We read with interest the recent paper by Zheng et al.1 The authors concluded that, in patients with chronic hepatitis B (CHB), hepatic steatosis (HS) was negatively associated with hepatitis B e antigen and hepatitis B virus (HBV) DNA, but negatively with metabolic factors.

It is important that treatment provided for CHB was not mentioned, although it may itself cause HS. Chang et al reported the incidence rate of new onset HS in patients receiving entecavir as 50 per 1000 person-years.2 This is almost twice as high as in the general population.3, 4 Ability to cause hepatic injury by lactic acidosis, microvesicular steatosis was shown for entecavir and tenofovir.5-8 The authors speculated that HS may alter the hepatic environment leading to decreased viral replication. However, the inhibitory effect of steatosis on viral replication may in fact be caused by a third factor, namely, anti-viral treatment.

In their systematic review, Zheng et al did not reveal an association between HS and advanced liver fibrosis in patients with CHB.1 However, in the study by Seto et al, severe steatosis (CAP ≥280 dB/m) was independently associated with increased liver fibrosis in both treatment-naïve and on-treatment patients achieving long-term virological suppression. The results suggest that, even during quiescent viral activity, fibrogenesis can still develop in the presence of HS.9 We obtained similar results from hepatitis B surface antigen-negative patients with NAFLD.10 In them, positive IgG antibody to hepatitis B core antigen (anti-HBc) was associated with 7.3-fold higher odds of advanced liver fibrosis or cirrhosis compared to those without markers of past HBV infection. The reverse association of dyslipidaemia with severe liver fibrosis may also support the importance of viral, rather than metabolic, factors in the disease progression and development of unfavourable outcomes.

We fully agree with Zheng et al on the need for further research on the pathogenesis and long-term outcomes in patients with HS and current or previous HBV infection.

Declaration of personal interests: Sergey Morozov has served as a speaker for Laborie, AstraZeneca, AlfaSigma, Dr Falk, Takeda, and has received research funding from Russian Science Foundation. Sergey Morozov is an employee of Federal Research Center of Nutrition and Biotechnology. Sergey Batskikh has served as a speaker for AbbVie, MSD, R-PHARM. Sergey Batskikh is an employee of Moscow Clinical Research Center named after AS Loginov.

Declaration of funding interests: This paper has no financial support.