Metabolic bone disorders in children with epilepsy

Abstract

Epilepsy during childhood is the most usual neurological disease and it is characterized by recurrent seizures influencing the everyday life of children. As a treatment, antiepileptic drugs (AEDs) affect the bone metabolism resulting in osteoporosis, osteomalacia, rickets, abnormal dentition and increased rate of fractures. Reduced bone mass density (BMD) has been found in the majority of children with epilepsy and a large proportion of these patients has osteoporosis. Furthermore, in many studies the BMD in the epileptic children is significantly lower than in the healthy one. Overall nutritional status affects the manifestation of seizures and the physiology of bone tissue. Especially the levels of vitamin D and calcium play a vital role in the expression of epilepsy related bone disease (ERBD) in children.In parallel, epileptic children should be adequately mobilized as less physical daily activity and inability to walk independently lead to decreased BMD levels which are the major cause of increased number of fractures. Close monitoring of BMD, nutritional status evaluation and prevention of ERBD is as crucial as treatment of epilepsy with antiepileptic drugs, in order to prevent the expression of fractures. Every specialty involved in the treatment of epileptic children must be aware of the consequences of epilepsy in bone tissue.

Genethormonal Outlook of Epilepsy: A Case Report Associated with Catamenial Epilepsy

“…There is strong evidence that patients taking carbamazepine and phenobarbital have decreased alkaline phosphatase levels which are in turn responsible for secondary hyperthyroidism. [18] Reductions in BMD were observed in the subject's taking carbamazepine or VPA, whereas subjects receiving lamotrigine showed no reductions. N-terminal telopeptide (NTX), a urinary marker for bone resorption, also increased.…”

“…This factor is inhibited by phenytoin and phenobarbital. [18] Drugs like phenytoin, phenobarbital and carbamazepine binds to the nuclear receptor Steroid and xenobiotic receptor (SXR) and pregnane X receptor (PXR). PXR translates 25-hydroxyvitamin D3,24-hydroxylase (CYP24) which is responsible for conversion of 25-hydroxyvitamin D to 24,25-dihydroxyvitamin and prevents the formation of active metabolite 1,25dihydroxyvitamin.…”

“…[20] At the same time intake of AEDs leads to sedation vertigo or dizziness which corresponds to increase in chances of bone fracture. [18] Treatment of bone diseases associated with AEDs can be relieved with the help of calcium, vitamin D supplements, bisphosphonates (alendronate and risedronate), hormone replacement, selective estrogen modulators (SERMs), and calcitonin. The daily vitamin D dose ranges from 400 to 4,000 IU [21] Adrenal hormones Chronic use of valproic acid causes an increase in plasma cortisol levels with no significant changes in ACTH levels.…”

Тригерні Фактори Порушення Мінеральної Щільності Кісток У Дітей З Хронічною Неврологічною Патологією (Літературний Огляд)

“…Рівні z-показника МЩК свідчили про остеопенію у 42 (75%) та остеопороз у 14 (25%) пацієнтів. Була відзначена кореляція низької МЩК із Таким чином, незважаючи на неоднозначні результати проведених досліджень, більшість авторів відзначають негативний вплив АЕП на фізіологію кісток та особливо мінеральну щільність кісткової тканини [30,31,32]. Основними предикторами низької МЩК та АЕП-індукованих остеопатій є група АЕП, їх комбінація та тривалість терапії, що проводиться.…”