No abstract

This study tested the hypothesis that asthma can promote obstructive sleep apnea (OSA) by looking at the prevalence of OSA among patients with difficult-to-control asthma receiving long-term oral corticosteroid (CS) therapy and examined some possible etiological factors. The study design was a prospective cohort study and was conducted in the pulmonary outpatient clinic of a tertiary care center in Haifa, Israel. Twenty-two consecutive patients with severe unstable asthma, 14 on continuous and 8 on bursts of oral CS, in addition to their standard therapy for a mean of 8.9 +/- 3.3 years, underwent a night polysomnography in a sleep laboratory regardless of sleep complaints. A standard questionnaire was completed upon attending the sleep laboratory. The OSA was defined as respiratory disturbance index (RDI) of > or = 5 and typical complaints. The correlation between RDI to asthma and morphometric parameters was tested. All but one patient had OSA [95.5% prevalence], with mean RDI of 17.7 +/- 2.5. The RDI values were significantly higher in the continuous CS therapy subgroup (21.4 +/- 3.4 vs. 11.1 +/- 1.6, p < 0.05]. The study group had above normal neck circumferences and body mass index. The former increased by 12.1% +/- 3.1% % to 29.8% +/- 1% during the oral CS therapy interval but had no significant effect on RDI as a covariant. This study showed an unexpectedly high prevalence of OSA among patients with unstable asthma receiving long-term chronic or frequent burst of oral CS therapy. It may be assumed that prolonged and especially continuous oral CS therapy in asthma increases airway collapsibility.

No abstract

The data suggest that PC expressed by lung uptake of 99mTc-MDP has no role in the pathogenesis of PHT among ESRD patients undergoing HD therapy via A-V access.

Patients with inherited α1-antitrypsin (AAT) deficiency (ZZ-AATD) and severe chronic obstructive pulmonary disease (COPD) frequently experience exacerbations. We postulated that inhalation of nebulised AAT would be an effective treatment.We randomly assigned 168 patients to receive twice-daily inhalations of 80 mg AAT solution or placebo for 50 weeks. Patients used an electronic diary to capture exacerbations. The primary endpoint was time from randomisation to the first event-based exacerbation. Secondary endpoints included change in the nature of the exacerbation as defined by the Anthonisen criteria. Safety was also assessed.Time to first moderate or severe exacerbation was a median of 112 days (interquartile range (IQR) 40–211 days) for AAT and 140 days (IQR 72–142 days) for placebo (p=0.0952). The mean yearly rate of all exacerbations was 3.12 in the AAT-treated group and 2.67 in the placebo group (p=0.31). More patients receiving AAT reported treatment-related treatment-emergent adverse events compared to placebo (57.5% versus 46.9%, respectively) and they were more likely to withdraw from the study. After the first year of the study, when modifications to the handling of the nebuliser were introduced, the rate of safety events in the AAT-treated group dropped to that of the placebo group.We conclude that in AATD patients with severe COPD and frequent exacerbations, AAT inhalation for 50 weeks showed no effect on time to first exacerbation but may have changed the pattern of the episodes.