A pilot study of sleep-related breathing disorders and hypersomnia in adult survivors of childhood Hodgkin lymphoma treated with thoracic radiation.

e21527 Background: Survivors of childhood Hodgkin lymphoma (HL) often report fatigue and daytime sleepiness. The presence of sleep disorders, such as obstructive sleep apnea (OSA), could further increase cardiovascular and cerebrovascular morbidity and mortality in these patients. The purpose of this pilot study was to assess for the presence of sleep-related breathing disorders and hypersomnia in adult survivors of childhood HL treated with thoracic radiation. Methods: Survivors, ≥18 years of age and ≥10 years from diagnosis, were randomly selected from the St. Jude Lifetime Cohort (SJLIFE) study and assessed with nocturnal polysomnography (PSG) and the multiple sleep latency test (MSLT). Enrollment was stratified by body mass index (BMI) to include an equal number of normal weight and overweight/obese survivors. Survivors with a history of neurotoxicity related to cancer therapies, and neurological, genetic, or neurodevelopmental conditions associated with neurocognitive impairment were excluded. Results: Thirty adult survivors of childhood HL (60% male; 73% white; mean age 35.8 years [range,19.9-52.8]; BMI 28.6 [range, 18.2-43.5]) enrolled, and 14 (47%) met PSG criteria for mild or moderate OSA (OSA; apnea-hypopnea index 5-30). Of those with OSA, 11 had concurrent hypersomnia using the MSLT criteria and 3 of these 11 met diagnostic criteria for narcolepsy. Twelve (40%) had hypersomnia without OSA and 3 of these 12 met diagnostic criteria for narcolepsy. Within the cohort, 86% had objective evidence of OSA and/or hypersomnia/narcolepsy. Conclusions: Findings suggest adult survivors of childhood HL may be at increased risk for OSA, which when concurrent with treatment-related cardiopulmonary and cerebrovascular risk may further increase morbidity and mortality. Future studies are warranted to compare the prevalence of OSA in this population with a matched community control group and examine whether and how the mechanism for OSA might differ from that in the general population.