Abstract

Background: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients with pre-treatment CSPH are limited. Methods: We retrospectively included patients with long-term (>12 months) suppression of HBV replication and pre-treatment CSPH (i.e., varices, collaterals on cross-sectional imaging, or ascites). Patients were monitored by on-treatment liver stiffness measurement (LSM) and HVPG assessment. The primary outcome was (further) hepatic decompensation (including liver-related mortality). Results: Forty-two patients (n = 12 (28.6%) with previous decompensation, HBeAg-negative: n = 36 (85.7%)) were included and followed for 2.1 (0.6; 5.3) years. The median HVPG (available in n = 17) was 15 (10; 22) mmHg and the median LSM 22.5 (12.5; 41.0) kPa. LSM correlated strongly with HVPG (Spearman’s ρ: 0.725, p < 0.001) and moderately with the model for end-stage liver disease (MELD) score (ρ: 0.459, p = 0.002). LSM, MELD and albumin levels had good prognostic value for decompensation (area under the receiver operated characteristics curve (AUROC) >0.850 for all). LSM predicted (further) decompensation in competing risk regression (subdistribution hazard ratio (SHR): 1.05 (95% confidence interval(CI) 1.03–1.06); p < 0.001), even after adjusting for other factors. An LSM cut-off at 25kPa accurately stratified patients into a low-risk (n = 23, zero events during follow-up) and a high-risk (n = 19; n = 12 (63.2%) developed events during follow-up) group. Conclusions: Patients with HBV-induced CSPH who achieved long-term viral suppression were protected from decompensation, if LSM was <25 kPa. LSM ≥ 25 kPa indicates a persisting risk for decompensation, despite long-term HBV suppression.

Highlights

  • Nucleos(t)ide analog (NA) treatment is recommended for all patients with hepatitis B virus (HBV)-induced cirrhosis with detectable HBV-DNA [1,2]

  • On-treatment liver stiffness measurement (LSM) was available in all patients, whereas hepatic venous pressure gradient (HVPG) measurements were conducted in n = 17 (40.5%) patients

  • All patients were virally suppressed by NA therapy with no viral breakthroughs

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Summary

Introduction

Nucleos(t)ide analog (NA) treatment is recommended for all patients with hepatitis B virus (HBV)-induced cirrhosis with detectable HBV-DNA [1,2]. In a small uncontrolled trial involving 19 HBV patients with cirrhosis and CSPH, i.e., a hepatic venous pressure gradient (HVPG) ≥10 mmHg, one year of lamivudine (3TC) therapy induced a decrease in HVPG in all but one patient, who had experienced viral breakthrough [9]. In another observational study investigating the effects of different NA (including 3TC, adefovir and tenofovir disoproxilfumarate (TDF)), patients without varices at baseline rarely developed varices during follow-up, and patients who had already developed small varices prior to NA therapy showed regression in a vast majority of cases (67%) [10]. LSM ≥ 25 kPa indicates a persisting risk for decompensation, despite long-term HBV suppression

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