Objective: To investigate if we were able to reproduce our previous findings in an independent patient cohort and whether such a correlation also exists in PD‑patients treated with the two other available COMT-inhibitors.

Background: COMT-inhibitors are among the most frequently used drugs in Parkinson’s disease (PD). In a previous study, we found that treatment with entacapone (a COMT-inhibitor) showed a significant negative correlation with the abundance of Faecalibacterium prausnitzii and its putative metabolic product, butyrate, in fecal samples of PD‑patients.

Method: 33 subjects, 14 PD‑patients without previous or present treatment with a COMT‑inhibitor and 19 PD‑patients under a stable therapy with a COMT-inhibitor were enrolled in this study. Clinical data were collected using validated scores and questionnaires. All subjects were provided with sterile containers and instructed how to collect fecal samples. Bacterial DNA was extracted from the stool samples, and target bacteria were quantified by real-time quantitative PCR (qPCR). Short chain fatty acids (SCFA) were quantified by gas chromatography.

Results: PD‑patients treated with entacapone (n=10) showed a significantly reduced abundance of Faecalibacterium prausnitzii compared to PD patients without COMT-inhibitor treatment (n=14). PD patients treated with either opicapone (n=6) or tolcapone (n=3) showed a similar abundance of Faecalibacterium prausnitzii as PD‑patients without a COMT‑inhibitor therapy. All other investigated microbiota showed no group-specific significant differences. A trend towards lower concentrations of fecal butyrate in entacapone treated PD‑patients compared to those treated with opicapone or telcapone, and without treatment, was noticed.

Conclusion: In contrast to entacapone, the two other COMT inhibitors were not associated with a decreased abundance of the potentially beneficial Faecalibacterium prausnitzii and butyrate. This pilot study indicates that the correlation observed for entacapone in our previous study might not be due to a group-effect of COMT-inhibitors, but might rather be entacapone-specific. Yet, longitudinal studies in larger patient cohorts are necessary to clarify whether a cause-effect relationship between entacapone and gut microbiota truly exists.

References: Unger et al. Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls. Parkinsonism Relat Disord. 2016 Nov;32:66-72.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/impact-of-oral-comt-inhibitors-on-gut-microbiota-and-biologically-active-microbial-metabolites-in-patients-with-parkinsons-disease/