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首页> 外文期刊>The Internet Journal of Neurology >A Case Of Hyperammonemic Encephalopathy Due To Valproate And Topiramate Combination At High Doses
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A Case Of Hyperammonemic Encephalopathy Due To Valproate And Topiramate Combination At High Doses

机译：丙戊酸和托吡酯联合高剂量引起的高氨血症性脑病一例

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A 35 years old male patient was admitted for a mental and behavioral disorder during the last two months. He had been treated for intractable epilepsy with valproate for many years. Topiramate was added in the previous year without any adverse reactions. Due to increased seizure frequency, the dosages of both drugs were increased gradually. Following the adjustment of drug regimen as 2000 mgs valproate and 400 mgs topiramate daily, the patient presented an encephalopaty with prominent delta and theta waves in EEG. Either serum liver enzymes or serum valproate levels showed no abnormality, but ammonia level had had rised up to 2 folds of normal. After withdrawal of topiramate and then valproate the symptoms resolved and ammonia level fell into the normal limits. The diagnosis of hyperammonemic encephalopathy due to treatment with the combination of valproate and topiramate was supposed. In our patient, the halopathic features had extraordinarily appeared after elevation of both antiepileptic drugs to high levels, while no adverse reactions had observed with moderately low doses. While treating patients with intractable epilepsy, complications of combinations should be carefully considered in desicion making not only for initiation but also for follow-up of drug adjustments. Introduction Hyperammonemic encephalopathy (HE) is a nonspecific encephalopathy appearing in patients under valproate (VPA) treatment [1]. Serum ammonia levels are consistently high without any other biochemical abnormality. Recently a few cases were reported under topiramate (TPM) and VPA [2]. Here, we present a case of HE who tolerated this combination well at low doses, but developed encephalopathy following the elevation the dosages of both drugs. Case Report A thirty five years old male patient, with a history of intractable epilepsy of 15 years was admitted for aggressive behavior which was going on for the last 2 months. The frequency of complex partial seizures was more than 10 monthly, so that we decided to add TPM 200mgs to existing drug regimen, VPA 1000mgs. During the following year a good control of epileptic seizures was achieved. However the seizures recurred then, which led us to elevate the dosages of VPA to 2000mgs and TPM to 400mgs sequentially. After a short time interval under these high dosages, the patient became drowsy and lost sphincter control. He exhibited abnormal behaviors like playing with his faeces. In the second month of this presentation he's been hospitalized because of gradual worsening of his symptoms.The neurologic examination at the admission revealed a stuporous man in a good general health. He was oriented for people, but not place and time. Urinary and faecal sphincter control was lost. The rest of neurologic examinations were normal. He had no pathologic reflexes or meningeal irritation.CBC, blood sugar, BUN, creatinine, AST, ALT, GGT, creatin kinase, potassium, calcium and sodium levels were normal including thyroid function tests. VPA serum level was 64.3 microg/dl, which was also normal. Arterial ammonia level was 196 microgr/dl (N:17-80). Carnitine serum level was normal. A routine EEG showed diffuse slowing of background activity with prominent delta and theta waves (Figure 1). Cranial MRI was normal.This patient exhibited an encephalopathy with normal liver, renal and thyroid functions. With normal VPA and elevated serum ammonia levels, the diagnosis of HE was supposed. TPM and VPA were stopped with tapering and levetiracetam (LEV) was initiated. The patient gained his consciousness but this resulted in an increase of seizure frequency. Carbamazepine (CBZ) was added. In the last examination, he was receiving CBZ1600mgs and LEV 2000mgs daily. He was fully oriented with 2-3 seizures monthly. His EEG was also recovered (Figure2). The arterial blood ammonia level was normal (39,8microgr/dl).
机译：最近两个月，一名35岁的男性患者因精神和行为障碍而入院。他因丙戊酸盐治疗顽固性癫痫病已有多年治疗。托吡酯在前一年加入，没有任何不良反应。由于癫痫发作频率增加，两种药物的剂量逐渐增加。每天调整药物剂量为丙戊酸2000毫克和托吡酯400毫克后，该患者出现脑病，脑电图中出现明显的δ波和θ波。血清肝酶或丙戊酸盐水平均未见异常，但氨水平已上升至正常水平的2倍。停用托吡酯和丙戊酸盐后，症状缓解，氨水平降至正常范围。假定诊断为丙戊酸盐和托吡酯联合治疗导致的高氨性脑病。在我们的患者中，两种抗癫痫药均升高至高水平后，出现了特别的晕影特征，而中度低剂量未观察到不良反应。在治疗顽固性癫痫患者时，应在联合决策过程中认真考虑联合使用的并发症，不仅要考虑药物的启动，还应跟踪药物调整的随访。简介高氨血症性脑病（HE）是丙戊酸盐（VPA）治疗患者中出现的一种非特异性脑病[1]。血清氨水平始终很高，没有任何其他生化异常。最近报道了几例托吡酯（TPM）和VPA治疗[2]。在这里，我们介绍了一个HE病例，该患者在低剂量时能很好地耐受这种组合，但是在两种药物的剂量增加后都会出现脑病。病例报告一名患有顽固性癫痫病史为15岁的35岁男性患者因侵略性行为而入院，该行为持续了最近两个月。复杂的部分性发作的频率每月超过10次，因此我们决定在现有的药物治疗方案中将TPM 200mgs加到VPA 1000mgs上。在接下来的一年中，癫痫发作得到了很好的控制。然而，随后发作再次发作，导致我们依次将VPA的剂量提高至2000mgs，将TPM的剂量提高至400mgs。在这些高剂量下短暂的时间间隔后，患者昏昏欲睡，失去了括约肌控制能力。他表现出不正常的行为，例如与他的粪便玩耍。在本次演讲的第二个月，由于症状逐渐恶化，他已住院。入院时的神经系统检查显示他的身体状况良好，身材矮胖。他为人着想，但没有时间和地点。尿和粪便括约肌失去控制。其余神经系统检查均正常。他没有病理反射或脑膜刺激.CBC，血糖，BUN，肌酐，AST，ALT，GGT，肌酐激酶，钾，钙和钠水平正常，包括甲状腺功能检查。 VPA血清水平为64.3 microg / dl，也正常。动脉氨水平为196 microgr / dl（N：17-80）。肉碱血清水平正常。例行脑电图显示背景活动呈弥漫性减慢，并伴有明显的δ波和θ波（图1）。颅脑MRI正常，该患者表现出脑病，肝，肾和甲状腺功能正常。如果VPA正常且血清氨水平升高，则可以诊断为HE。逐渐减少TPM和VPA，并开始使用左乙拉西坦（LEV）。患者意识增强，但癫痫发作频率增加。添加了卡马西平（CBZ）。在上次检查中，他每天接受CBZ1600mgs和LEV 2000mgs。他完全适应，每月发作2-3次。他的脑电图也被恢复（图2）。动脉血氨水平正常（39,8microgr / dl）。

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