Based on the study by Jeng et al., the APASL stopping rule results in approximately 50% relapse within 1 year and also resulted in hepatic decompensation in 1 patient with cirrhosis. Therefore, this study, in our opinion, confirms earlier observations in studies performed with

lamivudine[12, 13] that finite duration of nucleos(t)ide analog treatment is not really feasible in the majority of HBeAg-negative HBV patients, even not with the usage of more-potent antiviral U0126 chemical structure drugs and stringent cessation criteria. At this moment, long-term, if not lifelong, treatment may still be considered for the vast majority of patients. This recommendation definitely applies to patients who have already progressed to liver cirrhosis, because withdrawal hepatitis flares can result in

subsequent liver failure and death.[18] We also think that in future withdrawal studies, patients with cirrhosis should not be included until more data have become available from patients without advanced liver disease. Despite our concerns, the possibility that treatment cessation is feasible in a selected group of patients should drive Belnacasan mw further research in this field. Unfortunately, it is currently unclear what criteria and which markers can be helpful to identify those patients in whom it may be safe to stop antiviral therapy with a low risk of relapse of disease. The usage of quantitative HBsAg levels[19] may help to find these patients who prevent the glass from becoming completely empty. Jurriën G.P. Reijnders, M.D., Ph.D.1 PRKACG ”
“Aim:  The diagnosis of Wilson disease is based on the results of several clinical and biochemical tests. This study aimed to clarify the clinical features and spectrum of Wilson disease, including severe Wilson disease. Methods:  Between 1985 and 2009, 10 patients with clinical, biochemical or histological evidence of Wilson disease were either diagnosed or had a previously established diagnosis confirmed at Fukuoka University Hospital. Severe Wilson disease was defined by a serum prothrombin time ratio of more than 1.5 or serum prothrombin activity of less than 50%. The 10 Wilson disease patients were divided into two groups, one

containing three non-severe patients and the other containing seven severe patients, and the biochemical features of the patients in these two groups were compared. Results:  The mean age at diagnosis was 21.5 ± 11.7 years (range, 7–39). Decreased serum ceruloplasmin, enhanced 24-h urinary copper excretion, presence of Kayser–Fleischer rings and histological signs of chronic liver damage were confirmed in 100%, 100%, 66.7% and 100% of patients, respectively. Severe Wilson disease patients had higher levels of serum ceruloplasmin and serum copper (P < 0.05, P < 0.05, respectively) than non-severe patients. Conclusion:  In severe Wilson disease patients, the serum ceruloplasmin and serum copper levels were higher than those in non-severe Wilson disease patients.