P-23 PORTAL VEIN THROMBOSIS IS ASSOCIATED WITH HEPATIC DECOMPENSATIONS WITHOUT LIVER STIFFNESS INCREASE IN HEPATOSPLENIC SCHISTOSOMIASIS

Conflict of interest: No Introduction and Objectives: Hepatosplenic schistosomiasis (HSS) is one of the main causes of non-cirrhotic presinusoidal portal hypertension. Although liver stiffness in HSS is typically lower than in cirrhosis, it is still unknown if over the years liver injury related to...

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Main Authors: Rafael Theodoro, Guilherme Grossi Lopes Cançado, Mateus Jorge Nardelli, Guilherme Augusto Lima Figueira, Carlos Eduardo Franca Vargas, Ludmila Resende Guedes, Fernanda Maria Farage Osório, Luciana Costa Faria, Claudia Alves Couto
Format: Article
Language:English
Published: Elsevier 2024-12-01
Series:Annals of Hepatology
Online Access:http://www.sciencedirect.com/science/article/pii/S1665268124004204
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Summary:Conflict of interest: No Introduction and Objectives: Hepatosplenic schistosomiasis (HSS) is one of the main causes of non-cirrhotic presinusoidal portal hypertension. Although liver stiffness in HSS is typically lower than in cirrhosis, it is still unknown if over the years liver injury related to periportal fibrosis, to metabolic disease or vascular complications can alter liver stiffness and impact in serious hepatic events. This study aims to determine whether metabolic factors, portal vein thrombosis (PVT), or changes in liver stiffness over time are associated with serious hepatic events (SHE) in HSS patients. Patients / Materials and Methods: In this prospective study, adults with laboratory and radiologically confirmed HSS, without concurrent cirrhosis or other liver diseases, were included. All participants underwent initial transient elastography, followed by a second assessment after at least 3 years. The primary outcome was the occurrence of SHE, defined as upper variceal bleeding and/or ascites. Results and Discussion: Among the 26 patients studied, 65.4% were male, with a mean age of 55 ± 9 years. The main metabolic comorbidities were obesity (27%), hypertriglyceridemia (8%), low HDL-c (4%), and diabetes (13%). Baseline liver stiffness measurement (LSM) was 9.9 kPa (±3.9) and the controlled attenuation parameter (CAP) was 238 dB/m (IQR 121-270). After a median follow-up of 59 months (IQR 51-64), serious hepatic events occurred in 46% of the patients. There was a non-significant median absolute increase in LSM of 1.4 kPa (IQR -1.5 to +3.6) and a median relative increase of +14% (IQR -17% to +50%), with no statistically significant differences in paired analysis (p = 0.140). No metabolic or anthropometric factors were associated with changes in liver stiffness. PVT occurred in 7 patients (26.9%) and was the only factor significantly associated with the occurrence of serious hepatic events (p = 0.026), although it did not significantly interfere with LSM (p = 0.842). Conclusions: LSM remained relatively stable in HSS patients over a median follow-up of almost 5 years, proving to be a useful tool in distinguishing HSS from cirrhosis. SHE were primarily associated with PVT, which may further elevate portal pressure.
ISSN:1665-2681