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普鲁卡因胺毒性所致的小脑性共济失调。

Cerebellar ataxia due to procainamide toxicity.

作者信息

Schwartz A B, Klausner S C, Yee S, Turchyn M

出版信息

Arch Intern Med. 1984 Nov;144(11):2260-1.

PMID:6497531
Abstract

It has become appreciated that drug levels of procainamide hydrochloride needed to suppress inducible ventricular tachycardia by programmed ventricular stimulation exceed the previously published therapeutic range. Cerebellar ataxia developed acutely in a patient receiving high-dose procainamide. This was associated with a marked increase in the serum drug level. Resolution occurred within three days after drug therapy was discontinued.

摘要

现已认识到,通过程控心室刺激抑制可诱发的室性心动过速所需的盐酸普鲁卡因胺药物水平超过了先前公布的治疗范围。一名接受高剂量普鲁卡因胺治疗的患者急性出现小脑共济失调。这与血清药物水平的显著升高有关。在停药后三天内症状消退。

相似文献

1
Cerebellar ataxia due to procainamide toxicity.普鲁卡因胺毒性所致的小脑性共济失调。
Arch Intern Med. 1984 Nov;144(11):2260-1.
2
Electropharmacologic testing in sustained ventricular tachycardia associated with coronary heart disease: value of the response to intravenous procainamide in predicting the response to oral procainamide and oral quinidine treatment.
Am J Cardiol. 1985 Nov 15;56(13):883-6. doi: 10.1016/0002-9149(85)90775-1.
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Thrombocytopenia following sustained-release procainamide.缓释普鲁卡因胺后的血小板减少症。
Arch Intern Med. 1985 Apr;145(4):700-2.
4
Sustained-release procainamide: use of serum concentrations to determine dosage.缓释普鲁卡因胺:利用血清浓度确定剂量。
South Med J. 1985 Oct;78(10):1190-3.
5
[Novocainamide in the treatment of paroxysmal supraventricular tachycardia and auricular fibrillation in premature ventricular excitation syndrome (relation between novocainamide dose, its blood level, and antiarrhythmia effect)].[新斯的明治疗室性早搏综合征中的阵发性室上性心动过速和心房颤动(新斯的明剂量、血药浓度与抗心律失常作用的关系)]
Ter Arkh. 1982;54(3):92-6.
6
[Transitory cerebellar ataxia from high dosage combination thymoleptic therapy].[高剂量联合抗抑郁药治疗所致的短暂性小脑共济失调]
Pharmacopsychiatria. 1983 Mar;16(2):64-7. doi: 10.1055/s-2007-1017451.
7
Interaction of bisoprolol and procainamide in human cardiac impulse generation and conduction.比索洛尔与普鲁卡因胺在人体心脏冲动产生与传导中的相互作用。
J Cardiovasc Pharmacol. 1990;16 Suppl 5:S193-5.
8
[Lethal arrhythmias in a patient with coarctation of the aorta and severe heart failure: their control by combination of low dose amiodarone with procainamide for 3 years].[一名主动脉缩窄合并严重心力衰竭患者的致死性心律失常:低剂量胺碘酮与普鲁卡因胺联合应用3年对其进行控制]
Kokyu To Junkan. 1993 Nov;41(11):1107-11.
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Bone marrow granulomas and neutropenia associated with procainamide. Report of a case.
Arch Intern Med. 1978 Nov;138(11):1731-2.
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Pure red cell aplasia associated with administration of sustained-release procainamide.与缓释普鲁卡因胺给药相关的纯红细胞再生障碍。
Arch Intern Med. 1987 Jun;147(6):1179-80.

引用本文的文献

1
Adverse effects of class I antiarrhythmic drugs.I类抗心律失常药物的不良反应。
Drug Saf. 1997 Jul;17(1):8-36. doi: 10.2165/00002018-199717010-00002.
2
Myopathy after short term administration of procainamide.短期服用普鲁卡因胺后出现的肌病。
Br Med J (Clin Res Ed). 1986 Mar 1;292(6520):593-4. doi: 10.1136/bmj.292.6520.593.
3
Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide.IA类抗心律失常药物中毒。奎尼丁、普鲁卡因胺和丙吡胺。
Drug Saf. 1990 Nov-Dec;5(6):393-420. doi: 10.2165/00002018-199005060-00002.