Hamartomas are the most common benign tumors of the lung. Endobnronchial hamartomas are even rarer and infrequently causes hemoptysis. We report a case of endobronchial hamartoma that was originating from a segment bronchus and invisible in chest X-ray. A 63-year-old man was admitted to hospital with hemoptysis. A CT scan revealed endobronchial mass obstructing anterior bronchus of the right lower lob of the right lung. It wasn’t radiographically presented. Flexible bronchoscopy detected a polypoid mass (1.5x1.0 cm) that arising from the posterior wall of the anterior segment of right lower lob. Histopathologic examination revealed lipoumatous hamartoma. It was resected with an electro-surgical snare. Cryotherapy was applied to residual lesion on surface of the bronchus. The patient was successfully recovered. In conclusion, lipoumatous hamartoma may presented as rare cause of hemoptysis. Endoscopic treatment is safe and currently modality used for select cases.

Objective: Paraoxonase1 (PON1) and arylesterase (ARE) enzyme have an important role in prevention of oxidative stress which was related to the pathogenesis of chronic obstructive pulmonary disease (COPD). PON1 level vary widely among individuals and ethnic groups, which is in part correlated with polymorphisms. Materials and Methods: We investigated paraoxonase 1 and arylesterase activity and phenotype distribution in COPD patients and healthy individuals. Sixty six COPD patients and fifty nine control subjects were involved in the study. Serum PON1 and ARE activities were detected by spectrophotometric method. The ratio of salt-induced PON1 to arylesterase activity was used for determination of phenotypes as QQ, QR and RR. Results: COPD patients exhibited higher PON1 activity (199.1 vs 129.2, p= 0.002) but lower ARE activity compared to control (21.3 vs 33.5, p= 0.021). There was a significant difference between COPD and control group with respect to PON1 phenotype characteristics. RR phenotypic distribution was more common in the COPD group than in control (60.6% [95% CI: 48.8-72.3] versus 22.0 % [95%CI: 12.0-31.9], p= 0.001). We also found that smoking (95.0% CI: 0.001-0.036, p< 0.001), and RR phenotype (95.0% CI: 0.006-0.59, p= 0.016) are independent determinants in COPD. Conclusion: We found that RR phenotype was more common in COPD pateints compared to control. Smoking and RR phenotype may be defined as independent factors associated with COPD. Cite this article as: Sarioglu N, Bilen C, Cevik C, et al. Paraoxonase Activity and Phenotype Distribution in Patients with Chronic Obstructive Pulmonary Disease. Eurasian J Med 2020; 52(2): 161-5.

Objective: This study aimed to investigate the smoking prevalence and associated factors among the students of Balıkesir University and determine the level of nicotine dependence in smokers. \ud \ud Methods: Six faculties and two graduate schools located at the Balıkesir University campus were enrolled. The cluster method was used as the sampling method. To observe the rates of smoking initiation while studying at the university, first-year and final year students were compared.\ud \ud Results: A total of 1096 students were enrolled, with a mean age of 20.4±2.2 years. The regular smoking prevalence rate was 25.5%, occasional smoking rate was 9.5%, alcohol consumption rate was 28.0%, and drug abuse rate was 5.0%. The mean age for attempting to smoke was 16.6±2.2 years. The leading causes of smoking were curiosity, spiritual space, affection, and to comply with friends. According to the Fagerström questionnaire, the level of nicotine dependence was low in 53.0% of the participants, moderate in 8.7%, and high in 28.4%. The average smoking prevalence rate was 23.6% in first-grade students, whereas it was 44.8% in last-grade students. The factors that influence smoking were as follows: being in the last grade, mother, siblings, and friends who smoke, higher allowance, use of alcohol and drugs. Smoking was found to be more prevalent among males. \ud \ud Conclusion: Last-grade students had a higher smoking prevalence rate than the first-grade students. Family, social environment, and smoking behavior of friends have an influence on smoking. All risk factors, including past history and university period, should be considered together in tobacco control

