No abstract

The goal of this study was to evaluate the role of oxidant-antioxidant balance in the pathogenesis of COPD. We included 30 healthy nonsmokers [24 male, 6 female; mean age (yr) +/- SD: 62.4 +/- 9.3], 30 healthy smokers [27 male, 3 female; mean age (yr) +/- SD: 58.7 +/- 6.0], 71 patients with stable COPD [68 male, 3 female; mean age (yr) +/- SD: 63.5 +/- 7.9], and 31 patients with COPD exacerbation [30 male, 1 female; mean age (yr) +/- SD: 64.2 +/- 7.3]. In all study groups the peripheral venous blood samples were taken for plasma malonyldialdehyde (MDA), a parameter of lipid peroxidation caused by the oxidants, and erythrocyte superoxide dismutase (SOD), an antioxidant enzyme. The mean plasma MDA level was higher in healthy smokers and in patients with COPD than in healthy nonsmokers (p < 0.05), and erythrocyte SOD enzyme activity in patients with COPD exacerbation (1048.2 +/- 226.5 Ug/Hb) was significantly higher than in healthy nonsmokers (947.9 +/- 198.0 Ug/Hb) (p < 0.05). Although mean erythrocyte SOD enzyme activity in healthy smokers and patients with stable COPD was higher than in healthy nonsmokers, the difference was not statistically significant. We found that healthy smokers and stable and exacerbated COPD patients had an impairment in oxidant-antioxidant balance. We suggested that new therapeutic interventions, which may repair the impaired oxidant-antioxidant balance in COPD, are needed to prevent the development of COPD.

It is recommended to evaluate the presence of latent tuberculosis infection (LTBI) before initiating antitumor necrosis factor alpha (anti-TNF) therapy for rheumatologic diseases. We aimed to present the follow-up results of 192 patients with rheumatologic diseases before anti-TNF therapy for LTBI. We enrolled 192 patients who were given anti-TNF therapy for their rheumatologic diseases between April 2005 and January 2008. The demographic characteristics of the patients were recorded. Chest X-ray was obtained and tuberculin skin test (TST) was performed in all patients before anti-TNF therapy. LTBI was assessed by detailed history of close contact with infectious cases within the last year, abnormal chest radiography, and positive TST (> or =5 mm) before initiating anti-TNF therapy. Patients with anti-TNF therapy were followed with 2-month intervals for active tuberculosis by pulmonary and extrapulmonary symptoms, physical examination, and chest X-ray. Of 192 patients, 104 (54.2%) patients were women, age (mean +/- SD) 43.1 +/- 12.7 years and 88 (45.8%) patients were men, age (mean +/- SD) 39.3 +/- 11.2 years. Ninety-one (47.4%) of them had rheumatoid arthritis (RA); 92 (47.9%) had ankylosing spondylitis (AS), and nine (4.7%) had psoriatic arthritis. Isoniazid treatment was started in 129 (67.2%) patients in whom LTBI was detected. No significant difference was observed for TST positivity (TST > or = 5 mm) between the patients with RA and AS (p = 0.101). Similarly, no significant difference was also observed for TST positivity between the patients who received immunosuppressive therapy and those who did not (p = 0.154). Only three (1.6%) patients developed active tuberculosis at the study period. We suggested that in despite of the presence of rheumatologic disease and/or immunosuppressive therapy, TST is an acceptable and available diagnostic test for detecting LTBI before anti-TNF therapy.

We investigated the oxidant-antioxidant balance and the effect of inhaled corticosteroids on this balance in mild stable asthmatics. Included in the study were 30 mild asthmatic patients (11 male, 19 female, mean age (year) +/- SD: 35.1 +/- 9.7) and 26 healthy adults (7 male, 19 female, mean age (year) +/- SD: 40.8 +/- 13.3). In all study groups, the peripheral venous blood samples were taken for plasma malonyldialdehyde (MDA), a parameter of lipid peroxidation caused by the oxidants, and erythrocyte superoxide dismutase (SOD), an antioxidant enzyme. The mean plasma MDA level was lower in the asthmatic group (5.7 +/- 1.2 nmol/ml) than in the healthy group (6.3 +/- 1.7 nmol/ml); and the mean erythrocyte SOD level was higher in asthmatic group (1086.4 +/- 247.4 U/gHb) than in the healthy group (1028.0 +/- 230.0 U/gHb). However, there were no significant differences in measurements of both plasma MDA levels and erythrocyte SOD enzyme activities between the groups (respectively, p = 0.1 and p = 0.4). When asthmatic patients were divided into subgroups as "inhaled steroid user" and "no inhaled steroid user", no significant differences were observed in the measurements of either plasma MDA level or erythrocyte SOD enzyme activity between the mentioned subgroups. According to the results of our study, we can say that oxidant-antioxidant balance is not significantly affected in mild asthmatics or measurement of plasma level of MDA and erythrocyte SOD enzyme activity is not sensitive to the oxidant-antioxidant balance in mild asthmatics.

