Introduction
The gut–liver axis has a central role in the pathophysiology of chronic liver diseases. Small intestinal bacterial overgrowth (SIBO), as a manifestation of intestinal dysbiosis, may contribute to hepatic inflammation, altered bile acid metabolism, and disease progression. However, the prevalence of SIBO across different liver disease phenotypes and its independent clinical predictors remain insufficiently defined
Aims & Methods
Aim: To determine the prevalence of SIBO in patients with liver diseases and to identify laboratory and disease-related factors independently associated with SIBO positivity.
Methods: In this cross-sectional study, consecutive patients with liver-related disorders were evaluated using a structured clinical and biochemical dataset. After data cleaning and exclusion of repeated header rows and records with unavailable SIBO status, 328 patients were included in the final analysis. Patients were stratified into SIBO-positive and SIBO-negative groups. Continuous variables were compared using non-parametric tests, while categorical variables were analyzed using chi-square testing. To identify independent predictors of SIBO, multivariable logistic regression was performed using a complete-case model including age, sex, alanine aminotransferase (ALT), alkaline phosphatase (ALP), and active/acute hepatitis C virus (HCV) status.
Results
Among 328 patients, 116 (35.4%) were SIBO-positive and 212 (64.6%) were SIBO-negative. On univariate analysis, SIBO-positive patients had significantly higher ALT [median 42.5 vs 32.0, p=0.0027], AST [33.9 vs 27.2, p=0.0115], and ALP [95.9 vs 80.8, p=0.0047] levels compared with SIBO-negative patients. No significant differences were observed for sex (p=0.173), platelet count (p=0.699), GGT (p=0.366), or FIB-4 score (p=0.967), while age showed a borderline trend (p=0.073). SIBO prevalence differed significantly across liver disease categories (p=0.0016), with the highest rate observed in active/acute HCV infection (64.3%), followed by other HCV-related disease (53.8%), whereas lower rates were found in MAFLD/NASH (31.3%), HBV (34.8%), cirrhosis (30.0%), and cured HCV (20.0%). In multivariable logistic regression, active/acute HCV emerged as a strong independent predictor of SIBO positivity (OR 7.20, 95% CI 2.92–17.74, p<0.001). Higher ALP also remained independently associated with SIBO (OR 1.04 per 10-unit increase, 95% CI 1.00–1.09, p=0.043), whereas age, sex, and ALT were not independently significant. The general distribution of patients is presented in Table 1.
Table 1. The general distribution of patients with liver diseases (SIBO(+) and SIBO(-)).
Disease Category
| Total (n)
| SIBO (+), n (%)
| SIBO (−), n (%)
|
HCV active/acute
| 42
| 27 (64.3%)
| 15 (35.7%)
|
HCV (other)
| 13
| 7 (53.8%)
| 6 (46.2%)
|
| HBV | 66 | 23(34.8%) | 43(65.2%) |
MAFLD/NASH
| 144 | 45 (31.3%)
| 99 (68.7%)
|
Cirrhosis
| 10 | 3 (30.0%)
| 7 (70.0%)
|
HCV cured
| 30 | 6 (20.0%)
| 24 (80.0%)
|
Conclusion
SIBO is common in patients with liver diseases, affecting more than one-third of this cohort. SIBO positivity was associated with higher cholestatic and hepatocellular enzyme levels on univariate analysis, while active/acute HCV and elevated ALP remained independent predictors after adjustment. These findings support a clinically relevant interaction between intestinal dysbiosis and liver disease phenotype and suggest that patients with active HCV-related disease may represent a subgroup at particularly high risk for SIBO.