Our previous study suggested CD36 may be a positive regulator of hepatitis B virus (HBV) replication
A total of 282 subjects were divided into healthy controls (HC,
There was a step-wise increase of sCD36 with the progression of chronic HBV infection, and it was the highest in the HBV- LC group with liver failure (1.50, IQR:1.04–2.00) as compared with HC (0.38, IQR:0.27–0.38), CHB (0.75, IQR:0.40–1.13), and HBV-LC without liver failure (1.02, IQR,0.61–1.35) group. Circulating sCD36 was not correlated with serum HBV DNA levels, but correlated with liver function parameters. Additionally, ROC analysis confirmed sCD36 could be used to predict liver failure for HBV-LC patients, which yielded an AUC of 0.775 with 71.0% sensitivity and 72.2% specificity. Multivariate logistic regression analysis revealed sCD36 is an independent risk factor in predicting liver failure. Moreover, plasma sCD36 in HBV-LC patients was significantly correlated with prognostic indices, including MELD, MELD-Na and CHILD-PUGH scores. On the other hand, CD36 expression on monocytes or platelets was positively correlated with plasma sCD36 levels, whereas they were not strongly associated with the disease severity.
Circulating sCD36 could be used as a novel noninvasive biomarker for predicting liver failure and prognosis in chronic HBV infected patients.