Diagnostic value of adenosine deaminase in bronchoalveolar lavage fluid for patients with lung cancer.

BACKGROUND: Lung cancer is both the most common seen malignity and cause of cancer-related deaths worldwide. Adenosine deaminase (ADA) is a hydrolytic enzyme that catalyses the conversion of adenosine to inosine in the purine metabolism pathway. Studies examining ADA levels in bronchoalveolar lavage (BAL) fluids of patients with lung malignancy are very limited in the literature. Our aim examine the clinical significance of ADA levels in BAL fluids of patients with lung malignancy. METHODS: A total of 89 patients undergoing fiberoptic bronchoscopy (FOB) with different indications from December 2017 to December 2018 were included in this study. The patients were divided into two groups as malignancy and non-malignancy groups. Demographic, laboratory data and ADA levels in bronchoalveolar lavage (BAL) were compared between the two groups. In addition, ADA levels in BAL were compared among the histopathological subtypes of patients in the malignant group. RESULTS: The mean age of the patients was 58.2 ± 14.5 years with 86% of male gender. ADA enzyme levels were statistically higher in the malignant patient group compared with the non-malignant group (37.2 [17.6-71] vs 17.1 [9-35.3], P < .001). When the patients in the malignant group were compared in terms of ADA levels according to their histopathological types, a statistically significant difference was obtained in small cell carcinoma patients (49 [12.5-75.3], P = .005). CONCLUSION: ADA levels in BAL may be a diagnostic biomarker in lung malignancies. In patients where a biopsy cannot be taken or histopathological typing cannot be performed because of tissue insufficiency, ADA levels in BAL can be an auxiliary parameter in making malignancy / histopathological diagnosis accompanied by radiological and clinical findings.

Peripheral DNA damage in active pulmonary tuberculosis.

In pulmonary tuberculosis patients, little is known about peripheral DNA damage, although increased oxidative stress is a well documented entity. Therefore, we aimed to investigate DNA damage along with oxidative status parameters in pulmonary tuberculosis patients. Twenty-seven pulmonary tuberculosis patients and 26 controls were included. DNA damage was assessed by comet assay. Total oxidant and antioxidant status, and oxidative stress index were determined. DNA damage, total oxidant status and oxidative stress index were higher in pulmonary tuberculosis patients than controls (all P < 0.05), while total antioxidant status was lower (P < 0.05). DNA damage was correlated with total oxidant and antioxidant status, and oxidative stress index (r = 0.69, P < 0.05; r = 0.48, P < 0.05, r = -0.47, P < 0.05; respectively) in pulmonary tuberculosis patients. Oxidative stress and DNA damage are increased in pulmonary tuberculosis patients. Increased oxidative stress associated DNA damage may be one of the pathogenetic mechanisms involved in the disorders suggested to be associated with pulmonary tuberculosis.

PON1 activity and total oxidant status in patients with active pulmonary tuberculosis.

OBJECTIVES: The aim of this study was to the investigate effect of tuberculosis infection on paraoxonase-1 (PON1) activity and oxidative status in patients with pulmonary tuberculosis (PTB). DESIGN AND METHODS: Twenty-five active PTB subjects and 33 healthy controls were included in the study. Serum PON1 activity, total oxidant status (TOS), lipid hydroperoxide (LOOH) and total free sulfydryl (-SH) groups were determined. RESULTS: Serum basal/salt-stimulated paraoxonase activities, arylesterase activity and total -SH group levels were significantly lower in patients with PTB than controls (p<0.05, p<0.05, p<0.001 and p<0.01 respectively), while TOS and LOOH levels were significantly higher (p<0.01 and p<0.05, respectively). In PTB patients, TOS, LOOH and total -SH group levels were significantly correlated with paraoxonase (r=-0.371, p<0.05; r=-0.286, p<0.05; r=0.625 p<0.01; respectively) and arylesterase (r=-0.437, p<0.01; r=-0.352, p<0.05; r=0.653, p<0.01; respectively). CONCLUSIONS: Patients with active PTB are exposed to potent oxidative stress and they have decreased PON1 activity. These predisposal factors may, in part, play a role in the pathogenesis of atherosclerosis in PTB.