Abstract
Up to 50–65% of patients with cirrhosis exhibit interrupted night sleep, delayed sleep habits and excessive daytime sleepiness. These have been variously attributed to disease complications (i.e. ascites, pruritus), hepatic encephalopathy or impaired hepatic melatonin metabolism, but the understanding of their pathophysiology remains limited and their treatment problematic. In addition, use of common hypnotics is contraindicated in these patients because of impaired hepatic disposition and increased cerebral sensitivity to psychoactive medication.
Sleep is regulated by the interaction of a homeostatic and a circadian process. The homeostatic process determines sleep propensity in relation to sleep history, so that the need to sleep increases in parallel with the duration of the wake period. The circadian process, which is marked by the 24-h rhythm of the hormone melatonin, is responsible for the alternation of high/low sleep propensity in relation to dark/light cues.
Circadian sleep regulation has been studied in some depth in patients with cirrhosis, who show considerable delays in the 24-h melatonin rhythm, mostly in relation to impaired sensitivity to light cues. However, while circadian abnormalities are associated with delayed sleep habits, they do not offer a comprehensive explanation to the sleep–wake changes exhibited by these patients. Limited data are available on homeostatic sleep control in patients with cirrhosis, which is worthy of further study.