Turkthoracj, Turkish Thoracic Journal

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.

We aimed to report outcomes of pregnant patients with asthma under omalizumab treatment and their infants in our county. Patients with asthma who received omalizumab for at least 6 months and at least one dose during their pregnancy were retrospectively evaluated using a questionnaire regarding their disease and therapy, the health of their infants. 20 pregnant patients and their 23 infant?s data were analyzed. The mean delivery age was 31.8±7.4 years. They received omalizumab for 28.9±21.8 months. Eight (36.4%) patients showed exacerbation of the disease during pregnancy. Forced expiratory volume in 1 second (FEV1) and asthma control test (ACT) scores at the starting time of omalizumab administration, first month of the pregnancy, and after delivery were 71±18%, 83.4±10.5%, and 80.5±13% (FEV1), and 11.9±4.9, 20.2±2.6, and 20.4±2.2 (ACT), respectively. One patient gave birth to twin infants, two patients to two infants each in different years, and 17 to one infant each. Three (13%) infants had low birth weight and five (21.7%) were born prematurely. No congenital anomalies were detected. Seven (30.4%) infants presented atopic diseases during their life. Omalizumab treatment during pregnancy seems to be safe for both patients and their infants.

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.