Experimental Therapeutics, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, CRC Unit 7 Southeast, Room 7-3445, Bethesda, Maryland, 20892-1285, USA.
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Aug 16;34(6):819-21. doi: 10.1016/j.pnpbp.2010.02.027. Epub 2010 Mar 3.
Recent evidence suggests that purinergic system dysfunction may play a role in the pathophysiology and therapeutics of bipolar disorder (BPD). Uric acid is a key nitrogenous end product of purine metabolism. In addition to being a potential marker of treatment response, high levels of uric acid may represent a state marker during mania. In this study, we assessed the presence of purinergic dysfunction in 20 treatment-naïve first episode patients with BPD who were experiencing a manic episode. Patients were matched with 24 healthy controls. We found that acutely manic patients had significantly higher levels of plasma uric acid (4.85+/-1.60 mg/dL) compared to healthy controls (2.96+/-0.63 mg/dL, p<0.001; F=28.1). No association between uric acid levels with severity of manic symptoms was observed. These results support the role of purinergic system dysfunction in BPD early in the course of illness, and suggest that this phenomenon is not the result of chronicity or medication exposure. Overall, our findings suggest a novel mechanism in the pathophysiology of BPD.
最近的证据表明,嘌呤能系统功能障碍可能在双相障碍(BPD)的病理生理学和治疗中起作用。尿酸是嘌呤代谢的关键含氮终产物。除了作为治疗反应的潜在标志物外,高水平的尿酸可能代表躁狂期间的状态标志物。在这项研究中,我们评估了 20 名未经治疗的首次发作的 BPD 患者在躁狂发作期间嘌呤能功能障碍的存在情况。患者与 24 名健康对照者相匹配。我们发现,急性躁狂患者的血浆尿酸水平明显高于健康对照组(4.85+/-1.60 mg/dL 比 2.96+/-0.63 mg/dL,p<0.001;F=28.1)。尿酸水平与躁狂症状严重程度之间没有关联。这些结果支持嘌呤能系统功能障碍在疾病早期在 BPD 中的作用,并表明这种现象不是慢性或药物暴露的结果。总的来说,我们的发现表明了 BPD 病理生理学中的一个新机制。