Objectives: The severity of inflammation occurring during chronic obstructive pulmonary disease (COPD) is closely associated with oxidative stress. The aim of this study was to investigate the diagnostic value of Thiol/disulphide homeostasis (TDH) and ischemia modified albumin (IMA) levels in evaluating oxidative stress in COPD patients. Methods: This prospective study was performed with COPD patients presenting to the Kırıkkale University Hospital and with healthy volunteers. Subjects’ demographic data (age, sex, body mass index, and smoking status), native thiol (NT), total thiol (TT), disulphide (Ds), IMA levels and Ds/NT, Ds/TT and NT/TT ratios were recorded. Statistical analysis was performed with SPSS 21.0 software. Results: One hundred ninety subjects were enrolled in the study, 141 COPD patients and 49 healthy volunteers. No difference was determined between the patient and control groups in terms of age, sex or body mass index. The antioxidant markers; NT and TT levels and NT/TT ratio were significantly lower in the patient group compared to the control group (p < 0.001, p < 0.001, and p < 0.003, respectively). The oxidant markers; IMA levels and Ds/NT and Ds/TT ratios were significantly higher in the patient group (p = 0.006, p = 0.003, and p = 0.003, respectively). Significant negative correlation was determined between antioxidant and oxidant parameters. Sensitivity values were NT: 87.2%, TT: 83.3%, Ds/NT ratio: 68.1%, Ds/TT ratio: 68.1%, and IMA: 77.8%. Conclusions: TDH was impaired in favor oxidants in COPD patients. TDH parameters and IMA can be used to monitor oxidative stress emerging in COPD.
Carbon monoxide (CO) is an important cause of deaths via poisoning. CO poisoning causes inhibition of O2 transport and development of tissue hypoxia, which then causes cell apoptosis. A significant indicator of cell apoptosis, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) protein, is important for the stimulation of apoptosis. The primary purpose of this study is to determine whether apoptosis occurs during acute CO poisoning and to show that sTWEAK protein is an indicator of apoptosis that can be analyzed as a marker in the peripheral blood sample. The secondary aim is to determine the diagnostic and prognostic values of sTWEAK protein. The study was performed prospectively on 43 patients with CO poisoning and 30 healthy volunteer control individuals. The anamneses were taken from all patients, who also underwent physical examination. Complete blood count, biochemical markers, cardiac enzymes, and arterial blood gas measurements were analyzed. All the patients’ sTWEAK protein levels were also analyzed. The sTWEAK protein level of patients with CO poisoning was 2278 pg/mL (1197–7234), while the level of the control group was 1609 pg/mL (310–3721). The patients’ sTWEAK levels were significantly higher than the controls (area under the curve: 0.77 (0.66–0.89); p < 0.001), and the cutoff value was determined as 1895.50 pg/mL. The cutoff level had a sensitivity of 74.4%, a specificity of 76.7%, a positive predictive value of 82.0%, and a negative predictive value of 67.6%. sTWEAK is a significant indicator of apoptosis in CO poisoning that can be analyzed in the peripheral blood. However, further clinical trials are needed in terms of prognostic criteria.
Background and Objectives: Tobacco use and exposure to tobacco products remain a major public health challenge, even among athletes. This study aimed to evaluate tobacco use and second-hand smoke exposure in athletes through urinary cotinine levels and exhaled air carbon monoxide (CO) measurements. Materials and Methods: This cross-sectional study included licensed athletes who visited the sports medicine outpatient clinic of a tertiary hospital. Participants completed an electronic questionnaire on smoking habits and second-hand smoke exposure. Urine samples were analysed for cotinine levels, while CO levels were measured in exhaled breath. Results: A total of 421 athletes participated (57.8% male, median age: 18 years). Tobacco use was reported by 29.9% (n = 126) of participants. Median urinary cotinine levels were 22.9 ng/mL among daily tobacco users and 17.4 ng/mL among athletes exposed daily to second-hand smoke, with a statistically significant difference between exposure levels (p < 0.05). The optimal cut-off value for detecting second-hand smoke exposure was identified as 12.5 ng/mL. Median exhaled air CO levels were 5 ppm in daily tobacco users. Conclusions: This study demonstrates that tobacco use prevalence among athletes mirrors Türkiye’s national rates. Despite legal measures to curb tobacco use, direct use and second-hand smoke exposure remain pressing issues among athletes.
