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Significant liver histological changes (SLHC) were defined as moderate to severe liver inflammation (A2 or higher) and/or fibrosis (F2 or higher) using the METAVIR scoring system. This study aimed to develop an algorithm for the non-invasive detection of SLHC in patients with chronic hepatitis B (CHB) and normal or mildly elevated alanine transaminase (ALT) levels. Using liver histology as gold standard, we developed a simple algorithm for the diagnosis of SLHC in a training set (504 patients), and then validated the diagnostic accuracy in a validation set (166 patients). A new algorithm (AAG) attributed to age, ALT, and gamma-glutamyl transpeptidase (GGT) was developed. In the training set, the area under ROC curve (AUROC) of AAG was significantly higher than that of ALT, aspartate transaminase (AST), GPR, and APRI for the diagnosis of SLHC (0.74, 0.68, 0.65, 0.56, and 0.53, respectively; all P < .05). In the validation set, the AUROC of AAG was also higher than that of ALT, AST, GPR, and APRI (0.73, 0.65, 0.62, 0.62, and 0.61, respectively; all P < .05). Using AAG ≥ 2, the sensitivity and negative predictive value was 84% to 98% and 75% to 94%, respectively, for the diagnosis of SLHC. Using AAG ≥ 6, the specificity and positive predictive value was 93% to 97% and 67% to 79%, respectively, for the diagnosis of SLHC. The AAG algorithm represents a novel noninvasive method for the diagnosis of SLHC in CHB patients with normal or mildly elevated ALT levels.

Liver steatosis could affect the accuracy of FibroScan in patients with chronic hepatitis B (CHB) and nonalcoholic fatty liver disease (NAFLD). This study aimed to assess the accuracy and cut-off values of FibroScan for diagnosing liver fibrosis and cirrhosis in patients with concomitant CHB and NAFLD. A total of 116 patients with concomitant CHB and NAFLD who underwent FibroScan test and liver biopsy were retrospectively enrolled. Liver fibrosis was staged according to the METAVIR scoring system. Calculations of the areas under receiver-operating characteristic curves (AUROC) were performed and compared for the staging of liver fibrosis. The AUROCs for FibroScan, gamma-glutamyl transpeptidase to platelet ratio (GPR), aspartate aminotransferase to platelet ratio index (APRI), fibrosis index based on 4 factors (FIB-4), and NAFLD Fibrosis Score (NFS) were 0.87, 0.73, 0.69, 0.57, and 0.57 for the diagnosis of significant liver fibrosis (METAVIR ≥ F2); 0.89, 0.77, 0.75, 0.68, and 0.60 for severe liver fibrosis (METAVIR ≥ F3); and 0.94, 0.86, 0.80, 0.74, and 0.63 for cirrhosis (F4), respectively. The cutoff values of FibroScan for staging liver fibrosis with sensitivity at least 90% were: 8.0 kPa for significant liver fibrosis, and 10.5 kPa for cirrhosis. The cutoff values of FibroScan for staging liver fibrosis with specificity at least 90% were: 10.8 kPa for significant liver fibrosis, and 17.8 kPa for cirrhosis. FibroScan provides high value for the diagnosis of liver fibrosis and cirrhosis in patients with concomitant CHB and NAFLD.

This study aimed to explore the value of baseline serum exosome‐derived miRNAs for predicting HBeAg seroconversion in chronic hepatitis B (CHB) patients treated with peginterferon (Peg‐IFN). A total of 120 treatment‐naïve HBeAg‐positive CHB patients who received Peg‐IFN therapy (48 weeks) were enrolled. Next‐generation sequencing was performed to screen the serum exosomal miRNAs that were associated with Peg‐IFN treatment outcome, and qRT‐PCR was used to validate them. The area under the receiver operating characteristic curve (AUROC) was used to evaluate the predictive efficacy of biomarkers. Thirty‐three patients (27.5%) achieved HBeAg seroconversion (response group), and 87 patients (72.5%) did not achieve HBeAg seroconversion (nonresponse group). In the identification cohort, 40 serum exosome‐derived miRNAs were differentially expressed between the response group (four patients) and the nonresponse group (four patients). In the confirmation cohort, the expression levels of serum exosomal miR‐194‐5p (p < .001) and miR‐22‐3p (p < .001) were significantly downregulated in the response group (29 patients) compared to the nonresponse group (83 patients). Multivariate analysis identified baseline serum exosomal miR‐194‐5p, miR‐22‐3p, alanine aminotransferase (ALT), and HBV DNA as independent predictors of HBeAg seroconversion (all p < .05). The AUROCs of serum exosomal miRNAs (0.77 and 0.75 for miR‐194‐5p and miR‐22‐3p, respectively) were higher than that of ALT (0.70) and HBV DNA (0.69). The combination of exosomal miR‐194‐5p and miR‐22‐3p further improved the predictive performance with an AUROC of 0.82. Baseline serum exosomal miR‐194‐5p and miR‐22‐3p may serve as novel biomarkers to predict HBeAg seroconversion in CHB patients treated with Peg‐IFN.