(in Wingard et al). Photomicrographs illustrating the evolution of histological abnormalities of sinusoidal obstructive syndrome (SOS).

A and B. Fatal SOS 23 days post-autograft (H&E). A, showing hemorrhage in zone 3 with sparing of zone 1 (PV, portal vein); B, high power section showing early changes of concentric venular luminal narrowing by a widened subendothelial zone (double arrow) containing entrapped red cells. The surrounding changes include necrotic hepatocytes, disrupted sinusoids, and hemorrhage into the space of Disse.

C. Severe SOS 21 days post-allograft (Gomori trichrome). Hepatocyte dropout, sinusoidal congestion, and embolization of a cluster of hepatocytes (arrow) into a partially collagenized venule.

D. Immunostained liver section of early SOS with anti-factor VIII/vWF, showing intense perivenular and adventitial staining, loss of the hepatocyte staining in zone 3, and preservation of portal and zone 1 anatomy.

E. Fatal SOS 31 days post-allograft (Mallory trichrome). A small sublobular venule nearly occluded by loose extracellular matrix and red cells within the widened subendotheial zone (double arrows). Extensive necrosis has obliterated the liver cords which are replaced by fine curvilinear strands of connective tissue admixed with red cells.

F and G. Fatal SOS 37 days after gemtuzamub ozogamicin infusion for relapsed AML post-transplant. F illustrates extensive zone 3 sinusoidal fibrosis adjacent to a non-occluded sublobular venule (Mallory trichrome). G is an immunostain of the same specimen with anti-alpha smooth muscle actin showing proliferation of activated hepatic stellate cells lining perivenular sinusoids.

H. Fatal SOS 67 days post-allograft (Mallory trichrome), showing a pattern of “reverse” cirrhosis with confluent bridging between collapsed, fibrotic perivenular zones containing venules occluded by fibrous matrix.