Figure 2

Sinusoidal obstruction syndrome pathogenesis. (a) Normal hepatic sinusoid; (b) sinusoidal endothelial cells damaged during conditioning round up favoring the appearance of gaps in the sinusoidal barrier; (c) RBCs, leucocytes and cellular debris penetrate into the space of Disse detaching the endothelial lining; (d) the sloughed sinusoidal lining cells embolize downstream and obstruct the sinusoidal flow (sinusoidal obstruction syndrome). Adapted from 'The role of the endothelium in the short-term complications of hematopoietic SCT' by E Carreras and M Diaz-Ricart.2