Search

Background and Aims Methods Results Conclusions We aimed to explore the risk factors associated with virological and clinical relapse, as well as their impact on overall mortality, in hepatitis B virus (HBV)‐infected patients receiving nucleos(t)ide analogues (NUCs) therapy prior to chemotherapy initiation.From 2010 to 2020, we conducted a prospective cohort study involving patients with HBV infection undergoing cytotoxic chemotherapy. We utilized the Kaplan–Meier method and Cox proportional hazard regression models to assess risk factors.We observed that TDF or TAF (HR: 2.16, 95% CI 1.06–4.41; p = .034), anthracycline (HR: 1.73, 95% CI 1.10–2.73; p = .018), baseline HBV DNA (HR: 1.55, 95% CI 1.33–1.81; p < .001) and end‐of‐treatment HBsAg titre >100 IU/mL (HR: 7.81, 95% CI 1.94–31.51; p = .004) were associated with increased risk of virological relapse. Additionally, TDF or TAF (HR: 4.91, 95% CI 1.45–16.64; p = .011), baseline HBV DNA (HR: 1.48, 95% CI 1.10–1.99; p = .009) and end‐of‐treatment HBsAg titre >100 IU/mL (HR: 6.09, 95% CI .95–38.87; p = .056) were associated with increased risk of clinical relapse. Furthermore, we found that virological relapse (HR: 3.32, 95% CI 1.33–8.32; p = .010) and clinical relapse (HR: 3.59, 95% CI 1.47–8.80; p = .005) significantly correlated with all‐cause mortality in HBV patients receiving cytotoxic chemotherapy with prophylactic NUCs therapy.The risk of virological and clinical relapse was linked to baseline HBV DNA, end‐of‐treatment HBsAg levels and TDF or TAF for prophylaxis; additionally, experiencing relapse heightens the risk of all‐cause mortality. Further research is warranted to explore potential strategies for preventing virological and clinical relapse in high‐risk patients. [ABSTRACT FROM AUTHOR]

Abstract: Background & Aims: Although hepatitis B virus (HBV) and hepatitis C virus (HCV) infections remain major risk factors for hepatocellular carcinoma (HCC), non‐viral causes of HCC, particularly non‐alcoholic fatty liver disease (NAFLD), are becoming increasingly prevalent. The aim of this study was to compare the clinical characteristics and survival of cryptogenic and viral HCC. Methods: We conducted a retrospective cohort study involving 3878 consecutive HCC patients seen at two tertiary centres in the United States and one in Taiwan from 2004 to 2014. We compared the clinical characteristics, treatment and survival of patients by underlying aetiology: cryptogenic (n = 696), HBV (n = 1304) or HCV (n = 1878). Results: Cirrhosis was present in 66.8% of the cryptogenic HCC patients, compared with 74.7% of HBV‐related HCC (HBV‐HCC) (P = .001) and 85.9% of HCV‐HCC (P < .001). Compared to viral HCC, cryptogenic HCC patients presented with larger tumours and at later stages of disease. Five‐year overall survival was 16.3% among cryptogenic HCC patients compared with 31.9% among HBV‐HCC patients and 27.7% among HCV‐HCC patients (P < .001 for both by the log‐rank test). HCC aetiology was not an independent predictor of survival, though ethnicity, cirrhosis status, meeting Milan criteria and treatment allocation were. Conclusions: Compared with viral HCC patients, those with cryptogenic HCC had lower prevalence of cirrhosis, were diagnosed with larger tumours at more advanced stages of disease, and had poorer overall survival. Additional efforts are needed to identify patients at risk of cryptogenic HCC and to identify cryptogenic HCC at earlier stages of disease. [ABSTRACT FROM AUTHOR]