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Letter: diabetes mellitus increases the risk of hepatic encephalopathy in patients with cirrhosis—authors’ reply

EDITORS, We thank Liu and colleagues for their important comment on our recent manuscript demonstrating an independent effect of diabetes mellitus on the presence of covert hepatic encephalopathy (CHE) and the development of overt hepatic encephalopathy (OHE) in patients with cirrhosis.1 Liu et al validated our findings by performing a systematic literature search with pooled analysis of studies on diabetes mellitus and the risk of hepatic encephalopathy (HE).2 They demonstrated a significant association between diabetes mellitus and HE with an odds ratio of 1.7. These findings remained consistent across sensitivity analyses. Globally, non-alcoholic fatty liver disease (NAFLD) is the most common liver disease with an estimated prevalence of 24% and increasing incidence predicted for Europe.3 Diabetes mellitus is a common comorbidity in patients with NAFLD and adds independently to the risk of advanced fibrosis or cirrhosis.4 In patients with cirrhosis, it is of pivotal importance to prevent decompensation and consequently to improve prognosis. HE is one of the most severe complications of cirrhosis and an indicator for poor survival.5 Additionally, even the lowest grades of HE impair quality of life and sleep.6 Although some modifiable factors to decrease the risk of HE have been recently described, there is still an urgent need to improve the quality of care in the management of patients with cirrhosis and this important complication.7 As more exhaustively described in our study, diabetes mellitus and, more specifically, poor glycaemic control may be a target to potentially improve cognitive function and prevent development of OHE.1 Although the demonstrated association seems comprehensible from a pathophysiological point of view, our findings regarding the impact of poor glycaemic control on the risk of HE have to be validated in future multi-centre studies. In addition, interventional studies should investigate the potential effect of intensified anti-diabetic therapy on the development of HE and target values for HbA1c must be defined in this special population. Taken together, we fully agree with the comment of Lui and colleagues that more attention needs to be paid to adequate glycaemic control in patients with cirrhosis and diabetes mellitus. In metabolically burdened patients, this may be an additional step to improve the quality of care in the management of HE. ACKNOWLEDG EMENT The authors‘ declarations of personal and financial interests are unchanged from those in the original article.1