Background: Understanding the effect of systemic inflammation on the pathophysiology of thromboembolism may provide an approach to determine the course and prognosis of the disease. The aim of this study was to investigate the usability of systemic inflammatory markers in the risk stratification of pulmonary embolism in patients with acute pulmonary thromboembolism (PTE). Methods: The data of 234 patients diagnosed with pulmonary embolism by computed tomography pulmonary angiography (CTPA) or ventilation perfusion scintigraphy were evaluated retrospectively. Demographic data, co-morbid conditions, and laboratory parameters of the patients were obtained from the hospital data system. Pulmonary embolism risk classification was performed according to the 2019 ESC guidelines as low, intermediate (intermediate-low, intermediate-high), and high risk. Neutrophil - lymphocyte ratio (NLR), platelets-to-lymphocyte ratio (PLR), lymphocyte - monocyte ratio (LMR), lymphocyte / CRP ratio (LCRPR), systemic inflammatory response index (SIRI) (Neutrophil×Platelet/Lymphocyte) and systemic immune-inflammation index (SII) (Neutrophil×Monocyte/Lymphocyte) were calculated using the patients’ hemogram (White blood count (WBC), hemoglobin, hematocrit, platelet, neutrophil, lymphocyte, monocyte), C-reactive protein (CRP), lactate, troponin, and d-dimer values at the time of diagnosis. Results: In our study, WBC, neutrophils, NLR, PLR, SIRI, SII and CRP levels were significantly lower in low risk, while lymphocyte count and LCRPR were significantly higher. Platelet counts were significantly lower in high risk. D-dimer levels were significantly higher in intermediate-high and high risk. Lactate levels were significantly higher in high risk. Troponin levels were significantly higher in intermediate-high risk and high risk. WBC, neutrophils, D-dimer, troponin, lactate levels and NLR, SII, indices were found to be significant biomarkers in predicting high-risk embolism. Conclusion: Our findings suggest that systemic inflammatory markers may be a clinically important risk determinant in patients with acute pulmonary thromboembolism.

Aim: In cases where standardized maximum uptake (SUVmax) values in positron emission tomography (PET-CT) were not sufficient to differentiate mediastinal lymphadenopathy and masses from malignant or benign, the contribution of Hounsfield unit (HU) values in thorax computed tomography to the diagnosis was evaluated. Material Method: The study was conducted by evaluating the data of 182 patients between 2019 and 2023. HU values on non-contrast thorax computed tomography and PET-CT SUV_max values of biopsied masses and lymph nodes were compared with histopathological diagnoses. Results: Patients, 58 females (31.9%) and 124 males (68.1%), who underwent EBUS were included in the study. Biopsies were taken from 233 stations (199 lymph nodes, 34 masses) from 182 patients. A total of 135 of the biopsies taken from 233 stations were histopathologically malignant and 98 were benign. While PET-CT SUV_max values of cases with benign histopathology were 4.5 ± 3.5, it was 7.6 ± 4.2 in patients with malignant pathology (p< 0.05). The HU value on non-contrast thorax tomography in patients with benign histopathology was 43.1 ± 15.7, and in patients with malignant histopathology it was 40.5 ± 13.7 (p> 0.05). When HU was compared according to lung cancer type, it was found to be significantly higher in non-small cell lung cancer (p=0.035). A weak (r=0.182) positive and significant relationship (p< 0.01) was found between PET-CT values and HU values in thorax computed tomography. Conclusion: While positron emission tomography maintains its importance in the differentiation of mediastinal lymphadenopathy and masses from malignant to non-malignant, it was concluded that HU values in computed tomography are not sufficient to distinguish malignant/non-malignant.

Purpose: Alpha-1 antitrypsin deficiency (AATD) is a rare inherited condition characterized by low serum levels of alpha-1 antitrypsin (AAT). In this study, we aimed to determine the frequency of AATD in patients with emphysema, to show the distribution of AATD genotypes according to the type and localization of emphysema, and to evaluate patients in terms of augmentation therapy. Patients and Methods: This cross-sectional descriptive study included 794 patients with emphysema on high-resolution thoracic tomography (HRCT) between December 2022 and December 2024 at the chest disease clinic of the Samsun Training and Research Hospital. During screening, demographic characteristics (age and sex), smoking status (smoker, ex-smoker, and non-smoker), types of emphysema (centriacinar emphysema, panacinar emphysema, and paraseptal emphysema), and location (upper, middle, and lower lobes) were recorded. Dried blood spot samples collected from the fingertips of patients with emphysema were screened for Alpha-1 Antitrypsin (AAT) genotype deficiency. AAT levels and PFT were evaluated in patients with AATD. Results: In the AAT genotyping results, no mutations were detected in 763 (96%) patients, while AATD mutations were detected in 31 (4%) patients. While AATD was more common in panacinar emphysema, no mutations were detected in paraseptal emphysema. The most common mutations were PI*M/M malton (n=9), PI*M/Z (n=7), PI*M/I (n=4), and PI*M malton/M malton (n=4). AAT level was found to be low in PI*Z/Z (n=3), PI*M malton/M malton (n=4) and PI*Z/M malton (n=1) genotypes (0.20± 0.2 g/L). Six patients received augmentation therapy for AATD: three had PI*Z/Z, two had PI*M malton/M malton, and one had the PI*Z/M malton genotype. Conclusion: As a result, analyzing AAT genotypes in patients with emphysema may provide an early diagnosis of AATD, allowing the application of preventive measures and augmentation therapy strategies.

