Neonatology Research Center, Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz Endocrinology and Metabolism Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
J Bone Miner Metab. 2019 May;37(3):537-544. doi: 10.1007/s00774-018-0951-y. Epub 2018 Sep 6.
Epilepsy might have adverse effect on bone density due to underlying disease, drugs, vitamin D deficiency, immobilization and malnutrition. We investigated the bone mineral density in ambulatory vitamin-D supplemented children with epilepsy. This case-control study was conducted on 90 epileptic children aged 11.4 ± 3.3 years, and age and gender matched controls in pediatric neurology clinics of Shiraz, in Southern Iran, 2016. Anthropometric measurements, puberty, sun exposure, physical activity and biochemical variables were assessed. Bone mineral density was evaluated by dual-energy X-ray absorptiometry method. Data were analyzed by SPSS.v21. Prevalence of low bone mass in femur was more in patients (27%) than the controls (9%) (P value = 0.002). Age, weight Z score and height Z score were the most significant associated factors on lumbar BMD, BMAD, and femur BMD. Seizure duration and how it responded to anticonvulsants were the most associated factors with both lumbar and femur bone density. Sodium valproate and carbomazepin usage had negative association with lumbar Z score (beta = - 0.216, P = 0.017 and beta = - 0.336, P = 0.027, respectively). We hypothesized that epilepsy per se could affect bone density by an unknown pathophysiology, which was independent from vitamin D deficiency, effects of anticonvulsant and physical activity.
癫痫可能由于潜在疾病、药物、维生素 D 缺乏、固定和营养不良对骨密度产生不利影响。我们研究了接受维生素 D 补充的门诊癫痫儿童的骨矿物质密度。这项病例对照研究于 2016 年在伊朗南部设拉子的儿科神经病学诊所进行,共纳入 90 名年龄为 11.4±3.3 岁的癫痫患儿和年龄、性别匹配的对照组。评估了人体测量学测量、青春期、阳光暴露、身体活动和生化变量。通过双能 X 射线吸收法评估骨矿物质密度。数据采用 SPSS.v21 进行分析。与对照组(9%)相比,患者(27%)股骨低骨量的患病率更高(P 值=0.002)。年龄、体重 Z 评分和身高 Z 评分是与腰椎 BMD、BMAD 和股骨 BMD 最显著相关的因素。癫痫发作持续时间及其对抗癫痫药物的反应是与腰椎和股骨骨密度最相关的因素。丙戊酸钠和卡马西平的使用与腰椎 Z 评分呈负相关(β=-0.216,P=0.017 和β=-0.336,P=0.027)。我们假设癫痫本身可能通过一种未知的病理生理学机制影响骨密度,这种机制独立于维生素 D 缺乏、抗癫痫药物的作用和身体活动。