Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) increasingly co-occur in low- and middle-income countries and aging populations. Prior pulmonary TB is a robust, smoking-independent determinant of COPD and is linked to persistent systemic inflammation, endothelial dysfunction, dyslipidemia, and hypercoagulability axes that also amplify cardiovascular disease (CVD) risk. We conducted a targeted narrative non-systematic review (2005–2025) of PubMed/MEDLINE, Embase, Scopus, and Web of Science, selecting studies for clinical relevance across epidemiology, clinical phenotypes, pathobiology, biomarkers, risk scores, sleep-disordered breathing, and management. No quantitative synthesis or formal risk-of-bias assessment was performed. Accordingly, findings should be interpreted as a qualitative synthesis rather than pooled estimates. Prior TB is associated with a distinctive COPD phenotype characterized by mixed obstructive–restrictive defects, reduced diffusing capacity (DLCO), radiographic sequelae, and higher exacerbation/hospitalization burden. Mechanistic insights: Convergent mechanisms chronic immune activation, endothelial injury, prothrombotic remodeling, molecular mimicry, and epigenetic reprogramming provide biologic plausibility for excess CVD, venous thromboembolism, and pulmonary hypertension. Multimarker panels spanning inflammation, endothelial injury, myocardial strain/fibrosis, and coagulation offer incremental prognostic value beyond clinical variables. While QRISK4 now includes COPD, it does not explicitly model prior TB or COPD-TB outcomes, but data specific to post-TB cohorts remain limited. Clinical implications: In resource-constrained settings, pragmatic screening, prioritized PAP access, guideline-concordant pharmacotherapy, and task-shifting are feasible adaptations. A history of TB is a clinically meaningful modifier of cardiopulmonary risk in COPD. An integrated, multimodal assessment history, targeted biomarkers, spirometry/lung volumes, DLCO, 6 min walk test, and focused imaging should guide individualized care while TB-aware prediction models and implementation studies are developed and validated in high-burden settings.

Non-small-cell lung cancer (NSCLC) is a widespread and aggressive form of cancer, and in cases of its occurrence, accurate diagnosis and precise staging play a crucial role in determining treatment and estimating prognosis. Flexible bronchoscopy (FB) is a minimally invasive method used to assess the local and regional extent of the disease. FB facilitates the identification of endobronchial lesions and the collection of biopsy samples for histopathological diagnosis. It also enables the evaluation of regional lymph node involvement via advanced techniques such as endobronchial ultrasound with fine-needle aspiration (EBUS-TBNA). This method has high sensitivity and specificity, reducing the need for more invasive interventions like mediastinoscopy. The integration of endobronchial ultrasound (EBUS) has revolutionized NSCLC staging by providing detailed images and guiding biopsies of suspicious lymph nodes. Additionally, FB is valuable in staging the extent of primary tumor growth, providing critical information about the invasion of adjacent structures. In conclusion, FB, supported by advanced technologies, is important for the staging of NSCLC, improving medical practice and patient prognosis.

Non-Small-Cell Lung Cancer (NSCLC) represents the most prevalent form of lung cancer and remains one of the leading causes of cancer-related morbidity and mortality worldwide. This disease has evolved far beyond traditional histopathological classification. While histology remains foundational, it is no longer sufficient to guide optimal patient management in the era of precision oncology. This review uniquely integrates the full spectrum of NSCLC evaluation, from underlying pathophysiological mechanisms to histological, immunohistochemical, and molecular analyses, culminating in individualized therapeutic planning. We highlight actionable genetic alterations—including EGFR, ALK, ROS1, BRAF, and KRAS—and their roles in guiding targeted therapies, alongside the transformative impact of immune checkpoint inhibitors in selected patients. By emphasizing the interplay between tumor biology, diagnostic workflows, and treatment selection, this review underscores the necessity of comprehensive molecular testing and data integration. Finally, we discuss emerging biomarkers and rational combination strategies that promise to further refine patient stratification and improve outcomes.

As shown in a Spanish study, patients with rheumatoid arthritis (PAR) have a 4-fold increased risk of developing TB (tuberculosis) compared to the general population. Abruptly stopping anti-TNF (tumor necrosis factor α) agents after the development of TB could cause a paradoxical response leading to severe complications and death. We present the case of a 54 years old female patient with seropositive PAR since 2012 in treatment with biological therapy, which was diagnosed 10 years after the start of immunosuppressive treatment with miliary TB. She has had an unfavorable prognosis, dying after one month from the initiation of antituberculosis treatment due to septic shock. Therefore, it is very important to evaluate the bacillary status before initiating any immunosuppressive treatment.