Patients with alcoholic hepatitis (AH) have hepatic infiltration of leukocytes. There is upregulation of cell adhesion molecules (CAMs) on endothelial cell (EC) activation which has a significant role to play in leukocyte transendothelial migration. EC surface can shed CAMs, which accumulate in the blood, and act as soluble markers for EC activation.

The current study evaluated the effects of heavy drinking on expression of soluble forms of EC activation markers, such as CD146, ICAM-1, VCAM-1, and VEGF-A, and the impact of alcohol abstinence on the reversal of these abnormalities in heavy drinkers with and without AH.

Investigators estimated soluble EC activation markers in plasma from 79 AH patients, 66 heavy drinkers without overt liver disease (HDC), and 44 healthy controls (HC) at baseline; 31 AH patients and 30 HDCs at 6-month follow-up; and 18 AH patients and 25 HDCs at 12-month follow-up.

At baseline, the 4 soluble markers were found to be significantly upregulated in AH patients when compared with HDCs and HCs, while only sVCAM-1 was shown to be raised in HDCs compared to HC. At follow-ups, CD146, VCAM-1, and VEGF-A continued to be higher in AH patients, even among those who stopped drinking. The dysregulated markers had a correlation with AH disease severity, clinical parameters, and several soluble inflammatory factors.

It was concluded that the levels of soluble CD146, ICAM-1, VCAM-1, and VEGF-A were considerably raised in AH patients, and that stopping alcohol intake could not completely reverse these deviations.

Source: Xia Y, Yang J, Sanyal AJ, et al.Persistent Hyperactivation of Endothelial Cells in Patients with Alcoholic Hepatitis. Alcoholism Clinical and Experimental Research 2020;44(5):1075-87.