Patients with sickle cell disease (SCD) often have obstructive sleep apnea (OSA) as well. Although previous research has suggested that presence of OSA is linked to clinical severity of SCD, results have been inconsistent. Recent research published in Frontiers in Physiology found that nocturnal hypoxemia, not necessarily OSA, was linked with SCD complications.
Nocturnal hypoxemia can be caused by OSA but also may result from other conditions, such as lung disease, heart disease, pneumonia, and asthma. The researchers explored associations between OSA, nocturnal oxyhemoglobin saturation (SpO2), and history of certain acute and chronic complications of SCD such as vaso-occlusive events.
The study population included 43 patients with SCD (22 men and 21 women). The subjects were aged 15–55 years and had symptoms of OSA, such as excessive daytime sleepiness, snoring, sense of suffocation during sleep, headaches, and nocturia.
The study protocol involved:
- clinical examination for heart rate, daytime SpO2, and blood pressure
- full night of polysomnography testing (PSG)
- blood testing the morning after to track hematologic biomarkers
The researchers also prospectively retrieved data on the patients’ experiences of vaso-occlusive crises and acute chest syndrome requiring hospitalization in the previous two years. The researchers also reviewed the patients’ charts to identify history of other complications, such as priapism, glomerulopathy, pulmonary hypertension, leg ulcer, osteonecrosis, and retinopathy.
Of the 43 patients, seven (16%) had nocturnal hypoxemia (16%) and 29 had OSA (67%). The study found no association between OSA and clinical severity of SCD. It also did not detect an association between nocturnal hypoxemia and OSA.
Instead, nocturnal hypoxemia was linked with complications such as glomerulopathy, leg ulcer, priapism, and pulmonary hypertension. Nocturnal hypoxemia also was linked with a decrease in red blood cell (RBC) deformability, enhanced hemolysis, and more severe anemia.
“Nocturnal hypoxemia could be responsible for changes in RBC deformability that would fragilize RBCs, resulting in enhanced hemolysis that could play a significant role in the development of complications such as leg ulcers, priapism, pulmonary hypertension, or glomerulopathy,” wrote the authors, led by Emeric Stauffer of the Inter-University Laboratory of Human Movement Biology in Lyon, France. “The identification of nocturnal hypoxemia and its causes, other than OSA, and treatment of sleep-disordered breathing could be helpful to decrease morbidity in SCD patients.”