Pathophysiology, clinical manifestation, and treatment of tuberculosis-associated chronic obstructive pulmonary disease: a narrative review.

Chronic obstructive pulmonary disease (COPD) is a leading cause of respiratory morbidity and mortality, most often linked to smoking. However, growing evidence indicates that previous tuberculosis (TB) infection is also a critical risk factor for COPD. This review aimed at providing a comprehensive perspective on TB-COPD, covering its epidemiologic significance, pathogenesis, clinical characteristics, and current management approaches. Tuberculosis-associated chronic obstructive pulmonary disease (TB-COPD) is characterized by persistent inflammatory responses, altered immune pathways, and extensive structural lung damage-manifested as cavitation, fibrosis, and airway remodeling. Multiple epidemiologic studies have shown that individuals with a history of TB have a significantly higher likelihood of developing COPD and experiencing worse outcomes, such as increased breathlessness and frequent exacerbations. Key pathogenic mechanisms include elevated matrix metalloproteinase activity and excessive neutrophil-driven inflammation, which lead to alveolar destruction, fibrotic scarring, and the development of bronchiectasis. Treatment generally follows current COPD guidelines, advocating the use of long-acting bronchodilators and the selective application of inhaled corticosteroids. Studies have demonstrated that indacaterol significantly improves lung function and respiratory symptoms, while long-acting muscarinic antagonists have shown survival benefits.