Obstructive sleep apnea is a risk factor for Barrett’s esophagus, according to findings published online September 11 in Clinical Gastroenterology and Hepatology.
Researchers from the Mayo Clinic in Rochester, Minn., studied 7,482 patients who had undergone both a diagnostic polysomnogram and esophagogastroduodenoscopy from January 2000 to November 2011.
"In this subset of patients, the presence of OSA [obstructive sleep apnea] was associated with an 80% increased risk of [Barrett’s esophagus], compared to subjects without OSA and [Barrett’s esophagus]," wrote study author Dr. Prasad G. Iyer and his colleagues (Clin. Gastroenterol. Hepatol. 2013 September;11:1108-14.e5).
Dr. Prasad G. Iyer
Several overlapping risk factors exist for obstructive sleep apnea and Barrett’s esophagus (BE), including obesity, gastroesophageal reflux disease (GERD), male gender, and older age. This study was designed to explore whether there is a relationship between obstructive sleep apnea and Barrett’s esophagus independent of these factors.
Subjects were categorized into four groups: diagnosis of BE but not OSA; OSA but not BE; both; or neither. Of the 7,482 patients, 2,480 did not have a diagnosis of OSA or BE; 83 had BE but not OSA; 4,641 had OSA but not BE; and 278 had a diagnosis of both.
The study authors used univariable models assessing age, sex, body mass index, GERD, and smoking history to determine the association between OSA and BE. GERD and OSA were associated with Barrett’s esophagus. A multiple-variable analysis was performed to observe the association of OSA with BE, adjusting for other factors. Patients with OSA were about 80% more at risk for having Barrett’s esophagus than were subjects without OSA or Barrett’s esophagus.
"This association was dose dependent, with an increase in severity of OSA being associated with an increased risk of Barrett’s esophagus," wrote the authors.
Additionally, since "the association of [Barrett’s esophagus] and OSA could be confounded by gastroesophageal reflux," the researchers also performed analyses to determine whether this relationship was independent of a GERD diagnosis. In a univariate analysis, both OSA and GERD were associated with BE, and in a multiple-variable analysis demonstrated that "both OSA and GERD were "independently associated with an increased risk of Barrett’s esophagus."
Dr. Iyer and his colleagues cited a few limitations to this study. First, the study’s design did not allow for exploration of a specific mechanism for how OSA predisposes individuals to Barrett’s esophagus. Second, the ability to accurately assess the association of OSA with GERD was limited by a lack of an established clinical definition of GERD. Finally, the use of ICD-9 codes to diagnose conditions may have resulted in overestimates in the sample.
The authors concluded that further research is needed to confirm that these findings can be applied to the general population and to explore whether treatment for OSA may help reverse this risk.
They also added that given the "asymptomatic nature" of Barrett’s esophagus and the higher risk of esophageal adenocarcinoma, patients with OSA may benefit from BE screening.
Dr. Iyer and his colleagues disclosed that this study was supported in part by the American College of Gastroenterology, the National Institute of Diabetes, Digestive and Kidney Disease; and the Edward C. Rosenow Endowed Professorship Internal Medicine Residency Award at the Mayo Clinic.