Hor Jia Wei, Lim Shen-Yang, Khor Eng Soon, Chong Kah Kian, Song Sze Looi, Ibrahim Norlinah Mohamed, Teh Cindy Shuan Ju, Chong Chun Wie, Hilmi Ida Normiha, Tan Ai Huey
Division of Neurology, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
The Mah Pooi Soo & Tan Chin Nam Centre for Parkinson's Disease and Related Disorders, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
J Mov Disord. 2022 May;15(2):106-114. doi: 10.14802/jmd.21085. Epub 2021 Dec 24.
Converging evidence suggests that intestinal inflammation is involved in the pathogenesis of neurodegenerative diseases. Previous studies on fecal calprotectin in Parkinson's disease (PD) were limited by small sample sizes, and literature regarding intestinal inflammation in multiple system atrophy (MSA) is very scarce. We investigated the levels of fecal calprotectin, a marker of intestinal inflammation, in PD and MSA.
We recruited 169 subjects (71 PD, 38 MSA, and 60 age-similar nonneurological controls). Clinico-demographic data were collected. PD and MSA were subtyped and the severity assessed using the MDS-UPDRS and UMSARS, respectively. Fecal calprotectin and blood immune markers were analyzed.
Compared to controls (median: 35.7 [IQR: 114.2] μg/g), fecal calprotectin was significantly elevated in PD (median: 95.6 [IQR: 162.1] μg/g, p = 0.003) and even higher in MSA (median: 129.5 [IQR: 373.8] μg/g, p = 0.002). A significant interaction effect with age was observed; between-group differences were significant only in older subjects (i.e., ≥ 61 years) and became more apparent with increasing age. A total of 28.9% of MSA and 18.3% of PD patients had highly abnormal fecal calprotectin levels (≥ 250 μg/g); however, this difference was only significant for MSA compared to controls. Fecal calprotectin correlated moderately with selected blood immune markers in PD, but not with clinical features of PD or MSA.
s Elevated fecal calprotectin suggests a role for intestinal inflammation in PD and MSA. A more complete understanding of gut immune alterations could open up new avenues of research and treatment for these debilitating diseases.
越来越多的证据表明肠道炎症与神经退行性疾病的发病机制有关。先前关于帕金森病（PD）患者粪便钙卫蛋白的研究因样本量小而受到限制，关于多系统萎缩（MSA）肠道炎症的文献非常稀少。我们研究了PD和MSA患者肠道炎症标志物粪便钙卫蛋白的水平。
我们招募了169名受试者（71名PD患者、38名MSA患者和60名年龄相仿的非神经疾病对照者）。收集临床人口统计学数据。对PD和MSA进行亚型分类，并分别使用MDS-UPDRS和UMSARS评估严重程度。分析粪便钙卫蛋白和血液免疫标志物。
与对照组（中位数：35.7[四分位间距：114.2]μg/g）相比，PD患者的粪便钙卫蛋白显著升高（中位数：95.6[四分位间距：162.1]μg/g，p=0.003），MSA患者的粪便钙卫蛋白更高（中位数：129.5[四分位间距：373.8]μg/g，p=0.002）。观察到与年龄有显著的交互作用；组间差异仅在老年受试者（即≥61岁）中显著，且随着年龄的增长变得更加明显。共有28.9%的MSA患者和18.3%的PD患者粪便钙卫蛋白水平高度异常（≥250μg/g）；然而，与对照组相比，这种差异仅在MSA中显著。在PD中，粪便钙卫蛋白与选定的血液免疫标志物中度相关，但与PD或MSA的临床特征无关。
粪便钙卫蛋白升高表明肠道炎症在PD和MSA中起作用。更全面地了解肠道免疫改变可能为这些使人衰弱的疾病开辟新的研究和治疗途径。
