International audienceSummaryBackground Neuraminidase inhibitors were widely used during the 2009–10 influenza A H1N1 pandemic, but evidence for their effectiveness in reducing mortality is uncertain. We did a meta-analysis of individual participant data to investigate the association between use of neuraminidase inhibitors and mortality in patients admitted to hospital with pandemic influenza A H1N1pdm09 virus infection. Methods We assembled data for patients (all ages) admitted to hospital worldwide with laboratory confirmed or clinically diagnosed pandemic influenza A H1N1pdm09 virus infection. We identified potential data contributors from an earlier systematic review of reported studies addressing the same research question. In our systematic review, eligible studies were done between March 1, 2009 (Mexico), or April 1, 2009 (rest of the world), until the WHO declaration of the end of the pandemic (Aug 10, 2010); however, we continued to receive data up to March 14, 2011, from ongoing studies. We did a meta-analysis of individual participant data to assess the association between neuraminidase inhibitor treatment and mortality (primary outcome), adjusting for both treatment propensity and potential confounders, using generalised linear mixed modelling. We assessed the association with time to treatment using time-dependent Cox regression shared frailty modelling. Findings We included data for 29 234 patients from 78 studies of patients admitted to hospital between Jan 2, 2009, and March 14, 2011. Compared with no treatment, neuraminidase inhibitor treatment (irrespective of timing) was associated with a reduction in mortality risk (adjusted odds ratio [OR] 0·81; 95% CI 0·70–0·93; p=0·0024). Compared with later treatment, early treatment (within 2 days of symptom onset) was associated with a reduction in mortality risk (adjusted OR 0·48; 95% CI 0·41–0·56; p<0·0001). Early treatment versus no treatment was also associated with a reduction in mortality (adjusted OR 0·50; 95% CI 0·37–0·67; p<0·0001). These associations with reduced mortality risk were less pronounced and not significant in children. There was an increase in the mortality hazard rate with each day's delay in initiation of treatment up to day 5 as compared with treatment initiated within 2 days of symptom onset (adjusted hazard ratio [HR 1·23] [95% CI 1·18–1·28]; p<0·0001 for the increasing HR with each day's delay). Interpretation We advocate early instigation of neuraminidase inhibitor treatment in adults admitted to hospital with suspected or proven influenza infection. Funding F Hoffmann-La Roche

Objectives; Pulmonary hypertension (PH) is a common and well established complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with decreased survival. This study was designed to investigate the PH frequency and its relations in hospitalized tobacco and biomass related COPD patients. Methods and Results; The study was a retrospective review of inpatients with COPD defined as a history of tobacco or biomass smoking, Pulmonary function tests (PFT) within stable status, an echocardiogram within stable status. PH was defined as systolic pulmonary artery pressure (sPAP) >35 mmHg. Of the 694 individuals, 600 had suitable aspects for inclusion of study. All Females were biomass exposer and males were tobacco smoker. The Prevalence of PH was found more frequent in females than males. It was more prominent in moderate level COPD cases (56,2% and 37,5%, P<0,002). Both groups had airflow limitation, hypercapnia and hypoxemia, but no differences were found in terms of PaCO2 and PaO2. However, FEV1 % was lower in males than females (p<0,005). On the other hand, FVC % was lower in the females compared with the males (p < 0.02). When analyzing the influence of PFT and demographic parameters on PH in separate COPD level groups, the results a bit varied among the groups. Conclusion; Our study demonstrated that PH frequency is higher in female COPD cases due to biomass smoke than in male COPD cases due to tobacco smoke. The influence of FVC % on the risk of a person having PH increased with increasing COPD level.

BACKGROUND: Oxidative damage is a major contributing factor to carcinogenesis and obstructive disorders in lungs. Current evidence suggests that the inflammatory processes yield to oxidative mechanisms, which underlie COPD, lung cancer, and obstructive sleep apnea syndrome (OSAS). This study aimed to evaluate the oxidative damage in these diseases by evaluating the oxidative and antioxidant biomarkers. METHODS: Malondialdehyde, 8-oxo-7,8-dihydro-2-deoxyguanosine, and coenzyme Q10 levels were evaluated in the blood samples of subjects with COPD, lung cancer, and OSAS by high-pressure liquid chromatography. RESULTS: A total of 111 participants (35 females, 76 males) with OSAS (n ‫؍‬ 29), COPD (n ‫؍‬ 26), and lung cancer (n ‫؍‬ 28) and healthy controls (n ‫؍‬ 28) were included in the study. The malondialdehyde and coenzyme Q10 levels were significantly higher in all 3 diseases when compared with controls (P < .01), whereas 8-oxo-7,8-dihydro-2-deoxyguanosine levels were only significantly higher than in healthy controls in subjects with lung cancer (P ‫؍‬ .005). The highest levels of malondialdehyde and coenzyme Q10 were determined in subjects with OSAS and lung cancer, respectively. The highest 8-oxo-7,8-dihydro-2-deoxyguanosine levels were also observed in subjects with lung cancer, but the differences of this biomarker with other diagnoses were not statistically significant (P ‫؍‬ .56). CONCLUSION: Oxidative damage was observed in all 3 diagnoses, and, as a response to oxidative stress, antioxidant mechanisms were also active in these diseases. Malondialdehyde and 8-oxo-7,8-dihydro-2-deoxyguanosine were found to be efficiently usable in the evaluation of oxidative damage in chronic respiratory diseases. (ClinicalTrials.gov registration NCT02406053.) Key words: malondialdehyde; 8-oxo-7,8-dihydro-2Ј-deoxyguanosine;coenzyme Q10; COPD; OSAS; lung cancer; oxidative damage; antioxidants. [Respir Care 2016;61(2):205-211.

