Bartoli Francesco, Crocamo Cristina, Dakanalis Antonios, Brosio Enrico, Miotto Alessio, Capuzzi Enrico, Clerici Massimo, Carrà Giuseppe
Department of Medicine and Surgery, University of Milano Bicocca, Via Cadore 48, Monza 20900, Italy.
Department of Medicine and Surgery, University of Milano Bicocca, Via Cadore 48, Monza 20900, Italy.
Compr Psychiatry. 2017 Feb;73:1-6. doi: 10.1016/j.comppsych.2016.09.011. Epub 2016 Sep 30.
Subjects with bipolar mania may have increased uric acid levels, based on a purinergic system dysfunction with reduced neurotransmission of adenosine. We investigated whether there were differences in uric acid levels between individuals with bipolar disorder (in manic or depressive phases) and those with major depressive disorder.
We conducted a cross-sectional study recruiting 128 subjects with bipolar disorder and 118 with major depressive disorder, admitted to a psychiatric inpatient unit. Standard demographic and clinical information were retrieved from electronic charts and relevant clinical records. Fasting serum values of uric acid, as well as metabolic (total cholesterol, triglycerides, and glycaemia), oxidative stress (albumin, bilirubin), and kidney function (creatinine), parameters, were collected.
Subjects with bipolar mania (5.27±1.63mg/dL), but not those with bipolar depression (4.89±1.94mg/dL), had higher levels of serum uric acid (p<0.05), as compared with individuals with major depressive disorder (4.59±1.62mg/dL). Relevant linear regression analyses, controlling for metabolic profile, oxidative stress markers, kidney function, and comorbid alcohol use disorder, showed a significant association between bipolar mania (p<0.01) and increased uric acid.
Findings of this study add evidence to the role of uric acid as state, rather than trait, marker in bipolar disorders. Explored, relevant, confounders do not seem to influence these results. The current study supports the hypothesis of a purinergic system dysfunction associated with manic phases of bipolar disorder.
基于嘌呤能系统功能障碍及腺苷神经传递减少,双相躁狂症患者可能存在尿酸水平升高的情况。我们调查了双相情感障碍患者(处于躁狂或抑郁阶段)与重度抑郁症患者之间尿酸水平是否存在差异。
我们进行了一项横断面研究,招募了128名双相情感障碍患者和118名重度抑郁症患者,这些患者均入住精神科住院部。从电子病历和相关临床记录中获取标准的人口统计学和临床信息。收集尿酸的空腹血清值,以及代谢参数(总胆固醇、甘油三酯和血糖)、氧化应激参数(白蛋白、胆红素)和肾功能参数(肌酐)。
与重度抑郁症患者(4.59±1.62mg/dL)相比,双相躁狂症患者(5.27±1.63mg/dL)的血清尿酸水平较高,但双相抑郁症患者(4.89±1.94mg/dL)并非如此(p<0.05)。在控制了代谢谱、氧化应激标志物、肾功能和合并酒精使用障碍的相关线性回归分析中,双相躁狂症与尿酸升高之间存在显著关联(p<0.01)。
本研究结果为尿酸作为双相情感障碍的状态而非特质标志物的作用提供了证据。所探讨的相关混杂因素似乎并未影响这些结果。当前研究支持与双相情感障碍躁狂阶段相关的嘌呤能系统功能障碍的假说。