Sivakova Natalia, Abramova Irina, Trukhina Irina, Rybasova Varvara, Sorokin Mikhail, Kasyanov Evgeny, Lukina Larisa, Mikhailov Vladimir, Mazo Galina
Consort Psychiatr. 2025 Jun 27;6(2):5-20. doi: 10.17816/CP15553. eCollection 2025.
Anticonvulsants are widely used in treating patients with mental and neurological disorders. Their long-term use increases the risk of a decrease in bone mineral density (BMD) and low-energy fractures. Despite the growing number of studies of drug-induced osteoporosis, the effect of anticonvulsants on bone microarchitecture remains poorly studied.
To study the effect of treatment duration with different generations of anticonvulsants on bone mineral density and fracture risk.
We examined 100 adult patients with epilepsy who had been on anticonvulsants for more than 12 months and 58 healthy subjects who had never taken anticonvulsants. All the participants underwent a general clinical and neuropsychological assessment, as well as bone densitometry using quantitative computed tomography in three regions of interest (lumbar vertebrae L1, L2 and femoral neck).
BMD reductions were observed in 47 patients (47%) taking anticonvulsants and 29 (50%) subjects in the control group. The mean duration of anticonvulsant therapy was 8.7 years (SD=8.05) in patients with normal BMD, 10.7 years (SD=7.07) in patients with osteopenia, and 9.5 years (SD=5.24) in patients with osteoporosis. Age was found to significantly affect BMD, while the duration of anticonvulsant therapy affected it to a lesser extent. Patients taking first-generation anticonvulsants had lower BMD (=0.018). ROC analysis confirmed the existence of a relationship between the duration of anticonvulsant therapy and the risk of fractures (<0.001). The "duration of anticonvulsant therapy" threshold at the cut-off point corresponding to the highest Youden index value was 10 years.
Long-term treatment with conventional anticonvulsants adversely affects BMD and can lead to pathological bone resorption, increasing the risk of fractures in patients. New-generation anticonvulsants did not show any significant negative impact on BMD. The results of this study indicate the need for further research to better understand the effects of anticonvulsants on bone tissue.
抗惊厥药物广泛用于治疗精神和神经疾病患者。长期使用会增加骨密度(BMD)降低和低能量骨折的风险。尽管药物性骨质疏松的研究越来越多,但抗惊厥药物对骨微结构的影响仍研究不足。
研究不同代抗惊厥药物的治疗持续时间对骨密度和骨折风险的影响。
我们检查了100名服用抗惊厥药物超过12个月的成年癫痫患者和58名从未服用过抗惊厥药物的健康受试者。所有参与者均接受了一般临床和神经心理学评估,以及使用定量计算机断层扫描在三个感兴趣区域(腰椎L1、L2和股骨颈)进行骨密度测定。
服用抗惊厥药物的47名患者(47%)和对照组的29名受试者(50%)观察到骨密度降低。骨密度正常的患者抗惊厥治疗的平均持续时间为8.7年(标准差=8.05),骨量减少患者为10.7年(标准差=7.07),骨质疏松患者为9.5年(标准差=5.24)。发现年龄对骨密度有显著影响,而抗惊厥治疗的持续时间对其影响较小。服用第一代抗惊厥药物的患者骨密度较低(=0.018)。ROC分析证实抗惊厥治疗持续时间与骨折风险之间存在关联(<0.001)。对应最高约登指数值的截断点处的“抗惊厥治疗持续时间”阈值为10年。
传统抗惊厥药物的长期治疗对骨密度有不利影响,并可导致病理性骨吸收,增加患者骨折风险。新一代抗惊厥药物对骨密度未显示出任何显著的负面影响。本研究结果表明需要进一步研究以更好地了解抗惊厥药物对骨组织的影响。