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Introduction: The Neutrophil-to-Lymphocyte Ratio (NLR) has been utilized to predict clinical outcomes in cardiovascular diseases, infectious diseases, and solid tumors and it has a potential association with the severity of Chronic Obstructive Pulmonary Disease (COPD). This study aimed to determine whether NLR is a possible predictor of inflammation severity and mortality in COPD. Methodology: A prospective analysis of NLR in 70 COPD patients, and its relation with biochemical, lung function parameters, and mortality was assessed. Results: NLR was negatively associated with oxygen saturation (p < 0.05) and positively related to C-reactive protein (CRP) (p < 0.05), matrix metalloproteinase-9 (MMP-9) (p ≤ 0.001), tissue inhibitor of metalloproteinase-1 (TIMP-1) (p < 0.05), MMP-9/TIMP-1 ratio (p < 0.05), and the modified Medical Research Council dyspnea scale (mMRC) score (p < 0.05). Deceased patients had significantly higher NLR (p < 0.05). Older age and lower levels of saturation were independently associated with higher mortality in COPD patients (p < 0.05). Conclusions: NLR in COPD correlates with inflammation and protease/antiprotease balance, with elevated NLR detected in deceased patients. These findings suggest that NLR can be a helpful clinical marker in COPD.

Background/Objectives: Idiopathic pulmonary fibrosis (IPF) registries are established to enhance understanding of its natural history. Methods: Serbia (RS) participated in the EMPIRE (European Multi-Partner IPF Registry) from June 2015 to October 2022, involving four centers. The registry included patients over 18 diagnosed with IPF based on the 2011 international criteria. We aimed to gather key clinical, functional, and survival data, along with treatment information for IPF patients in RS, using a centralized electronic case report for consistency. Results: 188 RS patients participated (median age at diagnosis 65, 63.8% male, 51% smoking history, 56% radiological usual interstitial pneumonia (UIP) pattern). At the diagnosis, median forced vital capacity (FVC) was 73.7% and diffusion capacity for carbon monoxide (DLCO) was 38%. At initiation of antifibrotic therapy, median FVC was 73.2% (71.5% for deceased, 75.8% for survivors (p = 0.455), and DLCO was 33.8% (19.9% for deceased, and 35.6% for survivors (p = 0.046)). The median long-term survival from diagnosis was 29.4 months (95% CI: 22.6–36.2 months), and 9.4 months (95% CI: 5.9–12.9 months) from the initiation of therapy, with no difference in the duration of antifibrotic treatment between survivors and deceased (p = 0.598). Conclusions: The RS EMPIRE cohort represents a younger, less comorbid population with fewer smokers and more probable UIP, factors linked to a favorable prognosis. Nevertheless, survival was poorer than expected, mainly due to advanced disease severity at the time of antifibrotic initiation, as indicated by lower DLCO. These findings highlight the importance of earlier diagnosis and treatment before significant physiological decline to improve outcomes.

Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive, unpredictable, fatal interstitial lung disease. Antifibrotic therapy with pirfenidone or nintedanib slows functional decline, yet comparative real-world evidence remains limited. Materials and Methods: This retrospective, single-center, comparative cohort study included 76 IPF patients treated at the Clinic for Pulmonology at the University Clinical Center of Serbia (February 2019–February 2025). Diagnosis of IPF was made according to the guidelines of the American Thoracic Society and the European Respiratory Society. Demographic features, comorbidities, forced vital capacity (FVC), diffusion capacity for carbon monoxide (DLCO), high-resolution computerized tomography (HRCT) patterns, 6-min walk test distance (6MWTD), echocardiography, and survival outcomes were analyzed. Disease progression was defined as a ≥10% decline in FVC and/or DLCO after 12 months. Results: Of the 76 patients, 31 received nintedanib and 45 pirfenidone. Baseline characteristics, comorbidities, and HRCT patterns were comparable between groups. Mean annual decline in FVC was −1.74% with pirfenidone and −2.38% with nintedanib, without a statistical difference. DLCO declined by −4.25% and −6.29%, respectively, with similar downward trends over time in both groups. Progression was recorded in 35 (46.1%) patients, of whom 18 (58.06%) were in the nintedanib group and 17 (37.77%) in the pirfenidone group, with no difference between therapies (p = 0.81). Definite and probable usual interstitial pneumonia (UIP) were evenly represented on HRCT, although progression correlated significantly with the probable UIP pattern (p = 0.006). 6MWTD decreased in both groups over 12 months, again without treatment-related differences (p = 0.566). During up to 6 years of follow-up, overall survival was 4.18 years, with no significant difference between the nintedanib (4.55 years) and pirfenidone (3.81 years) groups (p = 0.159). No association was found between disease stage (FVC or DLCO) and progression. Conclusions: This study demonstrates that pirfenidone and nintedanib are equally effective in the management of IPF in real-world settings. The absence of significant differences in functional decline, progression rates, and survival indicates that treatment choices should be guided by individual clinical profiles rather than efficacy alone, reinforcing antifibrotic therapy as the primary approach to alter the course of IPF. Importantly, disease progression was strongly associated with a probable UIP pattern on HRCT, supporting current guidelines suggesting that probable UIP has a natural history and prognosis similar to those of definite UIP.