Incidence of clinical outcomes in patients with MASLD and long-term follow up: results from a single center cohort study

Abstract

Introduction

The natural history of MASLD results from environmental and genetic factors, impacting hepatic and extrahepatic outcomes. This study aims to elucidate the incidence of clinical outcomes, and the impact of non-invasive tests (NITs) and genetic factors.

Materials and methods

A retrospective study was conducted on patients undergoing vibration-controlled transient elastography (VCTE) for liver stiffness measurement (LSM), with at least 6 months follow-up. Other etiologies than MASLD, previous decompensation or hepatocarcinoma (HCC) were excluded. Significant liver fibrosis was defined by LSM≥8 Kpa, clinically significant portal hypertension (CSPH) by LSM≥25 Kpa. Primary endpoints included incidence of major adverse liver outcomes (MALOs): cirrhosis, liver decompensation (ascites, encephalopathy, variceal bleeding), HCC and liver transplant.

Results

504 patients were selected (61.7% males, median age 59 years [IQR 50.0-67.0]), with a median follow-up of 45.5 months [9.5-94.5]. Median LSM was 6.4 Kpa [5.0-9.0], 21% had PNPLA3 GG. Overall, 11.3% experienced MALOs (33.3% liver decompensation), 2.6% died (46.2% liver-related events). Significant fibrosis increased MALOs incidence (log rank p<0.0001, HR14.4, 95%CI 5.5-13.3). CSPH raised liver decompensation occurrence (p=0.007, HR 6.1, 95%CI 3.3-22.4). Type 2 diabetes (T2D) and PNPLA3 GG increased MALOs incidence (p<0.001, HR 3.8, 95%CI 2.03-6.2; p=0.004, HR 2.3, 95%CI 1.38-5.61). Obese/overweight patients had higher MALOs incidence than lean individuals (p=0.008, HR 2.67, 95% Cl 1.31-3.94). Multivariable Cox regression analysis showed that significant fibrosis by LSM was independently associated with MALOs (aHR 18.5, p<0.0001, 95%Cl 5.65-60.7).

Conclusions

Overweight/obesity and T2D increase incidence of MALOs. LSM by VCTE and PNPLA3 genotyping are useful tools for risk stratification.