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用左乙拉西坦治疗首诊癫的疗效及对病人骨代谢和骨密度的影响

Effects of levetiracetam treatment on the patients with first diagnosed epilepsy and bone metabolism and bone mineral density
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摘要 目的:探讨用左乙拉西坦治疗首诊癫的疗效及对病人骨代谢和骨密度的影响。方法:选取2015年6月-2017年5月解放军第一O一医院收治的首诊癫病人66例,分为A组(左乙拉西坦片治疗,33例)和B组(卡马西平治疗,33例),比较两组病人的疗效、药品不良反应(ADRs)及治疗前、治疗后6个月骨代谢和骨密度水平。结果:A组病人与B组病人治疗总有效率比较差异无统计学意义。两组病人头晕、头痛、嗜睡、恶心、呕吐、肝功能损伤、情绪改变发生率比较差异无统计学意义。治疗前,两组病人血钙、血磷、碱性磷酸酶、甲状旁腺激素水平比较差异也无统计学意义。治疗6个月后,B组病人血钙水平低于A组及自身治疗前,血磷、碱性磷酸酶水平高于A组及自身治疗前(P<0.05)。治疗前,两组病人腰椎、股骨大转子、股骨颈、Ward三角骨密度水平比较差异无统计学意义;治疗6个月后,B组病人股骨大转子、股骨颈、Ward三角骨密度较自身治疗前均显著下降(P<0.05);A组病人这些部位骨密度与治疗前比较差异无统计学意义。结论:用左乙拉西坦治疗首诊癫病人具有显著疗效和较高用药安全性,相对卡马西平能减轻对病人骨代谢和骨密度的影响。 Objective: To investigate the curative effects of levetiracetam on the patients with first diagnosed epilepsy , as well as bone metabolism and bone mineral density (BMD). Methods : Totally , 66 cases of first diagnosed epilepsy treated in No. 101 Hospital of PLA from June 2015 to May 2017 were enrolled as study subjects, and were divided into group A (with levetiracetam treatment ,n=33 ) and group B (with carbamazepine treatment , n=33 ). The curative effects , adverse drug reac tions (ADRs), bone metabolism and BMD before treatment and 6 months after treatment were compared between the patients of the 2 groups. Results: Total effective rate of the patients in group A and group B was not statistically different . The rates of dizziness, headache, drowsiness, nausea and vomiting, hepatic function injury and mood change in the patients of both groups were also not statistically different . There was no statistical significance in the levels of serum calcium , phosphorus, alkaline phosphatase and parathyroid hormone, when comparisons were made between the 2 groups before treatment. However, 6 months after treatment , the level of serum calcium in group B was lower than that of group A , and was also lower than that of itself before treatment . The levels of serum phosphorus and alkaline phosphatase in group B were higher than those of group A and were also higher than those itself before treatment (P〈0.05). Before treatment , there was no statistical significance in the bone mass density of lumbar vertebrae , femoral trochanter, femoral neck and Ward triangle in the 2 groups . However, after 6 months of treatment , the BMD of femoral trochanter, femoral neck and Ward triangle of group B decreased significantly , as compared with that before treatment (P〈0.05), while for the patients of group A , there were no statistical differences in the BMD of these sites , when comparisons were made with those before treatment (P〉0.05). Conclusion: Levetiracetam in the treatment of patients with first diagnosed epilepsy could produce significant curative effects with high medication safety . Fur thermore, it could lower the impact on bone metabolism and BMD , as compared with carbamazepine .
作者 万琦 吴佳羽 曹君冬 朱金 WAN Qi;WU JiaYu;CAO JunDong;ZHU Jin(Department of Neurology,No.101 Hospital of PLA,Wuxi Jiangsu 214044,China)
机构地区 解放军第一
出处 《药学服务与研究》 CAS 2018年第5期343-346,共4页 Pharmaceutical Care and Research
关键词 癫痫 左乙拉西坦 药物疗效 卡马西平 骨代谢 骨密度 epilepsy levetiraeetam medicine efficacy carbamazepine bone metabolism bone density
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  • 1Ghodke-Puranik Y, Thom CF, Lamba JK,eZ al. Valproic acidpathway: pharmacokinetics and pharmacodynamics [J]. Phar-macog Genom,2013,23(4): 236-241.
  • 2Amini-Shirazi N,Ahmadkhaniha R,Shadnia al. Determi-nation of VP A and its two important metabolites in iranian o-verdosed patients[J]. Inter J Pharmacol, 2010,6(6) :854-862.
  • 3Dupuis RE’Lichtman SN, Pollack GM. Acute valproic acid o-verdose : Clinical course and pharmacokinetic disposition of val-proic acid and Metabolites [J〕. Drug Saf,1990,5(1): 65-71.
  • 4Loscher W,Nau Htetal. Valproic acid; metabolite concentra-tions in plasma and brain,antic- onvulsant activity and effectson GABA metabolism during subacute treatment in mice[J].Arch Int Pharmacodyn Ther,1982,257(1) :20-31.
  • 5Andrew S, Davison, Anna M, etal. The consequences of val-proate overdose [J]. Clinical Chemistry, 2011,57(9): 1233-1238.
  • 6Mock CM, Schwetschenau KH. Levocarnitine for valproicacid-induced hyperammonemic encephalopathy [ J ]. Am JHealth Syst Pharm, 2012,69(21) : 35-39.
  • 7Lewis C,Deshpande A, Tesar GE,et al. Valproate-inducedhyperainnionemic encephalopathy : a brief review[J]. Curr MedResOpin,2012,28(6); 1039-1042.
  • 8Otoul C, De Smedt H, Stockis A. Lack of pharmacokinetic in-teraction of LEV on carbamazepine,valproic acid, topiramate,and lamotrigine in children with epilepsy[J]. Epilepsia, 2007,48(11):2111-2115.
  • 9Roh SY, Jang HS, Jeong EH, et al. Valproic acid-induced hy-perammonemic encephalopathy promoted by levetiracetam [J].J Epilepsy Res, 2014,4(2) :82-84.
  • 10Jayakumar S, Thomas KH. Assessment of the role of in situGenerated (E)-2,4 diene-valproic acid in the toxicity of valpro-ic acid and (E )-2-ene-valproic acid in sandwich-cultured rathepatocytes[J]. Toxicol Appl Pharmacol, 2012, 264 (3) : 413-422.

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