Combined platelet count with sCD163 and genetic variants optimizes esophageal varices prediction in cirrhotic patients
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Updated: May 20, 2026

Endoscopic Injection Sclerotherapy Assisted by Cyanoacrylate and Clips for Gastroesophageal Varices
Published on: June 13, 2025
Ying-Ying Yang1, Ming-Chih Hou, Ming-Wei Lin
1Division of General Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. yangyy@vghtpe.gov.tw
Insights
New markers, including soluble CD136 (sCD163) and genetic variants, can improve the prediction of esophageal varices (EVs) and bleeding risk in cirrhotic patients.
Area of Science:
- Hepatology
- Gastroenterology
- Genetics
Background:
- Endoscopic screening for esophageal varices (EVs) is costly and invasive.
- Noninvasive markers are needed for predicting EVs in cirrhotic patients.
Purpose of the Study:
- To explore soluble CD136 (sCD136) and genetic variants as additional markers for predicting EVs.
- To assess the combined predictive value of these markers with clinical factors.
Main Methods:
- 951 cirrhotic patients were analyzed for clinical and genetic characteristics.
- Association between EVs and patient factors was evaluated.
- Multivariate analysis identified predictors of EVs.
Main Results:
- Higher serum sCD163 and heme oxygenase-1 (HO-1) levels were found in patients with EVs.
- EVs were predicted by low platelet count, high sCD163, splenomegaly, HO-1 AS, and VEGF GT risk haplotypes.
- Combined markers significantly improved EVs predictability and indicated higher bleeding risk.
Conclusions:
- High sCD163 levels and genetic risk variants are valuable additions to low platelet count for assessing EVs.
- These markers can optimize the prediction of EVs and bleeding risk in cirrhotic patients.
Background And Aim:
Endoscopic screening for esophageal varices (EVs) is expensive and invasive. Besides traditional noninvasive markers, we explore additional candidate markers including portal hypertension serum marker-soluble CD136 (sCD163) and genetic variants of splanchnic vasodilatation and revascularization pathways for prediction of EVs in cirrhotic patients.
Methods:
A total of 951 cirrhotic patients without history of variceal bleeding and an independent validation cirrhotic cohort were enrolled to evaluate the association between the presence of EVs and patients' clinical and genetic characteristics.
Results:
Cirrhotic patients with EVs had higher serum sCD163 and heme oxygenase-1 (HO-1) level, which was positively correlated with the number of risk alleles of HO-1 (S, A), vascular endothelial growth factor (VEGF [G, T]) and VEGF receptor-2 (VEGFR2 [Ile]) genes, than those without EVs. Multivariate analysis showed that EVs in cirrhotic patients was predicted by low platelet count, high sCD163 level, splenomegaly, HO-1 AS and the VEGF GT risk haplotypes. Additive effects in relation to predict EVs were observed in the simultaneous presence of HO-1 AS and VEGF GT risk haplotypes. Combining low platelet count with high sCD163/risk haplotypes significantly increased the predictability of EVs. Furthermore, cirrhotic patients carrying both HO-1 AS and VEGF GT risk haplotypes had lower probability of being free of EVs bleeding compared to patients without above risk haplotypes.
Conclusions:
This study suggested that high sCD163 levels and genetic risk variants are additional markers that can be combined with low platelet count to optimize assessment of EVs and bleeding in cirrhotic patients.
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