These results indicate that prolidase activity decreases in patients with COPD.

BACKGROUND:Obstructive sleep apnea (OSA) is a common sleep problem, in which patients are at increased risk for metabolic and cardiovascular problems, including metabolic syndrome, diabetes mellitus (DM), and dyslipidemia. Betatrophin is a novel protein that regulates fatty acid and triglyceride (TG) metabolism and is related to obesity and metabolic abnormalities, including metabolic syndrome, DM, and dyslipidemia. Although OSA and betatrophin share common abnormalities, their relationship has not been investigated.AIM:The aim of this study is to investigate the relationships among betatrophin, OSA, and the serum lipid profile.METHODS:Ninety consecutive patients with suspected OSA underwent polysomnography (PSG) to confirm OSA. Plasma betatrophin, leptin, adiponectin, and the full lipid profile were analyzed. The patients were categorized as OSA or control based on the apnea-hypopnea index (AHI).RESULTS:About 61% of patients had OSA, and 39% had normal PSG. The levels of betatrophin, leptin, and adiponectin were higher in patients with OSA (256.59 ± 29.35, 374.20 ± 37.93, and 17.86 ± 2.63 μg/mL, respectively) compared to the controls (141.86 ± 26.20, 205.53 ± 14.75, and 7.52 ± 1.02 μg/mL, respectively). Betatrophin levels were correlated with the AHI, leptin (r = 0.413, P = 0.002, r = 0.782, P = 0.000). TG levels were significantly higher, and high-density lipoprotein cholesterol (HDL-C) levels were lower, in OSA patients compared to controls (244 ± 20.33 vs. 138 ± 14.89, and 37.21 ± 1.26 vs. 43.78 ± 1.62, respectively). The TG level was correlated with betatrophin (r = 0.353, P = 0.013). Multiple regression analysis showed that the AHI, leptin, and arousals were independent predictors of betatrophin level (B = 1.70 P = 0.046 95%, B = 0.56 P < 0.005, and B = 1, 2, P = 0.003, respectively).CONCLUSIONS:Our results suggest a complex relationship between OSA, betatrophin, TG, and HDL, as well as other adipokines. Our results require further investigation to assess this complex association and re-evaluate previous related studies.

Objective: To determine whether there are significant differences between rapid-eye-movement (REM)-related obstructive sleep apnea (OSA) and non-REM (NREM)-related OSA, in terms of the demographic, anthropometric, and polysomnographic characteristics of the subjects. Methods: This was a retrospective study of 110 patients (75 males) with either REM-related OSA (n = 58) or NREM-related OSA (n = 52). To define REM-related and NREM-related OSA, we used a previously established criterion, based on the apnea-hypopnea index (AHI): AHI-REM/AHI-NREM ratio > 2 and ≤ 2, respectively. Results: The mean age of the patients with REM-related OSA was 49.5 ± 11.9 years, whereas that of the patients with NREM-related OSA was 49.2 ± 12.6 years. The overall mean AHI (all sleep stages combined) was significantly higher in the NREM-related OSA group than in the REM-related OSA group (38.6 ± 28.2 vs. 14.8 ± 9.2; p < 0.05). The mean AHI in the supine position (s-AHI) was also significantly higher in the NREM-related OSA group than in the REM-related OSA group (49.0 ± 34.3 vs. 18.8 ± 14.9; p < 0.0001). In the NREM-related OSA group, the s-AHI was higher among the men. In both groups, oxygen desaturation was more severe among the women. We found that REM-related OSA was more common among the patients with mild-to-moderate OSA, whereas NREM-related OSA was more common among those with severe OSA. Conclusions: We found that the severity of NREM-related OSA was associated mainly with s-AHI. Our findings suggest that the s-AHI has a more significant effect on the severity of OSA than does the AHI-REM. When interpreting OSA severity and choosing among treatment modalities, physicians should take into consideration the sleep stage and the sleep posture.

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Loeffler's syndrome is an acute pneumonia with an unclear cause. One fourth of Loeffler's syndrome patients are idiopathic, although the most common etiologic causes include parasites. Asymptomatic form is usually a reversible, self-limited disease, which does not require a specific treatment regimen. We presented a 17-year-old young man with diagnosis of Loeffler syndrome.