Obstructive sleep apnea (OSA) is known to be closely associated with cardiovascular disease. Carotid intima-media thickness (IMT) is widely used for assessment of atherosclerosis. Mean platelet volume (MPV) is a new marker associated with atherothrombosis. In this study, we aimed to detect early atherosclerosis by measuring carotid intima-media thickness and to investigate the relationship between MPV and IMT and OSA severity. The study population consisted of 158 patients who underwent polysomnography and did not have any overt cardiac disease or risk factors. Carotid IMT was measured by ultrasonography. Blood samples were taken for MPV determination. Subjects were divided into 4 groups according to OSA severity: control, mild, moderate, and severe OSA. The patients with OSA (mild, moderate, severe) had an increased carotid IMT (0.59±0.2, 0.60±0.1, 0.64±0.1, respectively) compared to controls (0.50±0.1, p<0.05). There were no differences found between groups regarding mean platelet volume. Carotid IMT was found to be positively correlated with age, systolic blood pressure, apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and time duration with oxygen saturation <90% (T90), and negatively correlated with minimum SpO2 and mean SpO2. MPV was not correlated with OSA severity or other parameters. Carotid IMT was found to be effective in predicting the presence of OSA [AUC=0.769 (0.683, 0.855), p<0.001)] but MPV was not found to be effective [AUC=0.496 (0.337,0.614) p=0.946)]. OSA patients appear to have increased carotid IMT suggestive of an atherosclerotic process. Carotid IMT could be a more useful indicator than MPV in these patients. Long-term prospective studies are needed to confirm these results.

Background/aim: Acute lung injury (ALI) is a major cause of death in the intensive care unit. Lipopolysaccharide (LPS) induced lung injury is the most widely used experimental ALI model and provides opportunities for new targeting therapy. In this study, we investigated the effects of tocilizumab, adalimumab, and methylprednisolone in LPS-induced acute lung injury. Materials and methods: Lung injury was established by intratracheal instillation of LPS. The rats were randomly divided into six groups: LPS, control, and treatment groups (adalimumab, tocilizumab, methylprednisolone, adalimumab + tocilizumab). Bronchoalveolar lavage (BAL) and lung tissues were collected at 48 h and 96 h following LPS administration from each group. For histological analysis, hematoxylin-eosin (H&E) staining was performed. The sections were obtained for immunohistochemical analysis. IL-6 and TNF-alpha immunoreactivity were measured. Results: Intratracheal LPS application resulted in inflammatory cell infiltration of interstitial and alveolar spaces and thickening of the alveolar wall. All treatment groups showed significantly amelioration compared to LPS at 48 h. Interestingly, adalimumab and adalimumab + tocilizumab groups showed a significant amelioration of the lung histoarchitecture, compared to the prednisolone group at 96 h (p = 0.028, p = 0.025, respectively). Compared to the control group, LPS stimulation resulted in a significant increase in IL-6 and TNF-alpha immunoreactivity (p < 0.001). IL-6 and TNF-alpha expression were markedly reduced in all treatment groups at 48 h but the reduction was greater in the adalimumab and tocilizumab group than in the steroid. Administration with adalimumab and/or tocilizumab effectively decreased expression of TNF-alpha (p = 0.001) and IL-6 (p < 0.001) at 96 h, but prednisolone did not exert an effective decrease (p > 0.05). Conclusion: Adalimumab and/or tocilizumab significantly reduce the release of proinflammatory cytokines and improve the tissue inflammation in the experimental model of ALI. Our results suggest that adalimumab and/or tocilizumab have a more potent antiinflammatory effect on lung injury than the steroid.

Chronic obstructive pulmonary disease (COPD) is currently a complex, multicomponent disorder. The COPD Assessment Test (CAT) has been increasingly used to assess COPD patients. This study aims to investigate the relationship between CAT and inflammation markers and other COPD components. We enrolled 110 stable COPD patients and 65 control subjects in this study. All patients completed the CAT questionnaire and the modified Medical Research Council (mMRC) dispnea scale. The quality of life of these patients was measured with St. George's Respiratory Questionnaire (SGRQ). Levels of TNFα, IL-6, CRP were determined in blood samples. In COPD patients, serum levels of TNFα (109.5 ± 58 pg/ml), IL-6 (10.3 ± 18 pg/ml), and C-reactive protein (CRP) (1.6 ± 1.7 mg/L) were found to be significantly higher compared to controls (TNF-α: 14.6 ± 18 pg/ml, IL-6: 2.14 ± 1.9 pg/ml, CRP: 0.4 ± 0.3mg/L, p<0.001). These markers were correlated with smoking (r from 0.27 to 0.35, p<0.001), FEV1 (r from -0.39 to -0.57, p<0.001), FVC (r from -0.32 to -0.37, p<0.001) and FEV1/FVC (r from -0.31 to -0.66, p<0.001). The CAT score correlated with GOLD spirometric stages, mMRC dyspnea score, number of exacerbations in the previous year and FEV1 (p<0.001). There was a significant correlation between levels of CRP and the CAT score (r=0.43, p<0.001) but no similar relationship between levels of TNFα and IL-6 and the CAT was observed. Systemic inflammation persists in the stable period of COPD. CRP, one of the inflammation markers, was correlated with the CAT. Further studies are required to confirm the relationship between CAT and biomarkers.