Hemangioma pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Pathogenesis

The pathogenesis of hepatic hemangiomas has not been elucidated, but there are two competing theories.

First theory

• The first theory supports the notion that there is overexpression of angiogenic factors such as:

• Vascular endothelial growth factor
• Basic fibroblast growth factor
• Matrix metalloproteinases

• And there is downregulation of some inhibitors of angiogenesis such as:

• Tissue inhibitor of metalloproteinase-I

Second theory

• The second theory is that the presence of liver hemangiomas involves a genetic background of mutations.
• Genetic errors in growth factor receptors have also been shown to affect development of hemangiomas.
• Zhang et al. presumed that metalloproteinases accumulate in the endoplasmic reticulum of the tumor cells causing:

• Self-digestion
• Vacuole formation

• Additionally, Hu et al. showed the cavernous hemangioma cell to downregulate Derlin-1.

• Derlin-1 is a protein that when overexpressed induces the dilated endoplasmic reticulum to return to its normal size.

Third theory

• The third theory suggests that hemangioma endothelial cells arise from disrupted placental tissue imbedded in fetal soft tissues during gestation or birth.

• Markers of hemangiomas have been shown to coincide with those found in placental tissue.
• This is further supported by the fact that they are found more commonly in infants following:

• Chorionic villus sampling
• Placenta previa
• Preeclampsia

Associated Conditions

Hemangioma may be associated with:

• POEMS syndrome
• Castleman disease