Abstract
Background: Synthesis of erythropoietin (EPO) is stimulated by tissue hypoxia. Sleep apnea- hypopnea syndrome (OSA) is characterized by the presence of repeated episodes of hypoxemia. Aim: The objective of this study is to investigate whether hypoxemia induced by OSA could be a stimulus to increase EPO production. Methods: The study was conducted in 24 patients being investigated for OSA. A full polysomnography through a night's sleep was recorded and analyzed manually according to standard criteria. We determined the EPO levels in samples of first morning urine (sandwich ELISA technique). Serum creatinine, hematocrit and hemoglobin levels were additionally determined. Results: Of the 24 patients studied, 18 were diagnosed from OSA (AHI> 10) with the following results (mean ± SD): apnea/hypopnea index (AHI) 30.8 ± 23.1, desaturation index (HDI) 27 ± 16.9, CT90% 5.7 ± 7.8, mean length of nocturnal desaturation 25.7 ± 10.5 sec., average nocturnal SatO2 93.9 ± 1.6. Creatinine was within normal limits for all patients. Hemoglobin and EPO were higher in the OSA group than in the non-OSA group (14.2 ± 1.3 g / dl vs 13.2 ± 0.8) (p <0.03) and 0.65 ± 0.5 vs 0.30 ± 0.3 (p <0.05), respectively. There was no dose-response relationship between the severity of the alterations of the PSG and the titles of EPO. In fact, no significant correlations (linear) were found between the levels of EPO in urine and AHI, HDI, length of desaturation, CT90% or average nocturnal saturation. Conclusions: OSA patients show increased urinary excretion of EPO and hemoglobin. Changes in EPO concentration are of low magnitude and non-linear. This response could be a protective mechanism against tissue hypoxia caused by OSA.
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