We aimed to evaluate tuberculin skin test (TST) and interferon-gamma (IFN-γ) test results for latent tuberculosis infection (LTBI) in patients with rheumatologic diseases prior to anti-TNFα therapy. Ninety patients were evaluated in the study at the Departments of Chest Diseases and Rheumatology for anti-TNFα therapy for their rheumatologic diseases. Tuberculin skin test was performed (Mantoux method) and peripheral blood samples were collected for IFN-γ assay (QuantiFeron TB-Gold In Tube) before the anti-TNFα therapy. Of 90 patients, TST positivity was detected in 56 (62.2%) patients, while IFN-γ positivity was detected in 34 (37.8%) patients. Among 56 TST positive patients, IFN-γ positivity was detected in 24 (42.9%) patients, and among 34 TST negative patients, IFN-γ positivity was detected in 10 (29.4%) patients. There was no significant agreement between TST and IFN-γ assay results (Kappa = 0.12, P = 0.2). Forty-three (47.8%) patients were using immunosuppressive drugs owing to their rheumatologic diseases. In this group, TST and IFN-γ positivity is significantly lower than in those who did not receive immunosuppressive treatment (P < 0.05). We conclude that the IFN-γ assay may not be preferred to TST as a diagnostic test in patients with rheumatologic diseases prior to anti-TNFα treatment.

Death receptor 4 (DR4) gene is a candidate tumor suppressor gene that has a role in apoptotic pathway. It was reported in literature that polymorphisms in DR4 gene lead to susceptibility to many cancers. In accordance with this information, we aimed to investigate the association between G422A, C626G, A683C and A1322G polymorphisms in DR4 gene and lung cancer. We selected 60 patients with lung cancer (LC) and 30 healthy, sex and age matched volunteers randomly. Four polymorhisms, G422A, C626G, A683C and A1322G, in DR4 gene were analyzed with Polymerase Change Reaction (PCR)--Restriction Fragment Lenght Polymorphism (RFLP) and Amplification Refractory Mutation System (ARMS) techniques in both groups. Our results showed that there are no statistically significances between the patients and controls in terms of the G422A, C626G, A683C and A1322G polymorphisms in DR4 gene (p > 0,05). Our findings showed no role of DR4 gene polymorphisms in susceptibility to LC and provide a plausible explanation for DR4 genetic heterogeneity in LC susceptibility.

In this study, we investigated the safety and toxicity of isoniazid (INH) intervention therapy to the patients with latent tuberculosis who were given tumor necrosis factor alpha (TNFalpha) for the treatment of their rheumatologic diseases. In this prospective clinical study, we enrolled 86 patients receiving anti-TNFalpha therapy for their rheumatologic diseases between April 2005 and September 2006. Of all the subjects, 45 had rheumatoid arthritis, 36 had ankylosing spondylitis, and 5 had psoriatic arthritis. In addition to anti-TNFalpha therapy, 60 of the 86 patients were given INH intervention for revealed latent tuberculosis. INH at a dosage of 300 mg daily was given for 9 months. Hepatotoxicity due to the INH therapy was considered when the serum alanine aminotransferase (ALT) and/or aspartate aminotransaminase (AST) levels showed at least threefold increase with respect to their baseline serum levels. Serum ALT and AST levels were measured by enzymatic colorimetric method in fasting peripheral blood samples at 0 (baseline), 1, 2, 3, 6, and 9 months. Of 86 patients, 47 (54.7%) were women (mean age+/-SD, 44.1 +/- 10.9 years) and 39 (45.3%) were men (38.8 +/- 10.1 years). Except five patients (8.3%), liver toxicity due to the INH therapy was not encountered among the patients, and after temporarily discontinuing the INH therapy of these five subjects, serum transaminase levels returned to the normal ranges. No hepatotoxicity was observed in the non-INH group. However, there was no statistical significance between INH-treated and non-INH-treated group (p = 0.317). In addition, none of the 86 patients developed active tuberculosis infection during the treatment period. In conclusion, for those patients who were assigned to the TNFalpha treatment for their rheumatologic disorders and carrying risk for latent tuberculosis, INH intervention therapy was found to be safe and efficacious.

Aim To evaluate the risk factors associated with nocturia in patients with obstructive sleep apnea syndrome (OSAS). Materials and Methods Patients aged over 18 years who had been diagnosed with OSAS using polysomnography (PSG) from January to December 2019 were evaluated. The number of nocturia episodes had been assessed in a 3‐day bladder diary. We analysed the age, sex, body mass index (BMI) score, apnea‐hypopn ea index (AHI) score and severity, hypertension, diabetes mellitus, smoking and heart diseases in all patients. Results A total of 124 patients with a mean age of 49.9 ± 11.6 years (range: 25‐81 years) were included in the study. Ninety‐two (75.8%) patients had nocturia. The mean number of nocturia episodes of patients with nocturia was 2.4 ± 1.3. To determine factors affecting the risk of nocturia, the logistic regression analysis was performed. Patient age and BMI scores were found as the most effective risk factors determining nocturia (P < .05). The odds of patient age were 1.06 (odds ratio: 1.12; 95% confidence interval: 1.01‐1.11; P = .010) times higher for patients with nocturia. Every 1‐unit increase in the BMI score increased the risk of nocturia 1.12 times. In the study period, 48 patients with nocturia had undergone the continuous positive airway pressure (CPAP) therapy or surgical treatment. The mean number of nocturia episodes of these patients was 2.3 ± 1.4 before treatment and 1.7 ± 2.2 after treatment, showing a significant decrease (P = .032). Although the total daily urine volume increased significantly with the treatment, the total night‐time urine volume decreased significantly at night (P = .016 and P = .024, respectively). Conclusion The age and BMI score were the risk factors associated with nocturia in patients with OSAS.