Hepatic steatosis affects the outcome of anti-tuberculosis treatment in pulmonary tuberculosis patients.

BACKGROUND

Pulmonary tuberculosis (PTB) remains a major cause of infectious-disease mortality worldwide. Host metabolic status may shape treatment response, but whether hepatic steatosis affects sputum smear conversion in PTB remains poorly defined.

METHODS

We performed a retrospective single-center cohort study including newly diagnosed, smear-positive PTB patients treated at Taizhou People's Hospital between January 2022 and December 2025. Patients were classified according to sputum smear conversion status, with delayed conversion defined as persistent smear positivity beyond 8 weeks after initiation of standard anti-tuberculosis therapy. Baseline demographic, clinical, ultrasonographic, laboratory, and cytokine data were collected and compared between groups. Potential factors associated with delayed conversion were evaluated using correlation analysis, multicollinearity assessment, change-in-estimate confounder analysis with the R package chest, and multivariable logistic regression.

RESULTS

Clinical screening identified 11 candidate factors. After prioritisation by clinical relevance, correlation structure, collinearity and confounding assessment, six factors were entered into the multivariable model. Hepatic steatosis and IL-18 were positively associated with delayed smear conversion (hepatic steatosis: β = 2.401, OR = 11.036, 95% CI = 2.489-48.934; IL-18: β = 2.396, OR = 10.984, 95% CI = 1.832-65.862). By contrast, T-SPOT positivity was inversely associated with delayed smear conversion (β = -4.199, OR = 0.015, 95% CI = 0.001-0.172).

CONCLUSIONS

Hepatic steatosis was independently associated with delayed smear conversion in PTB. Baseline cytokine profiles, including IL-6 and IL-18, also differed according to treatment response. These findings suggest that PTB patients with hepatic steatosis may benefit from closer monitoring of treatment response during anti-tuberculosis therapy.