This systematic review suggests that there is a high prevalence of OSA in asthma, particularly within severe asthma populations and that co-diagnosis of OSA in asthma patients is associated with worse clinical outcomes. However this outcome was not uniform and the number of studies using polysomnography to confirm OSA was small. This weakens the conclusions that can be drawn and prompts the need for adequately powered and well-designed studies to confirm or refute these findings.

Impaired pulmonary release of nitric oxide (NO) is one of the characteristic phenotypic changes of vascular cells in pulmonary hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with primary pulmonary hypertension. NOS-dependent whole body NO production was assessed by giving an intravenous infusion of L-[¹⁵N]₂-arginine (50 µmol/min for 30 min) and measuring isotopic urinary enrichment of ¹⁵N-nitrite and ¹⁵N-nitrate. Four female patients with no signs of infection were recruited and compared with 6 age-matched control subjects. Mean 12-hour excretion of ¹⁵N-nitrite and ¹⁵N-nitrate in the total urine over 36 h was smaller in patients than in control subjects (57.2 ± 27.6 vs. 229.1 ± 65.2 nmol/mmol creatinine, p< 0.01, Mann-Whitney U test, respectively). Neither mean 12-hour excretion of ¹⁴N-nitrite and ¹⁴N-nitrate (51.6 ± 10.0 vs. 72.4 ± 10.0 µmol/mmol creatinine, p = 0.3) nor glomerular filtration rates (84.5 ± 15.8 vs. 129.7 ± 16.0 ml/min, p = 0.1) were different between patients and control subjects. Our results suggest that either basal NOS-dependent whole body NO production is impaired or excess NO metabolism occurs in patients with primary pulmonary hypertension.

Asthmatics with co-existing OSA can experience improved quality of life with CPAP treatment. This effect appears more pronounced in severe OSA or poorly controlled asthma.

No abstract