Oslo University Hospital, National Centre for Epilepsy, Division for Clinical Neuroscience, Section for Adult Epileptology, Department of Neurology, P.O. Box 53, 1306 Baerum Postterminal, G.F. Henriksens vei 23, Sandvika 1337, Oslo 0027, Norway.
Expert Opin Drug Saf. 2010 Jul;9(4):561-71. doi: 10.1517/14740331003636475.
Epilepsy is a neurological disorder associated with several comorbidities, one of them being reduced bone health. As the bone loss most often is insidious and asymptomatic, they are usually not recognized, and thus untreated. The key message of this paper is to make clinicians aware of the problem.
This article reviews data from basic and clinical studies of bone loss associated with usage of antiepileptic drugs (AEDs) within the last 4 decades.
The reader will learn that there is accumulating evidence of biochemical abnormalities indicating a disturbed bone metabolism, a decreased bone density and a 2 - 6 times increased risk of fractures among those with epilepsy compared to the general population. These findings most likely have many causes, both internal and external, but long-term use of AEDs seems to play an important role. Enzyme-inducing drugs, such as phenytoin, phenobarbital and carbamazepine, but also the enzyme inhibitor valproate, appear to have bone-depleting properties. Reduced bone density may be detected during the first 1 - 5 years of treatment. Although many theories have been launched, the exact mechanisms by which the the drugs affect bone architecture are not fully understood.
We recommend clinicians to promote osteoprotective behavior among their epilepsy patients; that is, sunlight exposure and weight-bearing exercise as well as avoidance of risk factors such as bone-depleting drugs other than AEDs, smoking and heavy alcohol consumption. Enzyme inducing drugs should be avoided, if possible. Bone mineral density screening should be assessed on an individual basis, taking risk factors for bone loss into account. All patients taking AEDs on long-term basis ought to have adequate amounts of dietary calcium and vitamin D, and those who have developed bone loss should in addition be given specific antiosteoporotic treatment.
癫痫是一种与多种合并症相关的神经障碍，其中之一是骨骼健康状况下降。由于骨质流失通常是隐匿且无症状的，因此通常无法被识别，也因此得不到治疗。本文的关键信息是让临床医生意识到这个问题。
本文综述了过去 40 年来与抗癫痫药物（AEDs）使用相关的骨丢失的基础和临床研究数据。
读者将了解到，有越来越多的证据表明，生化异常表明骨代谢紊乱、骨密度降低以及癫痫患者骨折风险增加 2-6 倍，与普通人群相比。这些发现可能有许多原因，包括内在和外在的，但长期使用 AEDs 似乎起着重要作用。酶诱导药物，如苯妥英、苯巴比妥和卡马西平，以及酶抑制剂丙戊酸，似乎具有耗骨特性。在治疗的头 1-5 年内可能会检测到骨密度降低。尽管提出了许多理论，但这些药物影响骨骼结构的确切机制尚未完全了解。
我们建议临床医生鼓励其癫痫患者采取护骨行为；即阳光暴露和负重运动，以及避免除 AED 以外的耗骨药物、吸烟和大量饮酒等危险因素。如果可能的话，应避免使用酶诱导药物。应根据个体情况评估骨矿物质密度筛查，考虑到骨质流失的危险因素。所有长期服用 AED 的患者都应摄入足够的膳食钙和维生素 D，对于已经发生骨质流失的患者，还应给予特定的抗骨质疏松治疗。
