Hinz Marty, Stein Alvin, Cole Ted
Clinical Research, NeuroResearch Clinics, Cape Coral, FL, USA.
Stein Orthopedic Associates, Plantation, FL, USA.
Clin Pharmacol. 2014 Nov 14;6:189-94. doi: 10.2147/CPAA.S72234. eCollection 2014.
When l-dopa use began in the early 1960s for the treatment of Parkinson's disease, nausea and reversible dyskinesias were experienced as continuing side effects. Carbidopa or benserazide was added to l-dopa in 1975 solely to control nausea. Subsequent to the increasing use of carbidopa has been the recognition of irreversible dyskinesias, which have automatically been attributed to l-dopa. The research into the etiology of these phenomena has identified the causative agent of the irreversible dyskinesias as carbidopa, not l-dopa. The mechanism of action of the carbidopa and benserazide causes irreversible binding and inactivation of vitamin B6 throughout the body. The consequences of this action are enormous, interfering with over 300 enzyme and protein functions. This has the ability to induce previously undocumented profound antihistamine dyskinesias, which have been wrongly attributed to l-dopa and may be perceived as irreversible if proper corrective action is not taken.
20世纪60年代初开始使用左旋多巴治疗帕金森病时，恶心和可逆性运动障碍一直是其副作用。1975年，卡比多巴或苄丝肼被添加到左旋多巴中，仅仅是为了控制恶心。随着卡比多巴使用的增加，人们认识到了不可逆性运动障碍，而这些障碍自动被归因于左旋多巴。对这些现象病因的研究已经确定，不可逆性运动障碍的致病因素是卡比多巴，而非左旋多巴。卡比多巴和苄丝肼的作用机制会导致维生素B6在全身发生不可逆的结合和失活。这种作用的后果是巨大的，会干扰300多种酶和蛋白质的功能。这有可能诱发以前未被记录的严重抗组胺药运动障碍，这些障碍被错误地归因于左旋多巴，如果不采取适当的纠正措施，可能会被视为不可逆的。
