Hepatic Microvasculature in Liver Injury

Abstract

Injury to the hepatic microvasculature, the hepatic sinusoids, manifests in several ways. The sinusoidal endothelial cells (SECs) may lose porosity and scavenger function (capillarization); SECs may loosen from their tetherings to the space of Disse or even detach completely (ischemia-reperfusion injury, early sinusoidal obstruction syndrome, peliosis hepatis, early acetaminophen toxicity); the space of Disse may be completely denuded of sinusoidal lining cells that then embolize and obstruct the sinusoid (early sinusoidal obstruction syndrome); or the sinusoid may be obstructed by fibrosis (hepatic sinusoidal fibrosis, late sinusoidal obstruction syndrome). In many of these microvascular injuries, the change to the sinusoid is a primary event that may lead to hepatocyte hypoxia with liver dysfunction and disruption of the portal circulation. With the exception of hepatic fibrosis, which will be reviewed elsewhere in this issue, each of these types of microvascular injuries will be described in this article.

Gene Expression Profiling Provides Insights into Pathways of Oxaliplatin-Related Sinusoidal Obstruction Syndrome in Humans

“…This correlates directly with the histologic features of human SOS where a significant proportion of patients develop centrilobular perisinusoidal and vein occlusive fibrosis (1,2,4,15,40). In the animal model deposition of collagen in the sinusoids also occurs, albeit as late event (18), when activated, HSC acquire a myofibroblastic phenotype and are essential actors in hepatic fibrosis (41) as underlined by the diffuse perisinusoidal aSM actin expression (1).…”

“…SOS is morphologically characterized by centrilobular sinusoidal congestive dilatation and perisinusoidal hemorrhage, occasionally associated with perisinusoidal fibrosis and/or centrilobular hepatic vein fibrotic obstruction, nodular regenerative hyperplasia, or peliosis (15)(16)(17).…”

“…Sloughed SECs and Kupffer cells intermingled with erythrocytes subsequently embolize downstream within the sinusoidal lumen toward the centrilobular vein (19). Microcirculation plugging causes sinusoidal obstruction, a reduction of blood flow in the sinusoids, increasing portal pressure (20), leading to liver metabolic dysfunction, and affecting the viability of parenchymal cells through hypoxia (15)(16)(17). In humans, morphologic studies have confirmed that the sinusoids are the main site of injury.…”

Disruption of the transcription factor recombination signal‐binding protein‐Jκ (RBP‐J) leads to veno‐occlusive disease and interfered liver regeneration in mice†

“…10 Bone marrow transplantation, alcoholic liver insults, and other chemical offenses may result in sinusoidal obstructive syndrome (SOS) or veno-occlusive disease, which is characterized by congested LSs, fibrin deposition, subendothelial edema, and hepatocellular abnormalities. 11,12 Evidence has shown that damage of LSECs is an initial step leading to SOS.…”

Peliosis Hepatis Shows Isometabolism on 18F-FDG PET/CT: Two Case Reports

“…It is histologically characterized by blood-filled cystic spaces that are continuous with hepatic sinusoids [1,2]. Although the pathogenesis of PH is not well known, it is frequently associated with tuberculosis, malignancy (such as hepatocellular carcinoma), acquired immunodeficiency syndrome (AIDS), and drugs (including steroids and oral contraceptives) [3][4][5][6][7][8][9][10][11][12]. Given its benign nature, asymptomatic PH does not require treatment.…”