Alpha-1 antitrypsin deficiency (AATD) is an autosomal co-dominant condition caused by mutations in the SERPINA1 gene. Chronic obstructive pulmonary disease/emphysema, asthma, and bronchiectasis are lung diseases associated with AATD. This study was designed to identify AATD in patients with bronchiectasis without emphysema and to demonstrate the frequency and distribution of AATD genotypes according to the type of bronchiectasis. The study was conducted as a single-center retrospective analysis between December 01, 2022 and December 31, 2024 in patients with bronchiectasis without emphysema. Patients’ demographic characteristics (age, gender), smoking status (smoker, ex-smoker, nonsmoker), and types of bronchiectasis (cylindrical, varicose, cystic) according to the Reid classification were evaluated. Dried blood spot samples collected from fingertip pricks were used to screen for alpha-1 antitrypsin genotype deficiency. A total of 563 patients, 241 (42.8%) women, and 322 (57.2%) men, with bronchiectasis without emphysema were evaluated, with a mean age of 55.3 ± 14.9 years. An AATD mutation was detected in 16 patients (2.8%). Genotype deficiency was most commonly observed in the cylindrical type (n = 9). The most frequently identified genotypes were PI*M malton in 6 patients (1.1%), PI*P lowell in 4 patients (0.8%), and PI*I in 3 patients (0.6%). Additionally, 2 patients were found to have previously unidentified novel alpha-1 antitrypsin variants. One of these patients also had Kartagener syndrome. Our findings suggest an association between AATD and bronchiectasis, independent of emphysema, and suggest that alpha-1 antitrypsin genotypes should also be examined in cases of bronchiectasis without emphysema to determine its etiology.

Culture confirmation for tuberculosis (TB) and nontuberculous mycobacteria (NTM) is time-consuming, potentially delaying diagnosis and treatment. Identifying systemic inflammatory markers from routine blood tests may provide supportive information for differentiating TB from NTM infection or colonization. This study evaluates the diagnostic value of systemic inflammatory indices in distinguishing TB from NTM infection and colonization. This retrospective study included 480 patients diagnosed between January 2018 and December 2023. TB and NTM diagnoses were confirmed according to microbiological and clinical criteria. Hematological parameters, including neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio, lymphocyte-to-C-reactive protein ratio, systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI), were analyzed. Receiver operating characteristic analysis was performed for parameters showing statistical significance in differentiating TB from NTM colonization. Among the inflammatory markers assessed, lymphocyte count and mean platelet volume were significantly higher in TB compared with NTM colonization, while SII and SIRI indices were significantly lower. Receiver operating characteristic analysis identified optimal cutoff values for lymphocyte count (1.895; sensitivity 57.7%, specificity 71.8%) and SII (2.345; sensitivity 73.1%, specificity 69.4%). The 95% confidence intervals for the area under the curve values are presented in table and figures. Lymphocyte count, mean platelet volume, SII, and SIRI show potential as supportive diagnostic markers for differentiating TB from NTM colonization. These indices may aid clinical decision-making while awaiting culture results; however, further studies with larger sample sizes and prospective validation are warranted.

Aim: This study aimed to investigate the distribution of hereditary risk factors in patients with pulmonary thromboembolism (PTE) who have no acquired risk factors and to explore the relationship between genetic factors and the early mortality risk of embolism. Material and Methods: Data from 295 patients diagnosed with PTE were examined retrospectively. Of these, 44 patients who had no acquired risk factors and were screened for hereditary risk factors, including factor V Leiden (FVL), prothrombin (PT) G20210A, methylenetetrahydrofolate reductase (MTHFR) C677T, MTHFR A1298C, plasminogen activator inhibitor (PAI) 4G/5G, factor XIII, antithrombin (AT) III, protein C, protein S, and activated protein C resistance (APCR), were included in the study. Results: Of the patients, 14 (31.8%) were female and 30 (68.2%) were male, with a mean age of 46.5±17.3 years. Among the hereditary risk factors, the most common homozygous mutations were MTHFR A1298C (n=10, 22.7%), PAI 4G/5G (n=9, 20.5%), and FVL (n=5, 11.4%), while the most common heterozygous mutations were PAI 4G/5G (n=26, 59.1%), MTHFR A1298C (n=19, 43.2%), and MTHFR C677T (n=16, 36.4%). The heterozygous MTHFR A1298C mutation was detected in 10 (52.6%) patients with a history of recurrent PTE. Conclusion: This study highlights the presence of genetic mutations such as PAI 4G/5G, MTHFR A1298C, MTHFR C677T, FVL, factor XIII, and PT G20210A in patients with PTE. The results show a high prevalence of genetic causes, especially in patients under 50 years of age with no acquired risk factors, no history of recurrent PTE or thrombophilia in any family member.