Zesiewicz Theresa A, Wecker Lynn, Sullivan Kelly L, Merlin Lisa R, Hauser Robert A
Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, 33612, USA.
Clin Neuropharmacol. 2006 May-Jun;29(3):106-11. doi: 10.1097/01.WNF.0000220817.94102.95.
Levodopa treatment of Parkinson disease results in hyperhomocysteinemia (HHcy) as a consequence of levodopa methylation by catechol-O-methyltransferase (COMT). Although inhibition of COMT should theoretically prevent or reduce levodopa-induced HHcy, results from several prospective studies are conflicting. Our review of these studies suggests that the ability of COMT inhibition to reduce or prevent levodopa-induced HHcy in Parkinson disease patients may be attributed to differences in the vitamin status of the study participants. In patients with low or low-normal folate levels, levodopa administration is associated with a greater increase in homocysteine and concomitant entacapone administration is associated with a greater reduction in homocysteine.
左旋多巴治疗帕金森病会导致高同型半胱氨酸血症（HHcy），这是儿茶酚-O-甲基转移酶（COMT）对左旋多巴进行甲基化的结果。虽然理论上抑制COMT应能预防或减轻左旋多巴诱导的HHcy，但几项前瞻性研究的结果相互矛盾。我们对这些研究的综述表明，COMT抑制在帕金森病患者中减轻或预防左旋多巴诱导的HHcy的能力，可能归因于研究参与者维生素状态的差异。在叶酸水平低或略低于正常水平的患者中，服用左旋多巴会使同型半胱氨酸水平有更大幅度升高，而同时服用恩他卡朋则会使同型半胱氨酸水平有更大幅度降低。
