Post-Tuberculosis Lung Disease (PTLD), a persistent sequelae of Tuberculosis (TB) in which TB survivors continue to experience respiratory symptoms and diminished lung function after microbiological cure, poses a significant and growing public health challenge. Its prevalence varies widely due to differences in treatment adequacy, comorbidities, and environmental exposures and afflicts particularly high TB-burden countries. Recent advances in fundamental science, clinical investigations and exploratory trials have expanded our understanding of PTLD pathogenesis and progression. Yet, critical questions remain unanswered: Which patients are most at risk? How can we intervene early to prevent or mitigate disability? And how should healthcare systems adapt to monitor, manage, and support the growing population of TB survivors? This review aims to inform ongoing efforts in clinical care, research, and policy. We summarize recent evidence on PTLD-specifically disease mechanisms, clinical manifestations, diagnostic approaches, risk factors, and treatment strategies. It also highlights key knowledge gaps and implementation challenges and proposes research priorities to steer future inquiry and practice. Greater research investment and stronger global collaboration are needed to mitigate the long-term burden of PTLD and improve outcomes for TB survivors.

The Spanish COPD Guidelines (GesEPOC) were first published in 2012, and since then, several updates have incorporated new evidence regarding the diagnosis and treatment of COPD. GesEPOC is a clinical practice guideline developed with the collaboration of the scientific societies involved in COPD management and the Spanish Patients' Forum. Its recommendations are based on an evaluation of the evidence using the GRADE methodology and on a narrative description of the evidence in those areas where application of this methodology is not feasible. This article summarizes the updated recommendations on the pharmacological treatment of stable COPD, derived from the development of 12 PICO questions. The COPD treatment process comprises five stages: (1) diagnosis; (2) risk stratification; (3) characterization; (4) initiation and continuation of treatment; and (5) follow-up. For inhaled treatment selection, high-risk patients are classified into three phenotypes: non-exacerbator, eosinophilic exacerbator, and non-eosinophilic exacerbator. Treatable traits include general aspects, applicable to all patients-such as smoking cessation and inhaler technique-and more specific conditions, mainly affecting severe patients, such as chronic hypoxemia or chronic bronchial infection. The cornerstone of COPD treatment is long-acting bronchodilators, either as monotherapy or in combination, depending on the patient's risk level. Eosinophilic exacerbators should receive inhaled corticosteroids, whereas non-eosinophilic exacerbators require a detailed evaluation to identify the most appropriate therapeutic option. GesEPOC 2025 also includes recommendations on inhaled corticosteroid withdrawal, the introduction of biologics, and the indication for alpha-1 antitrypsin therapy. GesEPOC 2025 represents a more individualized approach to COPD treatment, tailored to the clinical characteristics of patients and their level of risk or complexity.

In patients with acute symptomatic pulmonary embolism (PE), embolic burden has an uncertain prognostic significance.

Lung cancer (LC), the leading cause of death due to malignancy in both males and females, is common in patients with coexisting respiratory comorbidities. Many of these share common etiologies with LC such as smoking, biomass fume or occupational exposure, and ambient air pollution, but also a genetic predisposition and/or common pathophysiologic mechanisms, chief among them chronic inflammation, altered immune surveillance, cell injury and increased turnover, to name a few. This common thread puts patients with respiratory comorbidities at increased risk of developing LC. The present article reviews why patients with 5 of the most prevalent chronic respiratory diseases (COPD, asthma, Interstitial Lung Disease, Obstructive Sleep Apnea and Bronchiectasis) are at increased risk of LC and the potential pathological mechanisms underlying this clinically relevant association.