Ultrastructural study of the vascular endothelium of patients with spontaneous rupture of hepatocellular carcinoma

Abstract

Background: Spontaneous rupture of hepatocellular carcinoma (HCC) is common in Asia and Africa, although the mechanism is unclear. In our previous study, we found that vascular injury exemplified by collagenase synthesis and collagen degradation in small arteries was related to the HCC rupture.

Methods: In this study, transmission electron microscopy was used to study 22 specimens from ruptured HCC and non-ruptured HCC.

Results: In nine specimens of ruptured HCC, there was evidence of vascular injury with fewer cell junctions and larger fenestrae in vascular endothelial cells. The phenomenon of increased endothelial protein synthesis was also present. In the specimens of non-ruptured HCC, evidence of vascular injury was found in only two cases (p < 0.01). Fewer cell junctions and larger fenestrae could increase the permeability of the vascular wall. Increased protein synthesis in endothelial cells correlates with the phenomenon that more collagenase is expressed in these cells. The resulting breakdown of collagen could render the blood vessels weak; hence, these blood vessels are more prone to splitting/breakage.

Conclusion: We conclude from our study that this vascular injury may result in HCC rupture.