J Mov Disord.
2022 May;15(2):106-114. 10.14802/jmd.21085.
Fecal Calprotectin in Parkinson’s Disease and Multiple System Atrophy
- Affiliations
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- 1Division of Neurology, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
- 2The Mah Pooi Soo & Tan Chin Nam Centre for Parkinson’s Disease and Related Disorders, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
- 3Aab Cardiovascular Research Institute (CVRI), University of Rochester Medical Center, Rochester, NY, USA
- 4Institute for Advanced Studies, University of Malaya, Kuala Lumpur, Malaysia
- 5Neurology Unit, Department of Medicine, Faculty of Medicine, The National University of Malaysia, Kuala Lumpur, Malaysia
- 6Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
- 7School of Pharmacy, Monash University Malaysia, Selangor, Malaysia
- 8Division Gasteroenterology, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
- KMID: 2530215
- DOI: http://doi.org/10.14802/jmd.21085
Abstract
Objective
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.
Methods
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.
Results
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.
Conclusions
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.
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