Hypoxaemia in sickle cell disease: biomarker modulation and relevance to pathophysiology

Nocturnal oxyhaemoglobin desaturation might have a role in CNS complications related to sickle cell disease, and rates of painful crises. We attempted to examine the biological relations, and describe the haematological risk factors for oxyhaemoglobin desaturation. The study population included children with sickle cell disease and controls. Cellular activation was assessed by measurement of soluble vascular cell adhesion molecule 1, P-selectin, L-selectin, and leukotriene B4. Erythrocyte-endothelial adhesion and routine haemato-logical variables were assessed. Oxygen saturation (SaO2) was measured by pulse oximetry while children were awake and asleep. Children with a mean sleeping SaO2 of 93% were identified as hypoxaemic. Children were divided into four groups: controls (ten children), HbSC (nine, all normoxic), HbSS normoxic (13), and HbSS hypoxaemic (15). Among haematological variables, sleeping SaO2 correlated only with packed-cell volume (r=0·7; p