CO026 | LIVER FIBROSIS, STEATOSIS, AND SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH HEMOPHILIA: A CROSS-SECTIONAL STUDY
Abstract
Background and Aims. Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasingly recognized as a driver of cardiovascular risk beyond traditional factors. At the same time, patients with hemophilia (PWH) are aging and accumulating metabolic comorbidities such as obesity, hypertension, and dyslipidemia and are therefore no longer protected from arterial disease. However, liver involvement in this population is heterogeneous and often reflects a complex interplay between metabolic dysfunction and previous viral infections. As a result, it remains unclear whether liver fibrosis and steatosis truly identify patients at increased cardiovascular risk in hemophilia. This study aimed to explore the relationship between liver fibrosis, steatosis, and subclinical atherosclerosis in a cohort of PWH. Methods. We report an interim analysis of a cross-sectional study evaluating liver health in PWH. Liver fibrosis was assessed and graded from F0 to F4, while liver steatosis was evaluated and graded from S0 to S3. Subclinical atherosclerosis was assessed and recorded as present or absent. Clinical data included age, hemophilia type and severity, viral history (HCV, HBV, HIV), liver enzymes, platelet count, FIB-4, and traditional cardiovascular risk factors. Fibrosis and steatosis were analyzed as both ordinal variables and clinically relevant categories. Associations with atherosclerosis were assessed using non-parametric tests and contingency-table analyses. Results. A total of 49 patients with hemophilia were included (median age 55 years). Baseline characteristics of the study population are summarized in Table 1. Subclinical atherosclerosis was detected in 8/45 patients (16.3%). Liver fibrosis was generally mild, with significant fibrosis (F2–F4) observed in 6/49 patients (12.2%). Steatosis was present in 21/41 patients (51.2%), with moderate-to-severe steatosis (S2–S3) in 11/41 (26.8%). No significant association was found between fibrosis stage and the presence of atherosclerosis (p=0.524). Similarly, steatosis was not associated with atherosclerosis (p=0.389). Traditional cardiovascular risk factors were common, with hypertension in 42.8%, dyslipidemia in 32.6%, and active or previous smoking in 71.4% of patients. Atherosclerosis was more frequently observed in patients with a higher burden of cardiovascular risk factors (p=0.043). The number of cardiovascular risk factors showed a trend toward association with atherosclerosis (OR 2.22, 95% CI 0.94–5.22; p=0.068). Conclusions. In this cohort of patients with hemophilia, liver fibrosis and steatosis were not associated with subclinical atherosclerosis. Cardiovascular risk appears to be mainly driven by traditional risk factors rather than liver-related parameters. These findings highlight the complex and heterogeneous nature of liver disease in this population and warrant further investigation in larger cohorts.
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BibTeX
@article{simion2026co026,
title = {{CO026 | LIVER FIBROSIS, STEATOSIS, AND SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH HEMOPHILIA: A CROSS-SECTIONAL STUDY}},
author = {Chiara Simion},
journal = {Bleeding, Thrombosis and Vascular Biology},
year = {2026},
month = oct,
url = {https://www.btvb.org/btvb/article/view/728},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - CO026 | LIVER FIBROSIS, STEATOSIS, AND SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH HEMOPHILIA: A CROSS-SECTIONAL STUDY
AU - Chiara Simion
PY - 2026
DA - 2026/10/26
JO - Bleeding, Thrombosis and Vascular Biology
UR - https://www.btvb.org/btvb/article/view/728
AB - Background and Aims. Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasingly recognized as a driver of cardiovascular risk beyond traditional factors. At the same time, patients with hemophilia (PWH) are aging and accumulating metabolic comorbidities such as obesity, hypertension, and dyslipidemia and are therefore no longer protected from arterial disease. However, liver involvement in this population is heterogeneous and often reflects a complex interplay between metabolic dysfunction and previous viral infections. As a result, it remains unclear whether liver fibrosis and steatosis truly identify patients at increased cardiovascular risk in hemophilia. This study aimed to explore the relationship between liver fibrosis, steatosis, and subclinical atherosclerosis in a cohort of PWH. Methods. We report an interim analysis of a cross-sectional study evaluating liver health in PWH. Liver fibrosis was assessed and graded from F0 to F4, while liver steatosis was evaluated and graded from S0 to S3. Subclinical atherosclerosis was assessed and recorded as present or absent. Clinical data included age, hemophilia type and severity, viral history (HCV, HBV, HIV), liver enzymes, platelet count, FIB-4, and traditional cardiovascular risk factors. Fibrosis and steatosis were analyzed as both ordinal variables and clinically relevant categories. Associations with atherosclerosis were assessed using non-parametric tests and contingency-table analyses. Results. A total of 49 patients with hemophilia were included (median age 55 years). Baseline characteristics of the study population are summarized in Table 1. Subclinical atherosclerosis was detected in 8/45 patients (16.3%). Liver fibrosis was generally mild, with significant fibrosis (F2–F4) observed in 6/49 patients (12.2%). Steatosis was present in 21/41 patients (51.2%), with moderate-to-severe steatosis (S2–S3) in 11/41 (26.8%). No significant association was found between fibrosis stage and the presence of atherosclerosis (p=0.524). Similarly, steatosis was not associated with atherosclerosis (p=0.389). Traditional cardiovascular risk factors were common, with hypertension in 42.8%, dyslipidemia in 32.6%, and active or previous smoking in 71.4% of patients. Atherosclerosis was more frequently observed in patients with a higher burden of cardiovascular risk factors (p=0.043). The number of cardiovascular risk factors showed a trend toward association with atherosclerosis (OR 2.22, 95% CI 0.94–5.22; p=0.068). Conclusions. In this cohort of patients with hemophilia, liver fibrosis and steatosis were not associated with subclinical atherosclerosis. Cardiovascular risk appears to be mainly driven by traditional risk factors rather than liver-related parameters. These findings highlight the complex and heterogeneous nature of liver disease in this population and warrant further investigation in larger cohorts.
SN - 2785-5309
ER -