Obstruktive Schlafapnoe und oxidativer Stress^[*]

Zusammenfassung

Hintergrund: Die unbehandelte obstruktive Schlafapnoe (OSA) ist mit erhöhtem systemischen und lokalen oxidativen Stress sowie Inflammation verbunden. Die nicht-invasive Bestimmung von Entzündungsmarkern und Stoffwechselmetaboliten im Atemkondensat (EBC) ist für die Beurteilung von systemischen Auswirkungen einer schweren Schlafapnoe von Interesse. Bei Patienten mit schwerer Schlafapnoe (AHI ≥ 30 /h) wurde untersucht, ob unter einer CPAP-Therapie mit Normalisierung des AHI Veränderungen der H₂O₂-Abgabe im Atemkondensat auftreten.

Methodik: Patienten mit obstruktiver Schlafapnoe (AHI ≥ 30 /h) erhielten nach der Nativnacht, nach der 1. CPAP-Titrationsnacht und nach 6-wöchiger CPAP-Therapie eine Atemkondensatsammlung mit H₂O₂-Messung. Eingeschlossen wurden nur Patienten, die nach der 6-wöchigen CPAP-Therapie einen Rückgang des AHI auf ≤ 10 /h aufwiesen.

Ergebnisse: 23 Patienten (21 Männer und 2 Frauen) konnten in die Auswertung eingeschlossen werden. Die erste CPAP-Therapienacht führte trotz signifikanten Rückgangs des AHI nicht zu einer Veränderung des H₂O₂-Wertes. Nach 6-wöchiger konsequenter CPAP-Therapie mit Normalisierung des AHI auf (3 ± 3 /h) sank der H₂O₂-Wert signifikant von 450 ± 163 nmol/l auf 294 ± 110 nmol/l. In der Subgruppenanalyse war die Absenkung des H₂O₂-Wertes bei Nie-Rauchern und insbesondere bei Rauchern weniger ausgeprägt als bei Ex-Rauchern.

Schlussfolgerung: Eine 6-wöchige CPAP-Therapie bei OSA mit Normalisierung des AHI reduziert im Gesamtkollektiv die H₂O₂-Konzentration im Atemkondensat signifikant. Dies deutet primär auf eine Reduktion lokaler inflammatorischer Prozesse und oxidativen Stresses in den Atemwegen, wie auch auf einen positiven Effekt auf den bei OSAS erhöhten systemischen oxidativen Stress hin. Allerdings bestehen Einflüsse durch den Raucherstatus, sodass weitere Untersuchungen erforderlich sind, die Subgruppenanalysen in ausreichender Fallzahlgröße einschließen sollten.

Abstract

Background: Untreated obstructive sleep apnoea (OSA) is characterised by elevated systemic and local oxidative stress and inflammation. Non-invasive measurement of metabolites and markers of inflammation in exhaled breath condensate (EBC) is of interest in the interpretation of systemic effects of severe obstructive sleep apnoea. In patients with severe sleep apnoea (AHI ≥ 30 /h) we investigated if CPAP therapy with normalisation of AHI induces changes of H₂O₂ concentrations in EBC.

Material and Methods: Patients with obstructive sleep apnea (AHI ≥ 30 /h) had H₂O₂ analysis of EBC after native PSG, after the first night and after 6 weeks of CPAP therapy. Only patients with normalisation of AHI (AHI ≤ 10 /h) were included in the further analysis.

Results: 23 patients (21 men and 2 women) fulfilled the inclusion criteria. The first night of CPAP therapy led to a significant reduction of AHI, but did not change the H₂O₂ concentration in EBC. After 6 weeks of CPAP therapy with normalisation of AHI (3 ± 3 /h) H₂O₂ in EBC showed a significant reduction from 450 ± 163 nmol/L to 294 ± 110 nmol/L. Subgroup analysis showed that in non-smokers and especially in smokers the reduction was less marked than in ex-smokers.

Conclusion: Normalisation of AHI after 6 weeks of CPAP therapy in OSA induces a significant reduction of H₂O₂ in EBC. This primarly represents a reduction of local inflammation and oxidative stress in the airways, but also indicates a positive effect on elevated oxidative stress in OSA. The influence of smoking status needs further investigations, including subgroup analysis with a sufficient number of patients.

^* Die Ergebnisse wurden in Teilen auf dem DGP-Kongress 2008 in Lübeck im Rahmen eines Kurzvortrages präsentiert.

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