Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression.

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 ( = 12 (28.6%) with previous decompensation, HBeAg-negative: = 36 (85.7%)) were included and followed for 2.1 (0.6; 5.3) years. The median HVPG (available in = 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, < 0.001) and moderately with the model for end-stage liver disease (MELD) score (ρ: 0.459, = 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); < 0.001), even after adjusting for other factors. An LSM cut-off at 25kPa accurately stratified patients into a low-risk ( = 23, zero events during follow-up) and a high-risk ( = 19; = 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.