of phenytoin at a dose of 20 mg / kg for 5 weeks induced decreased BMD without decreasing the level of serum calcium (2). Moreover, it is well recognized that the severity of drug-induced bone loss depends on several factors including calcium and vitamin D intake, sun-light exposure, physical exercise, doses and duration of antiepileptic agents, duration of therapy, and individual susceptibility (10).…”

Section: Discussionsupporting

confidence: 92%

“…Moreover, previous biochemical data indicated that the serum osteocalcin (OC), a marker of bone formation, was significantly decreased, but there were no significant differences in the levels of serum calcium, pyridinoline (PYD), 25-hydroxyvitamin D (25OHD), and parathyroid hormone (PTH) (1). These data and morphometric results indicated that phenytoin-induced osteopenia may be due to bone loss caused by inhibition of bone formation and / or by accelerating bone resorption rather than osteoid accumulation in rats (1,2).…”

Section: Introductionmentioning

confidence: 95%

“…Combined administration of either alfacacidol or vitamin K 2 with phenytoin for 5 weeks prevented the reduction of BMD induced by phenytoin (1,2). Moreover, previous biochemical data indicated that the serum osteocalcin (OC), a marker of bone formation, was significantly decreased, but there were no significant differences in the levels of serum calcium, pyridinoline (PYD), 25-hydroxyvitamin D (25OHD), and parathyroid hormone (PTH) (1).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2003

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2003

Self Cite

View full text Add to dashboard Cite

show abstract

“…Vitamin K is a cofactor in the post-translational carboxylation of several bone proteins, most markedly osteocalcin, which is a marker of bone formation. Rats treated with phenytoin had more bone loss over a 5-week period when compared with rats treated with phenytoin and vitamin K2 (menatetrenone) [35]. These findings suggest that insufficient vitamin K may have been contributing to the loss seen secondary to phenytoin exposure.…”

Section: Mechanisms Of Antiepileptic Drug-associated Bone Diseasementioning

confidence: 82%

Bone disease in epilepsy

Pack

2004

Curr Neurol Neurosci Rep

View full text Add to dashboard Cite

Recent literature demonstrates an association between antiepileptic drugs (AEDs) and bone disease. Decreased bone mineral density (BMD) has been found in adults and children receiving both enzyme-inducing AEDs and valproate, which is an enzyme-inhibiting AED. Biochemical abnormalities include hypocalcemia, elevated parathyroid hormone, and elevated markers of bone formation and resorption. Although patients in earlier studies had evidence of decreased vitamin D, low BMD has been found to be independent of abnormal vitamin D chemistries in more recently published studies. Multiple mechanisms have been postulated to explain AED-associated bone disease, but no single mechanism fully explains all the abnormalities seen. Therapies are available for bone disease. However, few studies have evaluated the effects of treatment in bone disease associated with AEDs.

show abstract

“…В более ранних работах рассматривались и другие ме-ханизмы воздействия фермент-индуцирующих ПЭП на ко-стную ткань: ингибирование ФТ всасывания кальция в ки-шечнике [23,24]; повышение активности остеокластов под влиянием ФТ [25]; ингибирование пролиферации остеобла-стов КБЗ или ФТ [6]; дефицит витамина К [26], дефицит кальцитонина [27]; увеличение уровня гомоцистеина [28]. Имеются противоречивые данные исследований о влиянии фермент-индуцирующих ПЭП на биохимические показате-ли костного метаболизма и МПК.…”

Section: традиционные пэпunclassified

Molecular mechanisms responsible for the impact of antiepileptic therapy on bone mineral density of epileptic patients

Жидкова

Казначеева

Демидова

et al. 2016

RJTAO

View full text Add to dashboard Cite

59В настоящее время в мировой эпилептологии накоп-лен научный материал, позволяющий поднять серьезную проблему влияния противоэпилептической терапии на ми-неральную плотность кости (МПК): отмечено, что пациен-ты с эпилепсией подвержены значительно более высокому риску возникновения переломов по сравнению с общей по-пуляцией [1][2][3], а частота развития остеопороза (ОП) у дан-ной категории больных в 1,7 раза выше по сравнению с об-щепопуляционной [4]. Данные изменения связывают с дли-тельным применением противоэпилептических препаратов (ПЭП), типом ПЭП, политерапией и другими факторами [5][6][7][8]. Кроме того, высокая частота приступов, низкая фи-зическая активность, снижение концентрации внимания, координаторные нарушения, вызванные, помимо прочего, и приемом ПЭП, приводят к повышенной травматизации пациентов с эпилепсией [9, 10] и увеличению риска перело-мов, обусловленных ОП.ОП определяется как хроническое системное прогрес-сирующее метаболическое заболевание скелета или клини-ческий синдром при других заболеваниях, характеризую-щийся снижением плотности кости, нарушением микроар-хитектоники и повышением хрупкости костей вследствие нарушения баланса обмена костной ткани с преобладанием процессов рассасывания над процессами образования, по-нижением прочности кости и нарастающим риском перело-мов [9, 11]. Развитию ОП предшествует остеопения, которая

show abstract

Effects of phenytoin and/or vitamin K2 (menatetrenone) on bone mineral density in the tibiae of growing rats

Cited by 40 publications

References 0 publications

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

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

Bone disease in epilepsy

Molecular mechanisms responsible for the impact of antiepileptic therapy on bone mineral density of epileptic patients

Contact Info

Product

Resources

About