# Clinical, microbial and metabolic characteristics of gas-forming pyogenic liver abscess and its potential formation mechanism

## TL;DR

This study investigates gas-forming pyogenic liver abscess, finding that it is linked to worse outcomes and specific metabolic changes, not just bacterial types.

## Contribution

The study identifies metabolic alterations linked to gas formation in liver abscesses, independent of microbial composition.

## Key findings

- GFPLA patients had worse liver function, higher inflammation, and mortality compared to non-GFPLA patients.
- Metabolomics revealed distinct metabolic profiles in GFPLA, correlated with blood glucose and inflammation.
- Diabetes is a key risk factor for GFPLA, and gas formation is likely due to metabolic changes, not microbial differences.

## Abstract

Pyogenic liver abscess (PLA) is a common intra-abdominal infection with substantial morbidity and mortality, among which gas-forming pyogenic liver abscess (GFPLA) represents a more severe clinical subtype. Basically, GFPLA is usually associated with more severe clinical outcomes compared to non-gas-forming PLA (non-GFPLA). The underlying mechanisms driving gas formation remain unclear. This study aimed to explore clinical, microbial, and metabolic characteristics of GFPLA.

A total of 176 PLA patients (39 GFPLA, 137 non-GFPLA) were retrospectively analyzed. Clinical variables were compared between groups. Pus samples collected from patients undergoing percutaneous drainage were analyzed using 16S rDNA sequencing and untargeted metabolomics to investigate microbial composition and metabolic differences.

GFPLA patients showed worse liver function, higher inflammatory markers, poorer glycemic control, and higher in-hospital mortality. 16S rDNA sequencing revealed no significant differences in bacterial richness, diversity, or community composition between groups, with Klebsiella dominating in both. Functional microbial predictions showed no association with gas formation. Untargeted metabolomics identified distinct metabolic profiles in GFPLA, with key differential metabolites positively correlated with blood glucose and inflammatory markers but not with Klebsiella abundance.

Diabetes mellitus is an independent risk factor for GFPLA. Gas formation in PLA is more likely linked to high blood glucose-induced metabolic alterations in the liver micro-environment rather than microbial composition. These findings suggest new potential therapeutic targets by modulating metabolic pathways to improve GFPLA outcomes.