Home Research Feeds Alterations of the Gut Microbiota in Hashimoto's Thyroiditis Patients

Alterations of the Gut Microbiota in Hashimoto's Thyroiditis PatientsOriginal 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?

Researchers compared the fecal gut microbiota of Hashimoto's thyroiditis (HT) patients against healthy controls, then tested whether microbiota patterns could serve as diagnostic biomarkers.

How was it studied?

A cross-sectional cohort of 28 HT patients and 16 matched healthy controls had fecal samples analyzed by 16S ribosomal RNA gene sequencing. An independent validation cohort of 22 HT patients and 11 healthy controls tested the diagnostic value of biomarkers identified in the first cohort.

What did they find?

Overall bacterial richness and diversity did not differ between groups. HT patients had higher Blautia, Roseburia, Ruminococcus_torques_group, Romboutsia, Dorea, Fusicatenibacter, and Eubacterium_hallii_group, and lower Fecalibacterium, Bacteroides, Prevotella_9, and Lachnoclostridium. Linear discriminant analysis found 27 differing genera correlated with clinical parameters, and a 10-species biomarker panel achieved AUC values of 0.91 in the exploration cohort and 0.88 in validation.

Why it matters

Gut microbiota composition tracked with clinical parameters in HT patients, suggesting microbiome data could support diagnosis and warrants further study of its role in HT pathogenesis.

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