Osteoporosis Associated with Epilepsy and the Use of Anti-Epileptics—a Review

Petty, Sandra; Wilding, Helen; Wark, John D.

doi:10.1007/s11914-016-0302-7

Cited by 51 publications

(47 citation statements)

References 124 publications

(151 reference statements)

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“…Also, another study from Nettekoven et al indicated that epilepsy is related with increased bone turnover although physical activity levels were not assessed during their study [29]. Bone biopsy studies in epileptic patients who sustained a fracture have found reduced bone formation and resorption, an increase in the size of haversian canals and an increased resorption of trabecular bone, a degree of osteoporosis, and also increased deposition of osteoid which is suggestive of osteomalacia [17,30].…”

Section: Aeds and Bone Cells And Bone Turnovermentioning

confidence: 98%

“…According to another study by Babayigit et al, oxcarvazepine, carvamazepine and valproate acid have been related to reduced BMD in the lumbar spine of epileptic children which comes along with hypocalcemia, hypophosphatemia and reduced vitamin D levels [16]. Another study by Petty et al compared the BMD in 21 epileptic children and concluded that carvamazepine, compared to valproate, lessen the BMD in L1-L4 in epileptic children [17].…”

Section: Aeds and Vitamin Dmentioning

confidence: 99%

“…Authors suggested that the direct influence of anticonvulsants to osteoblasts and osteoclasts may be one of the major mechanisms which lead to ERBD [7]. However, other studies have proposed that epilepsy is associated with increased bone turnover [4,8,10,11,17,20]. Although the major indication for this association is the elevated ALP levels, this can be also attributed to increased bone absorption as ALP is not a specific biomarker for bone turnover [6].…”

Section: Aeds and Bone Cells And Bone Turnovermentioning

confidence: 99%

“…The trabecular bone of epileptic children has increased resorptive activity and osteoporosis, perhaps due to reduced mobility and also increased levels of osteoid, indicative of osteomalacia [17]. In parallel, less physical daily activity, inability to walk independently and mental retardation lead to diminished levels of BMD, a sign that leads to the statement that decreased daily exercise and worse ambulatory status results to ERBD [3,7,13].…”

Section: Role Of Exercisementioning

confidence: 99%

“…Worst ambulatory status and increased bone mass index (BMI) is related with lower levels of vitamin D [31]. In parallel, the inadequate mobilization of many of the epileptic children has been seen to lead to a degree of osteoporosis due to immobilization [17]. As a result, the level of activity has been seen to be the main predictor of BMD [34].…”

Section: Role Of Exercisementioning

confidence: 99%

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Metabolic bone disorders in children with epilepsy

Manolis¹,

Lepetsos²,

Tzefronis³

et al. 2017

Rheumatol Orthop Med

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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.

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Section: Aeds and Bone Cells And Bone Turnovermentioning

confidence: 98%

Section: Aeds and Vitamin Dmentioning

confidence: 99%

Section: Aeds and Bone Cells And Bone Turnovermentioning

confidence: 99%

Section: Role Of Exercisementioning

confidence: 99%

Section: Role Of Exercisementioning

confidence: 99%

See 3 more Smart Citations

Metabolic bone disorders in children with epilepsy

Manolis¹,

Lepetsos²,

Tzefronis³

et al. 2017

Rheumatol Orthop Med

View full text Add to dashboard Cite

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Pharmacological interventions for bone health in people with epilepsy

Aghoram,

Nair,

Nair

et al. 2024

Cochrane Database of Systematic Reviews

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Osteomalacia and Vitamin D Status: A Clinical Update 2020

et al. 2020

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Historically, rickets and osteomalacia have been synonymous with vitamin D deficiency dating back to the 17th century. The term osteomalacia, which literally means soft bone, was traditionally applied to characteristic radiologically or histologically documented skeletal disease and not just to clinical or biochemical abnormalities. Osteomalacia results from impaired mineralization of bone that can manifest in several types, which differ from one another by the relationships of osteoid (ie, unmineralized bone matrix) thickness both with osteoid surface and mineral apposition rate. Osteomalacia related to vitamin D deficiency evolves in three stages. The initial stage is characterized by normal serum levels of calcium and phosphate and elevated alkaline phosphatase, PTH, and 1,25-dihydroxyvitamin D [1,25(OH) 2 D]-the latter a consequence of increased PTH. In the second stage, serum calcium and often phosphate levels usually decline, and both serum PTH and alkaline phosphatase values increase further. However, serum 1,25 (OH) 2 D returns to normal or low values depending on the concentration of its substrate, 25-hydroxyvitamin D (25OHD; the best available index of vitamin D nutrition) and the degree of PTH elevation. In the final stage, hypocalcemia and hypophosphatemia are invariably low with further exacerbation of secondary hyperparathyroidism. The exact,or even an approximate, prevalence of osteomalacia caused by vitamin D deficiency is difficult to estimate, most likely it is underrecognized or misdiagnosed as osteoporosis. Signs and symptoms include diffuse bone, muscle weakness, and characteristic fracture pattern, often referred to as pseudofractures, involving ribs, scapulae, pubic rami, proximal femurs, and codfish-type vertebrae. The goal of therapy of vitamin D-deficiency osteomalacia is to alleviate symptoms, promote fracture healing, restore bone strength, and improve quality of life while correcting biochemical abnormalities. There is a need for better understanding of the epidemiology of osteomalacia. Simplified tools validated by concurrent bone histology should be developed to help clinicians promptly diagnose osteomalacia.

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Osteoporosis Associated with Epilepsy and the Use of Anti-Epileptics—a Review

Cited by 51 publications

References 124 publications

Metabolic bone disorders in children with epilepsy

Metabolic bone disorders in children with epilepsy

Pharmacological interventions for bone health in people with epilepsy

Osteomalacia and Vitamin D Status: A Clinical Update 2020

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