1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 2(nd) Department of Neurology, Attikon Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Parkinsonism Relat Disord. 2021 Mar;84:1-4. doi: 10.1016/j.parkreldis.2020.12.020. Epub 2021 Jan 20.
Blood uric acid represents an important biomarker in sporadic Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is beginning to be assessed. The aim of the present study was to evaluate differences in serum uric acid level among PD patients harboring mutations in the glucocerebrosidase (GBA1) gene, sporadic PD, and healthy controls followed longitudinally.
Longitudinal 2-year serum uric acid measurement data of 120 GBA-PD patients have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. This cohort was compared with 369 de novo sporadic PD patients and 195 healthy controls enrolled in the same study.
Following adjustment for age, sex and BMI the GBA-PD cohort exhibited lower 2-year longitudinal uric acid level as compared to the controls (p = 0.016). Baseline uric acid measurements showed only a marginal difference (p = 0.119), but year 2 uric acid levels were lower in the GBA-PD cohort (p < 0.001). There was no difference in baseline, year 2 and 2-year longitudinal serum uric acid in the GBA-PD cohort as compared to sporadic PD (p = 0.664, p = 0.117 and p = 0.315).
This is the first study to assess serum uric acid in a GBA-PD cohort. Our findings suggest that low serum uric acid might be a progression biomarker in GBA-PD. However, more studies (ideally longitudinal) on the association between low serum uric acid and clinical data in GBA-PD are needed. These results are consistent with data from previous reports assessing uric acid as a biomarker in other genetic forms of PD.
血尿酸是散发性帕金森病（PD）的重要生物标志物。尿酸水平在 PD 的遗传形式中是否发生变化，目前正开始评估。本研究旨在评估携带葡萄糖脑苷脂酶（GBA1）基因突变的 PD 患者、散发性 PD 患者和健康对照组的血清尿酸水平差异，并进行纵向随访。
从帕金森进展标志物倡议（PPMI）数据库中下载了 120 名 GBA-PD 患者的 2 年纵向血清尿酸测量数据。该队列与同一研究中纳入的 369 名首发散发性 PD 患者和 195 名健康对照进行了比较。
校正年龄、性别和 BMI 后，GBA-PD 队列的 2 年纵向尿酸水平低于对照组（p=0.016）。基线尿酸测量值仅显示出轻微差异（p=0.119），但 GBA-PD 队列的第 2 年尿酸水平较低（p<0.001）。与散发性 PD 相比，GBA-PD 队列在基线、第 2 年和 2 年纵向血清尿酸水平方面没有差异（p=0.664、p=0.117 和 p=0.315）。
这是第一项评估 GBA-PD 队列中血清尿酸的研究。我们的研究结果表明，低血清尿酸可能是 GBA-PD 的进展生物标志物。然而，需要更多的研究（理想情况下是纵向研究）来评估 GBA-PD 中低血清尿酸与临床数据之间的关系。这些结果与以前评估尿酸作为其他遗传形式 PD 生物标志物的报告中的数据一致。
