Acute hyperleukocytic leukemia [AHL; WBC count >100 x 10(9)/l] is associated with a life-threatening complication. The mechanisms of hyperleukocytosis in acute myeloid leukaemia (AML) remain unclear. However, the interaction of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) plays an important role in the adhesion and migration of normal leukocytes and AML cells. Therefore, effects of ICAM-1 and LFA-1 were studied in hyperleukocytic AML. The adhesion of hyperleukocytic AML blasts and human umbilical vein endothelial cells (HUVECs) was significantly increased compared with that of blasts from non-hyperleukocytic AML (WBC < 100 x 10(9)/l). The adhesion of normal neutrophils and HUVECs treated with hyperleukocytic AML blast supernatant was increased significantly. Finally, we determined the ICAM-1 on the surface of HUVECs treated with the supernatant of hyperleukocytic AML blasts and LFA-1 on hyperleukocytic AML blasts by flow cytometry. It showed that the ICAM-1 expression on the surface of the HUVECs treated with hyperleukocytic AML blast supernatant for 24 h could be increased, and the expression of LFA-1 on hyperleukocytic AML was also increased significantly. Our data show that hyperleukocytic AML blasts stimulate the endothelium to secrete more ICAM-1 and promote their own adhesion to vascular endothelium, suggesting that ICAM-1 and LFA-1 may have a role in hyperleukocytic AML.