Diverse effects of hepatic steatosis on fibrosis progression and functional cure in virologically quiescent chronic hepatitis B

Mak, Lung‐Yi; Hui, Rex Wan‐Hin; Fung, James; Liu, Fen; Wong, Danny Ka‐Ho; Cheung, Ka‐Shing; Seto, Wai‐Kay

doi:10.1016/j.jhep.2020.05.040

Cited by 109 publications

(117 citation statements)

References 29 publications

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“…A population-based cohort study showed that the cumulative HCC incidence in patients who achieved HBsAg loss is significantly lower than that in CHB patients, yet is still slightly higher than that in HBsAg-negative individuals. 42 43,44 Immunologically, the proportion of patients with HBsAg seroconversion, that is, the detection of anti-HBs together with HBsAg seroclearance, was comparable between patients who had spontaneous and NA-induced HBsAg loss, which is in line with previous studies. 41,45 Anti-HBs positivity appears to protect against HBsAg seroreversion, that is, reappearance of serum HBsAg after HBsAg loss, in patients with spontaneous HBsAg seroclearance.…”

Section: Discussionsupporting

confidence: 88%

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Similarly low risk of hepatocellular carcinoma after either spontaneous or nucleos(t)ide analogue‐induced hepatitis B surface antigen loss

Yip

Wong

Tse

et al. 2020

Aliment Pharmacol Ther

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SummaryBackgroundIt is unknown whether patients with chronic hepatitis B (CHB) who achieved hepatitis B surface antigen (HBsAg) seroclearance spontaneously or following anti‐viral therapy have similar clinical outcomes.AimTo compare the risk of hepatocellular carcinoma (HCC) in patients with CHB who either cleared HBsAg spontaneously or following anti‐viral therapyMethodsAdult CHB‐monoinfected patients who cleared HBsAg between January 2000 and March 2019 were identified from a territory‐wide database in Hong Kong. Patients with liver transplantation and/or HCC before HBsAg loss were excluded. Patients’ demographics, comorbidities, anti‐viral treatment, laboratory parameters and HCC development were analysed.ResultsOf 7,124 identified patients with CHB who cleared HBsAg, mean age was 58.1 ± 13.8 years; 4,340 (60.9%) were male; 451 (6.3%) had cirrhosis; 5,917 (83.1%) and 1,207 (16.9%) had spontaneous and nucleos(t)ide analogue (NA)‐induced HBsAg seroclearance, respectively. Most patients had normal liver function at HBsAg loss. Patients with NA‐induced HBsAg seroclearance were younger, and more likely to be male and cirrhotic than patients with spontaneous HBsAg loss. At a median (interquartile range) follow‐up of 4.3 (2.2‐7.6) years, 97 (1.6%) and 16 (1.3%) patients with spontaneous and NA‐induced HBsAg loss developed HCC, respectively. Patients who achieved NA‐induced HBsAg loss had comparable HCC risk as those with spontaneous HBsAg loss (adjusted subdistribution hazard ratio 0.75, 95% CI 0.43‐1.32, P = 0.323). The results remained robust in propensity score weighting and matching analyses.ConclusionThe HCC risk was similarly low after either spontaneous or NA‐induced HBsAg seroclearance in a territory‐wide cohort of patients with CHB who had cleared HBsAg.

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Section: Discussionsupporting

confidence: 88%

“…DM is closely related to fatty liver. Previous study showed that presence of hepatic steatosis is associated with a higher likelihood of HBsAg seroclearance in treatment‐naïve CHB patients, whereas it is also associated with fibrosis progression 43,44 …”

Section: Discussionmentioning

confidence: 99%

Similarly low risk of hepatocellular carcinoma after either spontaneous or nucleos(t)ide analogue‐induced hepatitis B surface antigen loss

Yip

Wong

Tse

et al. 2020

Aliment Pharmacol Ther

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“…Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world, accounting for 90% of human liver cancer (21). The incidence of liver cancer is rising due to various factors such as hepatitis, alcoholic fatty liver, nonalcoholic fatty liver and a atoxin (22,23). Hepatectomy and liver transplantation are commonly used in patients with early stage HCC (24).…”

Section: Discussionmentioning

confidence: 99%

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Zhang

Fan

et al. 2020

Preprint

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Background: Increasing evidence shows that liver tumor-initiating cells (T-ICs) closely associated with the progression, metastasis, recurrence and chemo-resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. The purpose of our study was to explore the role of miR-361-3p in the expansion of liver T-ICs and the potential molecular mechanism.Results: Flow cytometry analysis was performed to isolate CD24+, CD133+ or EpCAM+ cells from primary HCC cells or HCC cell lines. Real-time PCR was used to detect the expression of miR-361-3p in liver T-ICs. The impact of miR-361-3p on liver T-ICS expansion was investigated both in vivo and in vitro. The correlation between miR-361-3p expression and TACE (transcatheter arterial chemoembolization) or sorafenib benefits in HCC was evaluated in patient cohorts. miR-361-3p expression is upregulated in liver T-ICs. Knockdown of miR-361-3p impairs the self-renewal and tumorigenicity liver T-ICs. Conversely, forced miR-361-3p expression enhances the self-renewal and tumorigenicity liver T-ICs. Mechanistically, miR-361-3p directly targets SOX1 via binding its 3’-UTR in liver T-ICs. Moreover, miR-361-3p knockdown hepatoma cells are more sensitive to cisplatin or sorafenib treatment. Clinical cohort analysis demonstrates that miR-361-3p low HCC patients are benefited from TACE or sorafenib treatment. Conclusions: Our findings revealed the crucial role of the miR-361-3p in liver T-IC expansion and TACE or sorafenib response, rendering miR-361-3p an optimal target for the prevention and intervention in HCC.

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“…The implications of MAFLD on the clinical outcomes of patients with CHB, such as the risk of fibrosis progression and HCC, remain unknown. Our recent work 7 showed that the presence of hepatic steatosis was associated with 3-fold increased probability of hepatitis B surface antigen seroclearance, but the presence of persistent severe hepatic steatosis was also associated with more than 2-fold increase in risk of fibrosis progression. Further studies should investigate the interaction between CHB and MAFLD, incorporating the new diagnostic criteria, and dissect the driver mechanisms for both favorable and unfavorable clinical outcomes.…”

Section: To the Editormentioning

confidence: 97%

Letter regarding “A new definition for metabolic dysfunction-associated fatty liver disease: An international expert consensus statement”

Mak

Yuen

Seto

2020

Journal of Hepatology

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Diverse effects of hepatic steatosis on fibrosis progression and functional cure in virologically quiescent chronic hepatitis B

Cited by 109 publications

References 29 publications

Similarly low risk of hepatocellular carcinoma after either spontaneous or nucleos(t)ide analogue‐induced hepatitis B surface antigen loss

Similarly low risk of hepatocellular carcinoma after either spontaneous or nucleos(t)ide analogue‐induced hepatitis B surface antigen loss

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Letter regarding “A new definition for metabolic dysfunction-associated fatty liver disease: An international expert consensus statement”

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