Hemangioma pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
==Pathogenesis== | ==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:<ref name="PapafragkakisMoehlen2011">{{cite journal|last1=Papafragkakis|first1=Haris|last2=Moehlen|first2=Martin|last3=Garcia-Buitrago|first3=Monica T.|last4=Madrazo|first4=Beatrice|last5=Island|first5=Eddie|last6=Martin|first6=Paul|title=A Case of a Ruptured Sclerosing Liver Hemangioma|journal=International Journal of Hepatology|volume=2011|year=2011|pages=1–5|issn=2090-3456|doi=10.4061/2011/942360}}</ref> | |||
:*[[Vascular endothelial growth factor]] | |||
:*[[Basic fibroblast growth factor]] | |||
:*[[Metalloproteinases|Matrix metalloproteinases]] | |||
*And there is downregulation of some inhibitors of angiogenesis such as:<ref name="PapafragkakisMoehlen2011">{{cite journal|last1=Papafragkakis|first1=Haris|last2=Moehlen|first2=Martin|last3=Garcia-Buitrago|first3=Monica T.|last4=Madrazo|first4=Beatrice|last5=Island|first5=Eddie|last6=Martin|first6=Paul|title=A Case of a Ruptured Sclerosing Liver Hemangioma|journal=International Journal of Hepatology|volume=2011|year=2011|pages=1–5|issn=2090-3456|doi=10.4061/2011/942360}}</ref> | |||
:*[[Metalloproteinase|Tissue inhibitor of metalloproteinase-I]] | |||
===Second theory=== | |||
*The second theory is that the presence of liver hemangiomas involves a genetic background of mutations.<ref name="PapafragkakisMoehlen2011">{{cite journal|last1=Papafragkakis|first1=Haris|last2=Moehlen|first2=Martin|last3=Garcia-Buitrago|first3=Monica T.|last4=Madrazo|first4=Beatrice|last5=Island|first5=Eddie|last6=Martin|first6=Paul|title=A Case of a Ruptured Sclerosing Liver Hemangioma|journal=International Journal of Hepatology|volume=2011|year=2011|pages=1–5|issn=2090-3456|doi=10.4061/2011/942360}}</ref> | |||
*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.<ref name="RichterFriedman2012">{{cite journal|last1=Richter|first1=Gresham T.|last2=Friedman|first2=Adva B.|title=Hemangiomas and Vascular Malformations: Current Theory and Management|journal=International Journal of Pediatrics|volume=2012|year=2012|pages=1–10|issn=1687-9740|doi=10.1155/2012/645678}}</ref> | |||
*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:<ref name="RichterFriedman2012">{{cite journal|last1=Richter|first1=Gresham T.|last2=Friedman|first2=Adva B.|title=Hemangiomas and Vascular Malformations: Current Theory and Management|journal=International Journal of Pediatrics|volume=2012|year=2012|pages=1–10|issn=1687-9740|doi=10.1155/2012/645678}}</ref> | |||
:*Chorionic villus sampling | |||
:*Placenta previa | |||
:*Preeclampsia | |||
==Genetics== | ==Genetics== | ||
==Associated Conditions== | ==Associated Conditions== | ||
| Line 10: | Line 35: | ||
*POEMS syndrome | *POEMS syndrome | ||
*Castleman disease | *Castleman disease | ||
==Gross Pathology== | ==Gross Pathology== | ||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
Revision as of 16:14, 12 November 2015
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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]
Overview
Pathophysiology
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:[1]
- And there is downregulation of some inhibitors of angiogenesis such as:[1]
Second theory
- The second theory is that the presence of liver hemangiomas involves a genetic background of mutations.[1]
- 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.[2]
- 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:[2]
- Chorionic villus sampling
- Placenta previa
- Preeclampsia
Genetics
Associated Conditions
Hemangioma may be associated with:
- POEMS syndrome
- Castleman disease
Gross Pathology
Microscopic Pathology
Gallery
References
- ↑ 1.0 1.1 1.2 Papafragkakis, Haris; Moehlen, Martin; Garcia-Buitrago, Monica T.; Madrazo, Beatrice; Island, Eddie; Martin, Paul (2011). "A Case of a Ruptured Sclerosing Liver Hemangioma". International Journal of Hepatology. 2011: 1–5. doi:10.4061/2011/942360. ISSN 2090-3456.
- ↑ 2.0 2.1 Richter, Gresham T.; Friedman, Adva B. (2012). "Hemangiomas and Vascular Malformations: Current Theory and Management". International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.