Cessation of nucleoside/nucleotide analogue (Nuc) therapy in patients with HBeAg-negative chronic hepatitis B (CHB) remains controversial.

In this prospective, single-center cohort study, we recruited 45 patients with HBeAg-negative CHB from The Fifth Medical Center of Chinese People's Liberation Army General Hospital in mainland China. Patients were classified into a Nuc cessation group (n = 27) and Nuc continuation group (n = 18) and followed-up for 36 months. Nuc were stopped after being inactive for at least 4 years (normal alanine aminotransferase (ALT), undetectable hepatitis B virus (HBV) DNA), with liver fibrosis ≤ Stage1 (S1) and inflammation ≤ Grade (G1).

Within 3 years of follow-up, 51.9% patients with Nuc cessation had virological relapse and 14.8% had ALT elevation, while all patients with Nuc continuation had undetectable HBV DNA and normal ALT. The rate of HBsAg loss after Nuc cessation was 22.2% compared with no seroconversion in patients with Nuc continuation. The hepatitis flare rate was 11.1% and there were no cases of hepatic decompensation after Nuc cessation. End of treatment (EOT) HBsAg, HBV RNA, and decline in HBV core-related antigen (HBcrAg) rate were predictive markers for HBsAg seroconversion at 6 months post-Nuc cessation.

This study showed favorable HBsAg loss and low hepatitis flare rates after Nuc cessation. EOT HBsAg, HBV RNA, and decline in HBcrAg rate were predictive markers for HBsAg seroconversion at 6 months post-Nuc cessation.

Nonalcoholic fatty liver disease (NAFLD) is hepatic steatosis that is require the exclusion of certain etiologies, including drug usage or alcoholic consumption. Conversely, metabolic dysfunction-associated fatty liver disease (MAFLD) needs not to. In this study, we aimed to examine whether MAFLD is more easily diagnosed than NAFLD in liver transplant (LT) recipients with abnormal liver function.

In this cross-sectional study, LT recipients with abnormal liver function were investigated for the prevalence of MAFLD and NAFLD.

We recruited 57 LT recipients with abnormal liver function at a referral hospital. Among these patients, the prevalence of MAFLD and NAFLD was 37.8% and 11.1%, respectively. 17 patients showed hepatic steatosis, with an average NAFLD activity score of 3.5 and a fibrosis score of 1.0. Compared with non-MAFLD patients, MAFLD patients had a significant difference in fasting blood glucose levels (p = 0.009). Among 17 MAFLD patients, 12 were overweight and four were diagnosed with diabetes mellitus. The majority of MAFLD diagnoses were based on body mass index (70.6%) and diabetes mellitus history (23.5%), biomarkers that are easily obtained. At 6, 12, 24, and 36 months after LT, MAFLD patients had higher levels of fasting blood glucose (6 months: p = 0.004, 12 months: p = 0.038) and higher trend of body mass index value and plasma triglyceride level but no significance.

MAFLD was more easily diagnosed in LT recipients with abnormal liver function and higher in prevalence than NAFLD. A larger sample size research is required to validate these conclusions.