Home Research Feeds Metabolic disorder and intestinal microflora dysbiosis in chronic inflammatory demyelinating polyradiculoneuropathy

Metabolic disorder and intestinal microflora dysbiosis in chronic inflammatory demyelinating polyradiculoneuropathyOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-05

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
China
Sample Site
Feces
Species
Homo sapiens

What was studied?

This study asked whether serum metabolites and gut microbes are altered in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), a rare immune-mediated nerve disease with no reliable biomarker. Researchers ran untargeted serum metabolomics by liquid chromatography-mass spectrometry and shotgun metagenomic sequencing of stool. They compared CIDP subjects with matched healthy controls, then used Pearson correlation to link bile acid changes to specific gut microbes.

Who was studied?

The cohort was 64 people in Jinan, China: 31 CIDP patients and 33 age- and sex-matched healthy controls, enrolled from December 2020 to February 2022 at Qilu Hospital. Serum was analyzed from all subjects. Qualified stool metagenomes came from 28 CIDP and 33 control subjects. All participants were human adults, and CIDP was diagnosed using established clinical guidelines.

What were the most important findings?

Primary bile acids surged in CIDP. Cholic acid rose 9.61-fold and 36.46-fold across ion modes, taurocholic acid rose 38.30-fold, while microbe-derived secondary bile acids fell. Arachidonic acid roughly doubled and its mediator thromboxane B2 rose about 42-fold in CIDP. Metagenomics showed opportunistic pathogens, including Klebsiella pneumoniae and Megamonas funiformis, enriched, while Bacteroides species declined. Decreased secondary bile acids correlated with reduced Bacteroides ovatus, Bacteroides caccae, and Ruminococcus gnavus.

What are the greatest implications of this study?

The findings suggest CIDP involves disrupted bile acid and arachidonic acid metabolism, possibly driven by gut microbial dysbiosis and opportunistic infection. The authors propose a combined bile acid and arachidonic acid panel as a candidate CIDP biomarker. This is a small cross-sectional study, so causation is not established, and the biomarker needs validation in larger prospective cohorts before clinical use.

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