Dysglycemia, Dyslipidemia, and Pulmonary Tuberculosis Outcomes: Clinical Associations and Proposed Mechanisms

Tuberculosis (TB) remains a leading global infectious disease burden. The rising global burden of dysglycemia and dyslipidemia—which geographically converges with TB in many low- and middle-income countries—poses substantial challenges to clinical management. Dysglycemia, encompassing prediabetes and diabetes mellitus, is a well-established risk factor for pulmonary tuberculosis (PTB) and adverse treatment outcomes; dyslipidemia frequently co-occurs with dysglycemia, yet its relationship with PTB outcomes is complex and varies by lipid phenotype, timing of measurement, and disease stage. Clinical evidence indicates that in the context of TB-DM, comorbid dyslipidemia is associated with more severe pulmonary pathology, heightened systemic inflammation, and increased risks of drug-induced liver injury (DILI) and mortality, although the overall evidence base remains associative. At the mechanistic level, chronic hyperglycemia and altered lipid metabolism may impair anti-tuberculosis immunity through complementary pathways—including macrophage effector dysfunction, T-cell exhaustion involving the advanced glycation end products (AGEs)–receptor for AGEs (RAGE) axis, and lipid-mediated modulation of inflammatory signaling—although translational evidence from preclinical models to human populations remains limited. This narrative review synthesizes current clinical and mechanistic evidence on the associations between dysglycemia, dyslipidemia, and PTB outcomes, identifies key methodological limitations in the existing literature, and outlines priorities for future research, including prospective longitudinal studies and integrated metabolic profiling, to advance evidence-based management of PTB patients with comorbid metabolic disorders.