Erythropoietin and obstructive sleep apnea

We tested the hypothesis that repetitive severe hypoxemia resulting from obstructive sleep apnea would increase serum erythropoietin, and that this increase would be attenuated by effective treatment of obstructive sleep apnea. We studied healthy untreated patients with obstructive sleep apnea (18 s...

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Veröffentlicht in:American journal of hypertension 2004-09, Vol.17 (9), p.783-786
Hauptverfasser: Winnicki, Mikolaj, Shamsuzzaman, Abu, Lanfranchi, Paola, Accurso, Valentina, Olson, Eric, Davison, Diane, Somers, Virend K.
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Sprache:eng
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Zusammenfassung:We tested the hypothesis that repetitive severe hypoxemia resulting from obstructive sleep apnea would increase serum erythropoietin, and that this increase would be attenuated by effective treatment of obstructive sleep apnea. We studied healthy untreated patients with obstructive sleep apnea (18 severe and 10 very mild) before and after acute treatment with continuous positive airway pressure, and 12 healthy control subjects free of obstructive sleep apnea. Baseline erythropoietin levels before sleep were similar in the obstructive sleep apnea and control groups. However, erythropoietin levels increased (by 20%, P = .037) in patients with severe obstructive sleep apnea after 3.5 hours untreated (lowest O 2, 77% ± 3%), and decreased after 4 hours of continuous positive airway pressure treatment ( P = .001). Erythropoietin responses in patients with severe obstructive sleep apnea were different (F = 4.0, P = .03) from controls, in whom erythropoietin levels remained stable throughout the night ( P = .94). Erythropoietin responses were similar in very mild obstructive sleep apnea and controls ( P = .58). Our results indicate that untreated severe obstructive sleep apnea results in increased erythropoietin, which decreases after continuous positive airway pressure treatment. Increased erythropoietin may be a potential reversible mechanism to explain the association between obstructive sleep apnea and cardiovascular disease.
ISSN:0895-7061
1879-1905
1941-7225
DOI:10.1016/j.amjhyper.2004.04.011