STUDY OBJECTIVES: Sleep disturbances in cirrhosis are assumed to be due to hepatic encephalopathy (HE). The interaction between cirrhosis, prior HE, and obstructive sleep apnea (OSA) has not been evaluated. We aimed to evaluate the additional effect of cirrhosis with and without prior HE on the sleep architecture and perceived sleep disturbances of OSA patients. METHODS: A case-control review of OSA patients who underwent polysomnography (PSG) in a liver-transplant center was performed. OSA patients with cirrhosis (with/without prior HE) were age-matched 1:1 with OSA patients without cirrhosis. Sleep quality, daytime sleepiness, sleep quality, and sleep architecture was compared between groups. RESULTS: Forty-nine OSA cirrhotic patients (age 57.4 ± 8.3 years, model for end-stage liver disease (MELD) 8.3 ± 5.4, 51% HCV, 20% prior HE) were age-matched 1:1 to OSA patients without cirrhosis. Apnea-hypopnea index, arousal index, sleep efficiency, daytime sleepiness, and effect of sleepiness on daily activities were similar between OSA patients with/ without cirrhosis. Sleep architecture, including %slow wave sleep (SWS), was also not different between the groups. MELD was positively correlated with time in early (N1) stage (r = 0.4, p = 0.03). All prior HE patients (n = 10) had a shift of the architecture towards early, non-restorative sleep (higher % [N2] stage [66 vs 52%, p = 0.005], lower % SWS [0 vs 29%, p = 0.02], lower REM latency [95 vs 151 minutes, p = 0.04]) compared to the rest. Alcoholic etiology was associated with higher latency to N1/N2 sleep, but no other effect on sleep architecture was seen. CONCLUSIONS: OSA can contribute to sleep disturbance in cirrhosis and should be considered in the differential of sleep disturbances in cirrhosis. Prior HE may synergize with OSA in worsening the sleep architecture.
STUDY OBJECTIVES:Sleep disturbances in cirrhosis are assumed to be due to hepatic encephalopathy (HE). The interaction between cirrhosis, prior HE, and obstructive sleep apnea (OSA) has not been evaluated. We aimed to evaluate the additional effect of cirrhosis with and without prior HE on the sleep architecture and perceived sleep disturbances of OSA patients. METHODS: A case-control review of OSA patients who underwent polysomnography (PSG) in a liver-transplant center was performed. OSA patients with cirrhosis (with/without prior HE) were age-matched 1:1 with OSA patients without cirrhosis. Sleep quality, daytime sleepiness, sleep quality, and sleep architecture was compared between groups. RESULTS: Forty-nine OSA cirrhotic patients (age 57.4 ± 8.3 years, model for end-stage liver disease (MELD) 8.3 ± 5.4, 51% HCV, 20% prior HE) were age-matched 1:1 to OSA patients without cirrhosis. Apnea-hypopnea index, arousal index, sleep efficiency, daytime sleepiness, and effect of sleepiness on daily activities were similar between OSA patients with/ without cirrhosis. Sleep architecture, including %slow wave sleep (SWS), was also not different between the groups. MELD was positively correlated with time in early (N1) stage (r = 0.4, p = 0.03). All prior HE patients (n = 10) had a shift of the architecture towards early, non-restorative sleep (higher % [N2] stage [66 vs 52%, p = 0.005], lower % SWS [0 vs 29%, p = 0.02], lower REM latency [95 vs 151 minutes, p = 0.04]) compared to the rest. Alcoholic etiology was associated with higher latency to N1/N2 sleep, but no other effect on sleep architecture was seen. CONCLUSIONS: OSA can contribute to sleep disturbance in cirrhosis and should be considered in the differential of sleep disturbances in cirrhosis. Prior HE may synergize with OSA in worsening the sleep architecture.
Authors: Javier Crespo; Jose Cifrián; Jose Antonio Pinto; Antonio Jiménez-Gómez; Fernando Pons-Romero Journal: Am J Gastroenterol Date: 2003-12 Impact factor: 10.864
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