National data on asthma characteristics and the factors associated with uncontrolled asthma seem to be necessary for every country. For this purpose, we developed the Turkish Adult Asthma Registry ...

Respiratory Infections,hemoptysis,COVID-19,presentation

Background: This experimental study investigated the protective effects of N-acetylcysteine (NAC) on peroxidative changes in fetal lungs in the offspring of rats exposed to cigarette smoke. Methods: Thirty fetal rats used for analysis, were divided into three groups as follows: control group (n = 10), whose mothers were exposed to fresh air; group I (n=10), whose mothers were exposed to cigarette smoke; and group II (n=10), whose mothers were exposed to cigarette smoke and given 10 mg/kg per day NAC. In groups I and II, smoke exposure was started 4 weeks before the pregnancy, and continued to the 14th day of pregnancy, and in Group II, NAC was administered intraperitoneally for 14 days. The mothers and their fetuses were decapitated on the 14th day of pregnancy. Malondialdehyde (MDA) and glutathione (GSH) levels were determined in the lung tissues of fetuses to determine the oxidant-antioxidant balance. Results: While tissue MDA levels in Group I were found significantly higher than the control group (129.7±65.4 versus 63.4±15.4 nmol/100 mg protein, P <0.05), GSH levels were significantly lower (17.1±7.3 versus 45.4±8.1 nmol/mg protein, P <0.01). Furthermore, in Group II, MDA levels were significantly lower (56.9± 20.6 versus 129.7±65.4 nmol/100 mg protein, P <0.05), and GSH levels were significantly higher (34.57±10.7 versus 17.1±7.3 nmol/mg protein, P 0.05). Conclusions: These results suggest that smoke exposure during pregnancy causes oxidative damage in fetal lungs. This smoke-induced damage might be prevented by NAC. Human & Experimental Toxicology (2007) 26, 99-103

Aim: To evaluate the effects of montelukast in smoke- induced lung injury.Methods: 28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg) dissolved in Na2CO3 was given in one group (MON), Na2CO3 only was given in another group (MON control) and placebo was injected in the third group (COPD control) intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analy- ses were performed on the lung tissues of sacrificed rats. Results: Serum TNF-α levels in the MON group were signifi- cantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p < 0.05). Furthermore there was no sta- tistically significant difference between the MON group and healthy controls with respect to serum TNF-α levels (38.84 ± 4.9 pg/ml vs. 29.5 ± 3.6 pg/ml, p > 0.05). Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respec- tively, p < 0.05), while there was no significant difference between the MON group and healthy controls (5.1 ± 0.6 vs 2.3 ± 0.2, p > 0.05). Conclusion: These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view.

The obese-asthma phenotype has gradually increased in the last few years. We aimed to assess the differences between obese and non-obese patients with asthma. This research is a subanalysis of the Turkish Adult Asthma Registry (TAAR). Clinical presentation, disease control, severity, and demographics of obese and non-obese (lean, normal-weight, overweight) patients were compared. The obesity rate in TAAR was 32.2% (n = 619/1919; 18-83 years; 527 F/92 M). Patients with asthma and obesity had higher rates of childhood obesity, longer symptom duration, later onset of asthma, and more severe asthma. These patients were more likely to be female, older, less educated, and live in rural areas. Patients with obesity had more scheduled visits and emergency visits compared with non-obese patients, but similar asthma control, oral corticosteroid use, hospitalizations, intensive care unit admissions, and unscheduled visits. They also had a higher frequency of T2-high but lower frequency of possible T2-low phenotypes compared with normal-weight asthmatics. The risk of severe asthma in patients with obesity was 6.04 times higher for allergic than non-allergic patients and 3.58 times higher for the T2-high phenotype than for possible T2-low phenotypes. A one-unit increase in the asthma control test reduced the risk of severe asthma by 22%. A good definition of this phenotype is important to ensure that appropriate treatment strategies are implemented to achieve the control goal. We also believe that prevention of childhood obesity is an effective and pivotal strategy to achieve the goal of asthma control.