Background: Preeclampsia (PE) remains a significant cause of maternal and fetal morbidity and mortality, with diagnostic criteria still evolving. Serum albumin, a potential marker of endothelial dysfunction and protein loss, has been proposed as a severity indicator in PE. This study evaluates the clinical utility of serum albumin levels, particularly values below 2 g/dL, in assessing PE severity and predicting maternal–fetal complications. Methods: We conducted a prospective and descriptive study including 59 pregnant women diagnosed with PE. The participants were divided into mild (n = 23) and severe (n = 36) PE groups based on national guidelines. Serum albumin, 24 h proteinuria, renal and hepatic function markers, and fetal outcomes were analyzed. ROC curve analysis was employed to determine albumin’s diagnostic performance. Results: Serum albumin levels were significantly lower in the severe PE group compared to the mild PE group (1.82 ± 0.50 vs. 2.44 ± 0.36 g/dL, p < 0.001). ROC analysis identified a threshold of 2.3 g/dL (sensitivity: 88.9%, specificity: 73.9%) for distinguishing PE severity. A strong association was observed between albumin < 2 g/dL and severe proteinuria (>3 g/24 h), but no significant association emerged with renal or hepatic dysfunction, fetal complications, or birth outcomes. Conclusions: Although serum albumin < 2 g/dL is associated with severe proteinuria, it does not independently correlate with other maternal or fetal complications in PE. These findings suggest that albumin may serve as a complementary, but not a standalone, marker in assessing PE severity.

Background: Scar carcinoma represents a distinct subtype of lung malignancy developing in areas of chronic pulmonary fibrosis, inflammation, and structural remodeling, frequently associated with previous pulmonary tuberculosis (TB). The present study aimed to evaluate the radiological, clinical, inflammatory, and histopathological characteristics associated with the scar carcinoma phenotype in patients with lung cancer (LC) and previous TB-related pulmonary abnormalities. Methods: A retrospective observational cohort study conducted between February 2020 and December 2025 included 844 patients diagnosed with lung cancer. The scar carcinoma phenotype was operationally defined by the coexistence of: (1) confirmed lung cancer, (2) post-tuberculous structural pulmonary abnormalities on thoracic imaging, and (3) clinical history compatible with prior pulmonary TB. Associations between the scar carcinoma phenotype and clinicopathological variables were evaluated using Pearson’s Chi-square and Fisher’s exact tests. Binary logistic regression analysis was performed to identify independent predictive factors associated with scar carcinoma. Receiver operating characteristic (ROC) curve and precision–recall curve analyses were additionally performed. Results: Post-TB sequelae were identified in 58.2% of patients, while active TB was present in 7.8% of cases. Adenocarcinoma represented the predominant histopathological subtype (63.3%). Fibrotic/interstitial/bronchial abnormalities (67.7%), cavitary/destructive lesions (69.0%), atelectatic/retractile changes (65.4%), and infectious/inflammatory pulmonary abnormalities (60.4%) were highly prevalent. Significant associations were identified between scar carcinoma and TB sequelae (χ² = 811.850, p < 0.001), adenocarcinoma histology (χ² = 655.545, p < 0.001), infectious/inflammatory changes (χ² = 635.168, p < 0.001), cavitary/destructive lesions (χ² = 508.347, p < 0.001), fibrotic/interstitial abnormalities (χ² = 539.895, p < 0.001), and atelectatic/retractile changes (χ² = 597.346, p < 0.001). Logistic regression identified haemoptysis (OR = 0.651 (95% CI: 0.486–0.871), p = 0.005) and pulmonary opacities and/or condensation (OR = 1.343 (95% CI: 1.014–1.779), p = 0.040) as independent predictive factors. ROC analysis demonstrated moderate predictive performance (AUC = 0.703). Conclusions: TB-associated pulmonary remodeling was strongly associated with the scar carcinoma phenotype, consistent with an associative role of chronic inflammation, fibrosis, and post-TB structural damage in lung carcinogenesis; however, causal inferences cannot be drawn from this retrospective observational design.

Background: Tuberculosis (TB) has long been suspected to contribute to lung carcinogenesis through chronic inflammation and immune dysregulation. However, contemporary controlled evidence quantifying this association remains limited. We aimed to systematically evaluate the relationship between prior TB and subsequent lung malignancy, using recent observational studies and complementary case reports. Methods: A systematic review and random-effects meta-analysis were conducted, including controlled cohort and case–control studies published from 2020 onward. Adjusted effect estimates were converted to the logarithmic scale for pooling. Heterogeneity and small-study effects were assessed using standard meta-analytic techniques. Additionally, published case reports were descriptively analyzed to explore clinicopathological patterns. Results: Across eligible studies, prior TB was consistently associated with an increased risk of subsequent lung cancer (LC). The pooled estimate demonstrated a statistically significant positive association, despite moderate heterogeneity. Larger nationwide cohorts contributed greater statistical weight, while smaller studies showed wider variability. Case reports revealed heterogeneous temporal patterns, including long-latency scar-associated carcinoma and concurrent inflammatory–malignant presentations. Conclusions: Contemporary controlled evidence supports an association between prior tuberculosis and increased risk of subsequent lung malignancy. However, despite strong biological plausibility and the abundant literature on cancer-associated tuberculosis, modern longitudinal studies specifically evaluating tuberculosis as a preceding independent risk factor remain limited. The small number of eligible post-2020 investigations identified in this meta-analysis highlights a significant contemporary research gap and underlines the need for well-designed prospective studies to clarify causality and guide surveillance strategies in TB-exposed populations.

