Background & Aims: Portal hypertension is the strongest predictor of hepatic decompensation and death in patients with cirrhosis. However, its discriminatory accuracy in patients with nonalcoholic fatty liver disease (NAFLD) has been challenged because hepatic vein catheterization may not reflect the real portal vein pressure as accurately as in patients with other etiologies. We aimed to evaluate the relationship between hepatic venous pressure gradient (HVPG) and presence of portal hypertension–related decompensation in patients with advanced NAFLD (aNAFLD). Methods: Multicenter cross-sectional study included 548 patients with aNAFLD and 444 with advanced RNA-positive hepatitis C (aHCV) who had detailed portal hypertension evaluation (HVPG measurement, gastroscopy, and abdominal imaging). We examined the relationship between etiology, HVPG, and decompensation by logistic regression models. We also compared the proportions of compensated/decompensated patients at different HVPG levels. Results: Both cohorts, aNAFLD and aHVC, had similar baseline age, gender, Child-Pugh score, and Model for End-Stage Liver Disease score. Median HVPG was lower in the aNAFLD cohort (13 vs 15 mmHg) despite similar liver function and higher rates of decompensation in aNAFLD group (32% vs 25%; P =.019) than in the aHCV group. For any of the HVPG cutoff analyzed (<10, 10–12, or 12 mmHg) the prevalence of decompensation was higher in the aNAFLD group than in the aHCV group. Conclusions: Patients with aNAFLD have higher prevalence of portal hypertension–related decompensation at any value of HVPG as compared with aHCV patients. Longitudinal studies aiming to identify HVPG thresholds able to predict decompensation and long-term outcomes in aNAFLD population are strongly needed.
Decompensation in Advanced Nonalcoholic Fatty Liver Disease May Occur at Lower Hepatic Venous Pressure Gradient Levels Than in Patients With Viral Disease / Bassegoda, O.; Olivas, P.; Turco, L.; Mandorfer, M.; Serra-Burriel, M.; Tellez, L.; Kwanten, W.; Laroyenne, A.; Farcau, O.; Alvarado, E.; Moga, L.; Vuille-Lessard, E.; Fortea, J. I.; Ibanez, L.; Tosetti, G.; Vanwolleghem, T.; Larrue, H.; Burgos-Santamaria, D.; Stefanescu, H.; Paternostro, R.; Cippitelli, A.; Lens, S.; Augustin, S.; Llop, E.; Laleman, W.; Trebicka, J.; Chang, J.; Masnou, H.; Zipprich, A.; Miceli, F.; Semmler, G.; Forns, X.; Primignani, M.; Banares, R.; Puente, A.; Berzigotti, A.; Rautou, P. E.; Villanueva, C.; Gines, P.; Garcia-Pagan, J. C.; Procopet, B.; Bureau, C.; Albillos, A.; Francque, S.; Reiberger, T.; Schepis, F.; Graupera, I.; Hernandez-Gea, V.. - In: CLINICAL GASTROENTEROLOGY AND HEPATOLOGY. - ISSN 1542-3565. - 20:10(2022), pp. 2276-2286.e6. [10.1016/j.cgh.2021.10.023]
Decompensation in Advanced Nonalcoholic Fatty Liver Disease May Occur at Lower Hepatic Venous Pressure Gradient Levels Than in Patients With Viral Disease
Turco L.;Schepis F.;
2022
Abstract
Background & Aims: Portal hypertension is the strongest predictor of hepatic decompensation and death in patients with cirrhosis. However, its discriminatory accuracy in patients with nonalcoholic fatty liver disease (NAFLD) has been challenged because hepatic vein catheterization may not reflect the real portal vein pressure as accurately as in patients with other etiologies. We aimed to evaluate the relationship between hepatic venous pressure gradient (HVPG) and presence of portal hypertension–related decompensation in patients with advanced NAFLD (aNAFLD). Methods: Multicenter cross-sectional study included 548 patients with aNAFLD and 444 with advanced RNA-positive hepatitis C (aHCV) who had detailed portal hypertension evaluation (HVPG measurement, gastroscopy, and abdominal imaging). We examined the relationship between etiology, HVPG, and decompensation by logistic regression models. We also compared the proportions of compensated/decompensated patients at different HVPG levels. Results: Both cohorts, aNAFLD and aHVC, had similar baseline age, gender, Child-Pugh score, and Model for End-Stage Liver Disease score. Median HVPG was lower in the aNAFLD cohort (13 vs 15 mmHg) despite similar liver function and higher rates of decompensation in aNAFLD group (32% vs 25%; P =.019) than in the aHCV group. For any of the HVPG cutoff analyzed (<10, 10–12, or 12 mmHg) the prevalence of decompensation was higher in the aNAFLD group than in the aHCV group. Conclusions: Patients with aNAFLD have higher prevalence of portal hypertension–related decompensation at any value of HVPG as compared with aHCV patients. Longitudinal studies aiming to identify HVPG thresholds able to predict decompensation and long-term outcomes in aNAFLD population are strongly needed.
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