Therefore, it can be hypothesized that treatment strategies aimed at reducing daytime sleepiness may also lead to an improvement in night sleep architecture in these patients. The two case reports confirmed that HE is associated with prominent, reversible changes of both wake and nap EEG structure. Interestingly, in these two cases the HE-related sleep EEG changes were particularly prominent within the sleep spindle range, an area of the spectrum that was only moderately affected by the AAC. Similar findings have been

reported once before in a group of patients with overt HE.10 Clearly, differences are to be expected between the electrophysiological profile of full-blown, spontaneous or TIPS-related overt HE and AAC-related hyperammonemia because Compound Library the latter is only a model of the former, it is not meant to induce severe neuropsychiatric dysfunction and it is not necessarily accompanied by the degree of hepatic failure and/or

the precipitants which are associated with spontaneous Selleck Pembrolizumab HE. In conclusion, profound changes were observed in response to the AAC in clinical (subjective sleepiness), wake and nap EEG indices, suggesting that such techniques are exquisitely sensitive to ammonia levels, which have limited neuropsychiatric/neuropsychological correlates. These findings have important clinical implications: (1) subjective sleepiness may be a useful surrogate marker of HE; (2) correction of excessive daytime sleepiness, either by pharmacological or chronotherapeutic see more strategies, may also result in improved night sleep. We thank all study participants

for their patient and cheerful cooperation. We thank Professor Carlo Merkel, University of Padua, for helpful discussions on the article and constant support. “
“HCC, hepatocellular carcinoma; HCV, hepatitis C virus; PBMC, peripheral blood mononuclear cell; SVR, sustained virologic response. About 10% to 45% of persons who develop acute hepatitis C recover spontaneously, signaled by improved symptoms, normalized liver-related chemistries, loss of hepatitis C virus (HCV) RNA from serum, and the development of hepatitis C antibody.1 If spontaneous recovery should happen, it is always within 6 months of the acute infection and almost never beyond that time, when the disease is now regarded as chronic hepatitis C. At this point, viral loss occurs only if treatment is successful. Currently being debated is whether spontaneous and treatment-induced conversion from detectable to nondetectable serum HCV RNA establishes cure of the infection and the resulting liver disease.