Seizure after pulse therapy with methyl prednisolone.
Seizure after pulse therapy with methyl prednisolone.
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甲基泼尼松龙冲击治疗后癫痫发作。
DOI：
10.1002/art.1780260123
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发表时间：
1983
影响因子：
--
通讯作者：
J. Leddy
中科院分区：
文献类型：
--
作者：
A. Suchman;J. J. Condemi;J. Leddy
我们希望报告一个潜在的并发症，静脉注射（IV）甲基强的松龙脉冲治疗，很少受到关注，迄今在风湿性疾病的文献。我们治疗的狼疮性肾炎患者在完成3天的高剂量甲泼尼龙静脉注射疗程后68小时首次全身性癫痫发作。他的案件概述如下。一位32岁男性电子技师于1972年罹患全身性狼疮，表现为脱发、疲劳、肾小球肾炎。肾病综合征、胸膜炎和心包炎。他对环磷酰胺和泼尼松反应良好。在接下来的6年里，他每天服用泼尼松，在此期间，他的疾病处于静止状态。1979年，肾病综合征复发，伴有高血压和严重的雷诺氏综合征伴指梗死。他最初接受常规剂量的泼尼松治疗。但经过这种治疗，他的尿蛋白损失达到了9 gdday。因此，他开始用甲基强的松龙进行脉冲治疗（每天1次，连续3天）;在1981年4月至1982年3月期间，他接受了6个疗程（3次口服，3次静脉注射）。患者突然出现左臂不自主运动和有节奏的喘息吸气。他倒在地板上不省人事，他的妻子观察到左臂和左腿强直阵挛性运动和喘鸣性呼吸。发作持续了3-5分钟，在此期间，他咬了舌头，但没有失禁。之后的5分钟里，他仍然昏迷不醒，又昏迷了30分钟。当他到达医院时，他已经完全清醒了。安伐他汀显示，他的血压为148/92。检查中唯一的异常是弥漫性反射亢进。不存在局灶性或偏侧性神经系统体征。他没有头部创伤、临床上明显的狼疮性脑炎或其他已知的神经系统疾病的病史。入院时，他的常规药物为泼尼松（80 mg，每隔一天）、吡唑星（2 mg，每日两次）和阿司匹林（325 mg，每日两次）。患者未接受利尿剂治疗。脑电图头部计算机轴向断层扫描和脊髓液分析均正常。入院时的其他相关实验室检查值为：肌酐，1.3 mg%;血尿素氮。23 mg%;钠，138 mEq/L;钾，3.5 mEq/L; CO？，31 mEq/L;白蛋白，3.0 gm%;总蛋白。5.1 gm%; 24小时尿蛋白3.5抗核抗体。未稀释-强阳性，边缘模式（I：100阴性）;抗DNA抗体（crithidia试验）。弱阳性：C3，正常; C4，正常; CHSO，78（正常> 80）;放射性-Clq结合试验，阴性。他没有出现额外的癫痫发作，
We wish to report a potential complication of pulse therapy with intravenous (IV) methyl prednisolone which has received little attention to date in the rheumatic diseases literature. A patient whom we have treated for lupus nephritis experienced his first generalized seizure 68 hours after completing a 3-day course of high-dose IV methyl prednisolone. His case is summarized below. A 32-year-old male electronics technician developed systemic lupus in 1972, presenting with alopecia, fatigue, glomerulonephritis. nephrotic syndrome, pleuritis, and pericarditis. He responded well to cyclophosphamide and prednisone. He was maintained for the next 6 years on daily prednisone, during which time his disease was quiescent. In 1979 the nephrotic syndrome returned, accompanied by hypertension and severe Raynaud’s syndrome with digital infarction. He was treated initially with conventional doses of prednisone. but with this treatment his urinary protein loss reached 9 gdday. Therefore, he began pulse therapy with methyl prednisolone (I &day for 3 successive days); he received 6 courses (3 oral, 3 intravenous) between April 1981 and March 1982.Three days after his most recent pulse therapy (administered intravenously over 15 minutes). the patient abruptly developed involuntary movements of his left arm and rhythmic, gasping inspirations. He fell to the floor unconscious, whereupon tonic clonic movements of the left arm and leg and stridorous respirations were observed by his wife. The episode lasted 3-5 minutes, during which time he bit his tongue but was not incontinent. For 5 minutes afterward he remained unconscious, and he was confused for another 30 minutes. By the time he reached the hospital, he was fully alert. On amval, his blood pressure was 148/92. The only abnormality on examination was diffuse hyperreflexia. No focal or lateralizing neurologic signs were present. He had no history of head trauma, clinically evident lupus cerebritis, or other known neurologic disease. At the time of admission, his regular medications were prednisone (80 mg every other day), prazocin (2 mg twice a day), and aspirin (325 mg twice a day). He was receiving no diuretic drug. Electroencephalography. computed axial tomography of the head, and spinal fluid analysis were all normal. Other pertinent laboratory values at the time of admission were: creatinine, 1.3 mg%; blood urea nitrogen. 23 mg%; sodium, 138 mEqAiter; potassium, 3.5 mEq/liter; CO?, 31 mEq/liter; albumin, 3.0 gm%; total protein. 5.1 gm%; 24-hour urine protein. 3.5 gm; antinuclear antibodies. undiluted-strongly positive, rim pattern (I: 100 negative); antiDNA antibody (crithidia assay). weakly positive: C3, normal; C4, normal; CHSO, 78 (normal> 80); radio-Clq binding assay, negative. He experienced no additional seizures and was