New research finds that testing for an inflammatory marker is a stronger predictor than apnea-hypopnea index alone.
By Lisa Spear
It’s no secret that obstructive sleep apnea (OSA) can lead to hypertension and other cardiometabolic diseases, but predicting who will go on to develop these conditions is not always straightforward.
New research from Penn State University suggests that a simple blood test can shed light on which patients may eventually experience these comorbidities. C-reactive protein (CRP), a general inflammatory marker easily obtained from a blood sample, could give clinicians a window into an OSA patient’s future metabolic health with more precision than current diagnostic tools, according to research published in the journal Physiological Reports.
The study compared the inflammatory biomarker CRP with the apnea hypopnea index (AHI) in identifying the presence and severity of hypertension and hyperglycemia in middle-aged adults with mild to moderate OSA. The study showed CRP to be a stronger predictor of elevated blood pressure and fasting glucose levels than AHI alone.
If sleep clinicians incorporate regular CRP testing into their clinical practice, they could offer more precision care to improve patient outcomes, explains coauthor Alexandros Vgontzas, MD, university chair in Sleep Disorders Medicine at Penn State.
“These preliminary findings suggest that including a measure of CRP improves the ability for clinicians to detect cases of mild-to-moderate OSA with true cardiometabolic risk, with implications in improving prognosis and treatment within this clinically gray area,” the authors wrote.
For example, patients who experience mild sleep apnea but have high levels of CRP should be monitored more closely than those with low inflammatory markers, Vgontzas says. Clinicians can then recommend specific lifestyle changes, including exercise and diet, that may help avoid future inflammatory diseases. Ongoing monitoring of CRP can help clinicians measure the effectiveness of interventions and the progression of inflammatory disease.
This research stemmed from the idea that visceral fat tissue drives inflammation in the body, leads to insulin resistance, hypertension, and plays a role in the vicious cycle of sleep-disordered breathing, explains Vgontzas.
“There’s been many studies on the association between inflammation and sleep apnea. In 2005, we proposed the hypothesis that sleep apnea is not a pulmonary disease…is not a neurologic disorder, but the manifestation of a metabolic syndrome,” says Vgontzas. “What we said is that the underlying pathophysiologic mechanism that leads to sleep apnea is visceral adiposity.”
Lisa Spear is associate editor of Sleep Review.