15 January 2020 in Journal of Health Sciences and Medicine
Objective: Migraine is one of the most common neurological diseases with headache attacks. Although its pathophysiology is still unclear, it is thought to be multifactorial. Oxidative stress is one of the topics discussed in the pathophysiology of migraine. The aim of this study was to investigate IMA and prolidase levels, which are oxidative stress markers in migraine. Material and Method: In this study, 35 migraine and 35 healthy controls were included. Serum IMA and prolidase levels were measured in serum obtained after centrifugation from venous blood samples by ELISA. Prolidase and IMA in migraine patients were compared with the control group. Results: The mean age was 40.06±11.14 years in migraine (34 female, 1 male) and 34.31±8.26 in controls (31 female, 4 male). There was no significant difference between the groups in terms of age and gender (p=0.08, p=0.29). Interictal IMA and prolidase levels of migraine subjects were significantly higher than the control group (p=0.02, p<0.001). Prolidase was significantly higher in the attack period than the control group (p0.05). Conclusion: Prolidase and IMA may be an indicator of oxidative stress in migraine patients. Prolidase, one of the oxidative stress indicators, also correlates with the frequency of attacks in migraine. It is thought that these markers may lead to antioxidant agent studies in prophylactic treatment of migraine.
30 September 2019 in Journal of Contemporary Medicine
Background: Passive smoking exposure is an important public health problem that causes pneumonia, bronchiolitis, bronchopneumonia, asthma formation and exacerbation, middle ear inflammation, tooth decay, growth retardation and development in children.Objectives: In this study, it was aimed to evaluate passive smokers objectively by cotinine level in urine.Method: Eighty children with at least one active smoker at home and 80 children who were not active smoker at home were admitted to the Ankara Education and Research Hospital . Parents were asked a questionnaire to the sociodemographic characteristics of their children and their families, the habits of smoking and the illnesses they had in a year. To assess passive smoking exposures, the first urine of children was collected and the level of cotinine, the main metabolite of nicotine in the urine, was measured using the solid phase competitive chemiluminescence immunoassay method on the Immulite 2000 Analyzer. A cut-off value of 10 ng / ml was obtained for diagnosis of passive smoking. Patients with cotinine levels above this value were assessed as "exposed to passive smoking".Results: In passive smoking exposures, the number of illnesses and wheezing has increased in the last year. The preterm birth and wheezing frequency of the smokers were significantly higher in the pregnant women (p <0, 05). Median cotinine level was found to be 10 ng / ml in the passive smoking group but median cotinine level was found to be 20,8 ng / ml in the cigarette group (p <0,01). The group with only mother smokers had significantly increased incidence of tooth decay compared with other groups (p <0.05). No relationship was found between birth weigth of infant and smoking behaviour during pregnancy (p=0,53), however the frequency of prematurity was found to be higher (p=0.03).The cotinine level of 68.7% of patients in the passive smoking group and 25% of the control group was above the threshold value of 10 ng / ml. The most sensitive and specific threshold level of cotinine was found as 14.75 ng/ml. Conclusions: Our study showed that 25% of children who do not smoke at home are exposed to passive smoking. This finding suggests that families are biased towards reporting smoking cessation alongside their sick children and those children are also exposed to cigarette smoke in out-of-home settings.
31 August 2019 in Kırıkkale Üniversitesi Tıp Fakültesi Dergisi
Amaç: Bakteriyel enfeksiyonlar önemli morbidite ve mortalite nedenidir. Serum prokalsitonin ve C-reaktif protein sistemik inflamasyon ve bakteriyel enfeksiyonların tanı, tedavi ve takibinde önemli belirteçlerdir. Bu çalışmada nihai tanıları pnömoni ve/veya KOAH alevlenmesi olan hastalarda son zamanlarda enfeksiyon takibinde sıklıkla kullanılmaya başlanan prokalsitonin ile klasik belirteç olarak kullanılan C-reaktif protein düzeyleri arasındaki korelasyon araştırıldı. Ayrıca alt solunum yolu enfeksiyonu tanısı ya da yönetimi için C-reaktif proteinin mi, prokalsitoninin mi maliyet etkililik açısından yararlı olduğunu saptamayı amaçladık.Gereç ve Yöntemler: Toplam 1948 hastadan elde edilmiş 4712 örnekten eş zamanlı çalışılan prokalsitonin ve C-reaktif protein sonuçları değerlendirildi. Örneklerden 499’u (%10.6) KOAH alevlenmesi (Grup I), 1480’i (%31.4) pnömoni (Grup II) ve 2733 (%58)’i KOAH alevlenmesi ve pnömoni (Grup III) tanısı almış hastaların örneklerinden oluşuyordu.Bulgular: C-reaktif protein ve prokalsitonin düzeyleri arasında pozitif güçlü korelasyon saptandı (rho=0.512, p<0.001). Yine prokalsitonin ve C-reaktif protein arasındaki grup içi değerlendirmede Grup I, Grup II ve Grup III’de pozitif güçlü korelasyon tespit edildi (sırasıyla rho=0.539, p<0.001; rho=0.509, p<0.001; rho=0.511, p<0.001).Sonuç: Prokalsitoninin C-reaktif protein ile korelasyon gösterdiği, enfeksiyonun ileri dönem takibinde yüksek maliyetli prokalsitonin yerine C-reaktif protein ölçümünün kullanılmasının uygun olacağı kanaatine varılmıştır.