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卡马西平诱发的高氨血症。

Carbamazepine-induced hyperammonemia.

作者信息

Adams Erin N, Marks Alla, Lizer Mitsi H

机构信息

Bernard J. Dunn School of Pharmacy, Shenandoah University, 1775 North Sector Court, Winchester, VA 22601, USA.

出版信息

Am J Health Syst Pharm. 2009 Aug 15;66(16):1468-70. doi: 10.2146/ajhp080454.

DOI:10.2146/ajhp080454
PMID:19667003
Abstract

PURPOSE

A case of carbamazepine-induced hyperammonemia is presented.

SUMMARY

A 26-year-old man with bipolar disorder, seizures, and mild mental retardation secondary to a traumatic brain injury began treatment with carbamazepine for aggression and seizure control. After three weeks of carbamazepine therapy, the patient arrived at the emergency department (ED) with severe agitation and aggressive behavior. His oral medications included topiramate, carbamazepine, olanzapine, quetiapine, guanfacine, and desmopressin acetate. The patient's medications had been stable for at least six months except for the addition of carbamazepine one month before his arrival at the ED. Upon admission, the patient's vital signs were found to be within normal limits, as were his liver profile results, complete blood count, thyroid-stimulating-hormone level, and serum chemistry panel. His serum carbamazepine concentration was 3.9 microg/mL (reference range, 4-12 microg/mL), and his serum ammonia concentration was 127 microg/dL (reference range, 19-60 microg/dL). Carbamazepine was discontinued upon admission, and the patient was treated with oral lactulose. Since carbamazepine was discontinued and had been prescribed for bipolar disorder, his olanzapine dosage was increased, and trazodone was added at bedtime for insomnia. Of note, the patient had been on carbamazepine therapy one year earlier and had experienced the same adverse event. He had also developed elevated serum ammonia levels while on valproic acid. The patient's serum ammonia level returned to normal by hospital day 4, and he was discharged to his group home.

CONCLUSION

A 26-year-old man with bipolar disorder developed hyperammonemia three weeks after initiating carbamazepine therapy.

摘要

目的

报告一例卡马西平诱发高氨血症的病例。

摘要

一名26岁男性,患有双相情感障碍、癫痫,因创伤性脑损伤继发轻度智力障碍,开始使用卡马西平治疗攻击行为和控制癫痫发作。卡马西平治疗三周后,患者因严重烦躁和攻击性行为被送至急诊科。他的口服药物包括托吡酯、卡马西平、奥氮平、喹硫平、胍法辛和醋酸去氨加压素。除了在入院前一个月加用卡马西平外,患者的药物治疗至少已稳定六个月。入院时,发现患者的生命体征、肝功能检查结果、全血细胞计数、促甲状腺激素水平和血清化学指标均在正常范围内。他的血清卡马西平浓度为3.9微克/毫升(参考范围为4 - 12微克/毫升),血清氨浓度为127微克/分升(参考范围为19 - 60微克/分升)。入院后停用卡马西平,患者接受口服乳果糖治疗。由于卡马西平已停用且曾用于双相情感障碍治疗,故增加了奥氮平的剂量,并在睡前加用曲唑酮治疗失眠。值得注意的是,该患者一年前曾接受卡马西平治疗,也曾发生过相同的不良事件。他在服用丙戊酸时也出现过血清氨水平升高。患者的血清氨水平在住院第4天时恢复正常,随后出院返回集体之家。

结论

一名患有双相情感障碍的26岁男性在开始卡马西平治疗三周后出现高氨血症。

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