Cachexia and Sarcopenia in Patients with Coexisting Chronic Obstructive Pulmonary Disease and Pulmonary Tuberculosis

Malnutrition, loss of muscle mass, and reduced muscle strength are common but underrecognized conditions in tuberculosis (TB) and chronic obstructive pulmonary disease (COPD). These abnormalities may persist after completion of TB treatment, and a normal or elevated body mass index does not exclude muscle depletion. Unlike the extensively studied conditions of hyperglycemia and obesity, the catabolic end of the spectrum of metabolic disturbances in coexisting TB and COPD remains insufficiently investigated. This narrative review focuses on cachexia and sarcopenia in patients with coexisting TB and COPD (TB–COPD). It examines the roles of systemic inflammation, immunometabolic remodeling, mitochondrial dysfunction, disturbances in protein metabolism and endocrine regulation, and ceramide signaling. Because direct evidence in TB–COPD is scarce, findings from TB or post-tuberculosis lung disease without confirmed COPD and from COPD alone are used as indirect evidence, and the level of evidence is indicated for each mechanism. The diagnostic approach is organized around current clinical guidelines and includes assessment of nutritional status, diagnosis of malnutrition using the Global Leadership Initiative on Malnutrition (GLIM) criteria, identification of sarcopenia using European Working Group on Sarcopenia in Older People 2 (EWGSOP2) or Asian Working Group for Sarcopenia (AWGS) criteria, pulmonary function testing to distinguish post-tuberculosis airflow obstruction from COPD, and evaluation for reversible causes of muscle weakness. The main treatment approaches are correction of malnutrition, pulmonary rehabilitation, and treatment of the underlying respiratory disease. The effectiveness of interventions is assessed through changes in muscle strength, physical performance, body weight, and body composition. The evidence base for patients with coexisting TB and COPD remains limited; most studies have investigated each disease separately. The efficacy of pharmacological agents targeting the molecular mechanisms of muscle wasting has not been established in this population. Priorities for future research include prospective assessment of muscle function in TB–COPD cohorts and the development of personalized strategies for nutritional and rehabilitation support.