Tuberculosis (TB) continues to be a major public health challenge in low- and middle-income countries (LMICs), where high burdens of coinfections exacerbate the disease’s impact. In 2023, an estimated 8.2 million people were newly diagnosed with tuberculosis worldwide, reflecting an increase from 7.5 million in 2022 and 7.1 million in 2019. In LMICs, limited access to healthcare, inadequate nutrition, and poor living conditions contribute to higher coinfection rates among TB patients, leading to delayed diagnosis and treatment, which in turn exacerbates disease severity and facilitates transmission. This narrative review synthesizes the epidemiology, clinical implications, diagnostic challenges, and management strategies related to TB coinfections with viral pathogens including HIV, SARS-CoV-2, and influenza, bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, and Pseudomonas aeruginosa, fungi such as Aspergillus and Candida species, and parasites. This review highlights that overlapping symptoms, immune system compromise, and socioeconomic barriers in LMICs lead to delayed diagnoses and suboptimal treatment outcomes, while also addressing the challenges of managing drug interactions particularly in HIV–TB coinfections and underscoring the need for integrated diagnostic approaches, improved treatment regimens, and strengthened healthcare systems, thereby consolidating current evidence to inform future research priorities and policy interventions aimed at reducing the overall burden of TB and its coinfections in resource-limited settings.

Tuberculosis (TB) induces a hypercoagulable state characterized by systemic inflammation, endothelial dysfunction, and alterations in the coagulation and fibrinolytic pathways. This review explores the pathophysiological mechanisms underlying hypercoagulability in TB, including increased pro-inflammatory cytokine release, endothelial damage, platelet activation, and reduced anticoagulant and fibrinolytic activity. These factors contribute to an elevated risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), which complicate TB prognosis and treatment. The potential role of adjunctive anti-inflammatory therapies, such as vitamin D, NSAIDs, corticosteroids, and anti-platelet agents, is highlighted as a strategy to mitigate systemic inflammation and reduce thrombotic risks in patients with TB. The challenges of anticoagulation therapy, particularly in managing the interactions between anti-TB medications and traditional anticoagulants, are discussed, along with the potential of novel oral anticoagulants (NOAs) as alternatives. We also address therapy of hypercoagulability in TB within resource-limited settings which requires low-cost diagnostics, accessible anticoagulation options, adjunctive therapies, and preventive strategies integrated into existing healthcare systems. Effective risk stratification and individualized management strategies are vital for reducing the morbidity and mortality associated with thrombotic complications in TB.

Chronic obstructive pulmonary disease (COPD) is an escalating global health burden, with a disproportionate impact on low- and middle-income countries (LMICs). Although tobacco smoking is a well-established risk factor, emerging evidence highlights the significant role of non-smoking exposure in driving the prevalence of COPD in these regions. This narrative review synthesizes current data on key non-smoking contributors, including household air pollution, ambient urban pollution, occupational exposure, early-life respiratory insults, chronic infections, and socioeconomic adversity. These risk factors are associated with distinct COPD phenotypes, often marked by increased airway inflammation, reduced emphysema, and variable airflow limitation. Such presentations are particularly common among women and younger populations in LMICs. However, diagnostic and therapeutic challenges persist, owing to limited disease awareness, under-resourced health systems, restricted access to essential medications, and financial constraints impacting adherence. Despite the proven effectiveness of non-pharmacological measures and public health interventions, their implementation remains inadequate because of infrastructural and funding limitations. Bridging these gaps requires region-specific clinical guidelines, improved diagnostic infrastructure, expanded access to affordable treatment, and culturally sensitive interventions. Future priorities include identifying robust biomarkers, refining disease definitions to accommodate non-smoking phenotypes, and advancing implementation science to improve interventions. A coordinated, context-aware global response is essential to reduce the growing burden of COPD in LMICs and to ensure equitable respiratory health outcomes.

Background: Pulmonary tuberculosis (TB) is increasingly recognized as a risk factor for chronic obstructive pulmonary disease (COPD), but its impact on COPD onset and severity remains poorly characterized, particularly in low- and middle-income countries. This multicenter study aimed to assess the impact of prior pulmonary TB on COPD onset, severity, the timing of the first severe exacerbation, and progression among Romanian patients with and without a history of pulmonary TB. Methods: This retrospective multicenter study included adults hospitalized for their first severe COPD exacerbation at two tertiary care centers in Romania between April 2020 and April 2025. Patients were grouped based on smoking status and prior TB history. Propensity score matching was used to control for confounding factors. Clinical characteristics, spirometry, and radiological TB patterns were analyzed comparatively between patients with prior TB and TB-naïve patients. Results: Among 403 COPD patients, those with prior TB had significantly earlier COPD onset (mean age 48.67 ± 6.42 vs. 65.61 ± 5.14 years in smokers, p < 0.001) and shorter intervals to their first severe COPD exacerbation compared to patients without prior TB (6.35 ± 4.71 vs. 15.14 ± 6.93 years in smokers, p < 0.001). COPD prevalence was higher among TB survivors compared to those without TB history, especially in smokers (OR = 5.73; 95% CI, 3.30–9.94, p < 0.001), versus non-smokers (OR =2.23; 95% CI, 1.37–3.64, p = 0.001). Radiological severity of TB lesions significantly influenced COPD prevalence among smokers (OR = 10.79, p < 0.001). Conclusions: Prior pulmonary TB substantially accelerates COPD onset, exacerbation timing, and disease severity, particularly in smokers. This multicenter comparative study demonstrates that prior pulmonary TB significantly accelerates COPD onset, exacerbation timing, and disease severity, especially among smokers. Recognizing TB history as a significant COPD risk factor underscores the importance of targeted COPD screening and tailored management in populations with high TB prevalence.

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.

Pulmonary oncological pathologies are an important public health problem and the association with other pulmonary lesions may pose difficulties in diagnosis and staging or require different treatment options. To address this complexity, we conducted a retrospective observational study at the Marius Nasta Institute of Pneumophthisiology, Bucharest, Romania. Our study focused on patients admitted in 2019 with non-small-cell lung carcinoma and associated pulmonary lesions identified through surgical resection specimens. Among the 314 included patients, multiple pulmonary nodules were observed on macroscopic examination, with 12% (N = 37) exhibiting nonmalignant etiologies upon microscopic examination. These findings underscore the challenge of preoperative staging. Patients with coexisting nonmalignant lesions were similar in age, smoking habits, and professional or environmental exposure by comparison with those who presented only malignant lesions. The presentation of coexisting malignant and nonmalignant lesions may pose difficulties in diagnosing and staging pulmonary cancer.