Profiling gut microbiome dynamics in subacute thyroiditis: Implications for pathogenesis, diagnosis, and treatment

TL;DR

This study finds that subacute thyroiditis is linked to changes in gut bacteria, which may help in understanding the disease and its treatment.

Contribution

The study identifies specific gut microbiome signatures in subacute thyroiditis and their response to treatment.

Findings

SAT patients showed increased abundance of Escherichia-Shigella, Bifidobacterium, and others.

Prednisolone treatment partially restored gut microbiota, with Lactobacillus and Prevotella as key post-treatment markers.

Strong correlations were found between gut microbiome and clinical markers in SAT patients.

Abstract

The aim of this study is to characterize gut microbiome alterations in newly diagnosed subacute thyroiditis (SAT) patients, and identify potential microbial signatures associated with SAT and treatment response.

Fecal samples collected from 20 newly diagnosed SAT patients and 20 healthy controls were analyzed using 16S ribosomal RNA gene sequencing. Bioinformatics analysis was performed to assess alpha and beta diversity, taxonomic composition, and differential abundance of gut microbiota between the groups. Correlations between gut microbiome and clinical parameters were also investigated.

Newly diagnosed SAT patients exhibited significant alterations in gut microbiota composition. There was increased abundance of Escherichia-Shigella, Bifidobacterium, Akkermansia, Veillonella, and Streptococcus, while the abundance of Bacteroidetes, Faecalibacterium, Prevotella, Roseburia, and Ruminococcus were significantly decreased. Prednisolone treatment partially normalized the gut microbiota, with Lactobacillus, Lactobacillaceae, Lactobacillus reuteri, and Prevotella emerging as key biomarkers in post-treatment SAT. Significant correlations were found between specific gut microbiome and clinical markers.

SAT is associated with distinct gut microbiome alterations, partially reversible with treatment, which suggest a potential role for the gut microbiome in SAT pathogenesis and treatment response.

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