Background: Pulmonary tuberculosis (PTB) and lung cancer (LC) are major causes of global respiratory morbidity and mortality. Increasing evidence suggests that tuberculosis may induce persistent pulmonary alterations that extend beyond microbiological cure, potentially facilitating lung carcinogenesis. This review synthesizes current epidemiological and mechanistic evidence linking PTB to subsequent LC development. Methods: A structured narrative appraisal of the literature was conducted using PubMed, Web of Science, Scopus, ScienceDirect, MDPI Journals, and Google Scholar, focusing on studies published between 2020 and 2025. Eligible publications included cohort studies, meta-analyses, observational reports, and mechanistic investigations addressing the TB–LC association. Studies were thematically categorized into epidemiological evidence, pathogenic mechanisms, diagnostic challenges, and therapeutic implications. Results: Population-based studies consistently demonstrate a two- to threefold increased risk of LC among individuals with prior PTB, independent of smoking and other major confounders. Mechanistically, the post-tuberculous lung is characterized by chronic inflammation, oxidative stress, fibrotic remodeling, immune checkpoint activation (including PD-1/PD-L1 signaling), dysregulated microRNA expression, and metabolic reprogramming. Clinically, overlapping radiological and histopathological features may delay cancer diagnosis. A history of TB may also influence therapeutic decisions, particularly regarding immune checkpoint inhibitors due to potential infection reactivation. Conclusions: PTB may represent an independent risk factor for LC through sustained structural and immunological remodeling. Structured post-TB surveillance and risk-adapted screening strategies may be warranted in selected high-risk populations.

Background/Objectives: Air pollution is progressively acknowledged not only as a carcinogenic exposure, but also as a potential modulator of tumor immune activation and molecular heterogeneity in lung cancer. However, integrated analyses combining long-term environmental exposure, molecular biomarkers and immune phenotype remain limited, especially in Eastern European populations. Methods: We conducted a regional retrospective study including patients diagnosed with lung cancer in Constanța County, Romania. Prolonged atmospheric pollution exposure over an average period of 15 years was estimated using historic environmental monitoring data. Tumor samples were assessed for histopathological subtype, PD-L1 expression and EGFR status, while ALK and KRAS alterations were descriptively analyzed because of the limited number of positive cases. Multivariate ordinal and binary logistic regression models and predicted probability analyses were used to evaluate the association between chronic pollution exposure, PD-L1 expression and EGFR positivity. Results: Chronic NO₂ exposure was significantly associated with increased PD-L1 expression (OR = 1.035, p = 0.017), suggesting an association between NO₂ exposure and an immune-related tumor phenotype. Similar trends were observed for PM10, NO and NOx exposures. Exploratory associations were observed between EGFR positivity and carbon monoxide exposure. Conclusions: Chronic atmospheric pollution was associated with differences in the immune and molecular profile of lung cancer. Long-term exposure to selected pollutants was associated with variations in PD-L1 expression and EGFR status, suggesting that environmental factors may contribute to tumor heterogeneity. However, causal relationships cannot be established from this retrospective observational study.

Background: Tuberculosis-related pulmonary changes may overlap radiologically and clinically with lung cancer, complicating diagnostic interpretation, staging, and therapeutic planning. This study evaluated the relationship between tuberculosis status, thoracic imaging patterns, and clinical characteristics in patients diagnosed with lung cancer. Methods: A retrospective cohort study was conducted between February 2020 and December 2025 at the Clinical Pneumophtisiology Hospital, Constanța, Romania. A total of 620 patients with lung cancer were analyzed. Patients were classified into three groups: no tuberculosis, post-tuberculosis sequelae, and active tuberculosis. Demographic, clinical, laboratory, histopathological, functional, and radiological variables were assessed. Associations between tuberculosis status and imaging findings were evaluated using chi-square testing, effect-size analysis, and multinomial logistic regression. Results: Post-tuberculosis sequelae were identified in 337 patients (54.4%), active tuberculosis in 51 patients (8.2%), and no tuberculosis-related disease in 232 patients (37.4%). Adenocarcinoma was the most frequent histological type, occurring in 359 patients (57.9%). Significant associations with tuberculosis status were observed for fibrotic/interstitial or bronchial changes, infectious-inflammatory changes, cavitary/destructive lesions, atelectatic/retractile changes, pulmonary opacities, pleural involvement, and mediastinal/hilar adenopathy. The strongest effects were found for fibrotic/interstitial changes, infectious-inflammatory changes, and cavitary/destructive lesions. In regression analysis, active tuberculosis was most strongly associated with infectious-inflammatory changes, cavitary lesions, pulmonary opacities, and fibrotic abnormalities, while post-tuberculosis sequelae were mainly associated with chronic fibrotic and structural pulmonary changes. Conclusions: Tuberculosis-related abnormalities frequently coexist with lung cancer and may mimic or obscure malignant findings. Recognition of these overlapping patterns is essential for accurate radiological interpretation and individualized clinical management.