Metabolites disorders are associated with the severity of pathological lung injury in patients with concurrent diabetes and tuberculosis: a cross sectional study.

BACKGROUND

Type 2 diabetes mellitus elevates the risk of developing tuberculosis, posing a substantial challenge to TB treatment and control. However, the underlying molecular mechanisms remain poorly understood.

METHODS

Non-targeted metabolomics analysis of serum samples collected from 20 patients with concurrent DM and TB (DM-TB) and 20 patients with TB only (TB) was performed using UPLC-MS/MS. Logistic regressions were applied to evaluate the associations between the metabolites and lung pathology.

RESULTS

Pathway analysis revealed that TCA cycle, steroidogenesis, ketone body metabolism were the key pathways enriched in the differential metabolites distinguishing DM-TB from TB patients. Multivariable logistic regression analysis suggested, high levels of C18 Sphingosine (OR = 2.207, 95% CI = 1.049-4.645), L-Saccharopine (OR = 4.407, 95% CI = 1.045-18.582) and arachidonic acid (AA) (OR = 2.845, 95% CI = 1.272-6.366) were associated with an increased risk of extensive lung lesions. In addition, C18 Sphingosine (OR = 3.596, 95% CI = 1.239-10.440) and AA levels (OR = 3.306, 95% CI = 1.200-9.112) were positively associated with the risk of prevalent multiple cavities.

CONCLUSIONS

Our results suggests that lipid metabolism disorders are significantly associated with severe lung lesions in TB-DM patients, suggest a potential link to exacerbated inflammatory and immunomodulatory responses.