Abstract
CD146, an element of the endothelial junction- has been evaluated in several pathological conditions with altered endothelial function but never before in patients with liver disease. As angiogenesis and inflammation were implicated in the development of liver fibrosis, we have explored this suggestion by evaluating levels of sCD146 in a group of patients with chronic liver diseases (CLD) and in cirrhotic patients. The results indicated that there is a clear connection between sCD146 levels and the progression of liver disease. They can differentiate noncirrhotic patients with CLD from cirrhotics, supporting the usefulness of CD146 in the noninvasive diagnosis of liver cirrhosis. Furthermore, our findings provided evidence of sCD146 upregulation in decompensated compared to compensated cirrhosis and sCD146 values were clearly associated with Model for End Stage Liver Disease (MELD) score. Thus, by using an easy to perform ELISA method, we demonstrated that sCD146 can accurately distinguish advanced fibrosis and prognosticate decompensation in cirrhosis.
Highlights
The cell adhesion CD146 (S-Endo 1 Ag), “a member of the immunoglobulin superfamily” referred as MUC18, was lately reported as a new element located at the endothelial cell-to-cell junction [1]
Since soluble form of CD146 (sCD146) can provide evidence for endothelial activation and proliferation, we investigated its performance in estimating liver fibrosis and cirrhosis, its relationship with Model-for-End-Stage-Liver Disease (MELD) score and its utility in differentiating compensated from decompensated cirrhosis [29]
We found that median sCD146 values were considerably higher in patients with cirrhosis in comparison with those with non-cirrhotic chronic liver disease (CLD) or to healthy controls
Summary
The cell adhesion CD146 (S-Endo 1 Ag), “a member of the immunoglobulin superfamily” referred as MUC18, was lately reported as a new element located at the endothelial cell-to-cell junction [1]. The levels of sCD146 were assessed in chronic renal insufficiency, in hemodialysis patients with atherosclerosis and in those with inflammatory bowel disease [9,10,11]. Since sCD146 can provide evidence for endothelial activation and proliferation, we investigated its performance in estimating liver fibrosis and cirrhosis, its relationship with Model-for-End-Stage-Liver Disease (MELD) score and its utility in differentiating compensated from decompensated cirrhosis [29].
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