Introduction Obstructive Sleep Apnoea (OSA) is a condition with increasing prevalence. Individuals with severe OSA have significant intermittent nocturnal hypoxia. Erythropoiesis is stimulated through the renal secretion of erythropoietin in response to hypoxia, and is responsible for polycythaemia found in chronic respiratory failure. There are case reports of secondary polycythaemia attributed to OSA, but there are limited data assessing the relationship of OSA physiological parameters and haemoglobin. We aimed to investigate this.
Methods Clinical information was collated prospectively from patients assessed at the Newcastle Regional Sleep Service with suspected OSA. None of those included had been referred to investigate polycythaemia. All patients included underwent either a domiciliary or in-patient sleep study as per standard clinical practise, and had a Full Blood Count (FBC) taken.
Results There were 103 patients included: 70% males, mean (SD) age 52 years (range 26–76 years), BMI 36.1kg/m2 (8.3), Epworth Sleepiness Scale 13 (5), daytime SpO2 on air 96% (2.7) [six patients had SaO2 <92%]. Sleep study results showed the Apnoea-Hypopnea Index (AHI) to be <5 in 13% [no OSA], ≥5 and <15 in 30% [mild OSA], ≥15 and <30 in 19% [moderate OSA], and ≥30 in 38% [severe OSA]. Analysis of FBC results showed no statistical difference in Haemoglobin between the four patient groups; mean (SD), no OSA 14.3g/dl (2.1), mild 14.6g/dl (1.5), moderate OSA 14.5g/dl (1.2), severe OSA 14.7g/dl (1.4). There was no correlation between Haemoglobin (Hb) and AHI, oxygen desaturation index (ODI), % time SpO2<90%, % time SpO2<80%, or awake SpO2. There was no significant difference in haematocrit or RBC between groups. A weak positive correlation was observed between total WBC and ODI, r=0.319, p=0.001, but there was no statistical difference between patient groups.
Conclusions In this sleep clinic patient group, we found no correlation between haemoglobin and any OSA severity marker. This suggests that the nocturnal intermittent hypoxia which occurs in OSA alone does not lead to secondary polycythaemia. Further work will evaluate the prevalence of OSA in people with secondary polycythaemia, and whether the OSA is contributory or reflects the general population prevalence of OSA.