The year 2020 will likely be remembered as the year dominated by COVID-19, or coronavirus disease. The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for this pandemic, can be traced back to late 2019 in China. The COVID-19 pandemic has significantly impacted the tuberculosis (TB) care system, reducing TB testing and reporting. This can be attributed to the disruption of TB services and restrictions on patient movement, consequently increasing TB-related deaths. This perspective review aims to highlight the intersection between COVID-19 and TB, highlighting their dual threat and identifying shared solutions to address these two infectious diseases effectively. There are several shared commonalities between COVID-19 and tuberculosis, particularly the transmission of their causative agents, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Mycobacterium tuberculosis. Both pathogens are transmitted via respiratory tract secretions. TB and COVID-19 are diseases that can be transmitted through droplets and airborne particles, and their primary target is typically the lungs. Regarding COVID-19 diagnostics, several methods are available for rapid and accurate detection. These include RT-PCR, which can provide results within two hours, and rapid antigen test kits that offer results in just a few minutes. The availability of point-of-care self-testing further enhances convenience. On the other hand, various approaches are employed for TB diagnostics to swiftly identify active TB. These include sputum microscopy, sputum for reverse transcription polymerase chain reaction (RT-PCR), and chest X-rays. These methods enable the rapid detection of active TB on the same day, while culture-based testing may take significantly longer, ranging from 2 to 8 weeks. The utilization of diverse diagnostic tools helps ensure the timely identification and management of COVID-19 and TB cases. The quality of life of patients affected by COVID-19 and tuberculosis (TB) can be significantly impacted due to the nature of these diseases and their associated challenges. In conclusion, it is crucial to emphasize the urgent need to address the dual threat of COVID-19 and TB. Both diseases have devastated global health, and their convergence poses an even greater challenge. Collaborative efforts, research investments, and policy reforms are essential to tackle this dual threat effectively.

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.

Among the most widespread childhood infections, Helicobacter pylori (H. pylori) develops potentially life-threatening conditions in adults if not appropriately treated. Helicobacter pylori is a common human pathogen that was first described in the stomach many years ago. The discovery of H. pylori was crucial in gastroenterology; this bacterium is associated with chronic gastritis, peptic ulcers, gastric cancer, and lymphoid tissue lymphoma related to the gastric mucosa. Studies published so far estimate that approximately 10% of subjects infected with H. pylori develop a peptic ulcer, and 1–3% of subjects develop gastric cancer. The clinical manifestations are variable and characteristically depend on the individual factors of the host. Various methods of detection and diagnosis of H. pylori infection have been developed, each with advantages, disadvantages, and/or limitations. Available diagnostic tests are usually performed using invasive (endoscopy, biopsy, rapid urease test, cultures, and molecular tests) and noninvasive methods (urea breath test, stool antigen examination, and serological and molecular tests). Although there is extensive accessibility for diagnosing and treating H. pylori infection, the prevalence of antibiotic resistance is not negligible. Thus, numerous studies and meta-analyses are focused on a new orientation of gastroenterologists in diagnosing and treating H. pylori infections. A fascinating perspective hypothesis is the administration of probiotics to reduce H. pylori adhesion to gastric epithelial cells, preventing H. pylori colonization, especially in children, or reinfection with H. pylori in high-risk adult patients.

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.

Background and objective: Analysis of inflammatory biomarkers, along with the neutrophil/lymphocyte ratio (NLR) or platelet/lymphocyte ratio (PLR), supports the connection between inflammation and carcinogenesis. Methods: We conducted a retrospective observational study at the Clinical County Hospital Mureș involving patients with lung cancer. The parameters analyzed included histopathological type (NSCLC: squamous cell carcinoma or adenocarcinoma; SCLC), molecular mutations (EGFR, ALK, PD-L1), parameters from the complete blood count, inflammatory parameters, and associated comorbidities. Results: A total of 380 patients were included: 115 patients in the cancer group and 265 patients in the control group. Among patients in the lung cancer group, 88 were diagnosed with NSCLC (44 adenocarcinomas, 44 squamous cell carcinomas) and 27 with SCLC. Both NLR and PLR were significantly higher in cancer patients than in the control group (5.30 versus 2.60, p < 0.001; 217 versus 136, p < 0.001, respectively). NLR and PLR differ between men and women (p = 0.005 and p = 0.056, respectively). C-reactive protein was not correlated with either NLR (p-value: 0.0669) or PLR (p-value: 0.6733) in lung cancer patients. Conclusions: The NLR and PLR values may serve as new predictive biomarkers for the diagnosis of disease in patients with lung cancer, especially those with NSCLC.

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.