Ying-Ying Yang and Han-Chieh Lin are co-corresponding authors of this paper.
Combined platelet count with sCD163 and genetic variants optimizes esophageal varices prediction in cirrhotic patients
Article first published online: 19 DEC 2012
© 2012 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 28, Issue 1, pages 112–121, January 2013
How to Cite
Yang, Y.-Y., Hou, M.-C., Lin, M.-W., Chen, P.-H., Liao, W.-C., Chu, C.-J. and Lin, H.-C. (2013), Combined platelet count with sCD163 and genetic variants optimizes esophageal varices prediction in cirrhotic patients. Journal of Gastroenterology and Hepatology, 28: 112–121. doi: 10.1111/j.1440-1746.2012.07245.x
- Issue published online: 19 DEC 2012
- Article first published online: 19 DEC 2012
- Accepted manuscript online: 31 JUL 2012 07:45AM EST
- Manuscript Accepted: 20 JUL 2012
- National Science Council. Grant Numbers: NSC100-2314-B-075-058-MY3, NSC100-2314-B-075-015
- Taipei Veterans General Hospital. Grant Numbers: V100C-035, VGH100C-21
- esophageal varices;
- genetic polymorphism;
- heme oxygenase-1;
- vascular endothelial growth factor
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.
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.
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.
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.