Cherry hemangioma

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Cherry angioma
A cherry angioma
Classification and external resources
Specialty cardiology
ICD-9-CM 448.1
DiseasesDB 30744
MedlinePlus 001441
eMedicine derm/73

Cherry angiomas, also known as Campbell De Morgan spots or senile angiomas,[1] are cherry red[2] papules on the skin containing an abnormal proliferation of blood vessels. They are the most common kind of angioma. They are called Campbell de Morgan spots after the nineteenth-century British surgeon Campbell De Morgan, who first noted and described them.

The frequency of cherry angiomas increases with age.

Signs and symptoms[edit]

Cherry hemangioma, H&E stain

Cherry angiomas are made up of clusters of capillaries at the surface of the skin, forming a small round dome ("papule")[citation needed], which may be flat topped[citation needed]. They range in colour from bright red to purple. When they first develop, they may be only a tenth of a millimeter in diameter and almost flat, appearing as small red dots. However, they then usually grow to about one or two millimeters across, and sometimes to a centimeter or more in diameter[citation needed]. As they grow larger, they tend to expand in thickness, and may take on the raised and rounded shape of a dome. Multiple adjoining angiomas are said to form a polypoid angioma. Because the blood vessels comprising an angioma are so close to the skin's surface, cherry angiomas may bleed profusely if they are injured.[citation needed]

One study found that the majority of capillaries in cherry hemangiomas are fenestrated because of staining for carbonic anhydrase activity.[3]


Cherry angiomas appear spontaneously in many people in middle age but can also, less commonly, occur in young people. They can also occur in an aggressive eruptive manner in any age. The underlying cause for the development of cherry angiomas is not understood.

Findings suggest that cherry angioma may occur through two different mechanisms: angiogenesis (the formation of new blood vessels from pre-existing vessels), and vasculogenesis (the formation of totally new vessels, which usually occurs during embryonic and fetal development).[4]

The first study trying to bring light to the molecular and genetic mechanisms behind cherry/senile hemangioma was published in 2010.[5] The study found that the level of microRNA 424 is significantly reduced in senile hemangiomas compared to normal skin resulting in increased protein expression of MEK1 and cyclin E1. By inhibiting mir-424 in normal endothelial cells they could observe the same increased protein expression of MEK1 and cyclin E1 which, important for the development of senile hemangioma, induced cell proliferation of the endothelial cells. They also found that targeting MEK1 and cyclin E1 with small interfering RNA decreased the number of endothelial cells.

Chemicals and compounds that have been seen to cause cherry angiomas are mustard gas,[6][7][8][9] 2-butoxyethanol,[10] bromides,[11] and cyclosporine.[12]

A significant increase in the density of mast cells has been seen in cherry hemangiomas compared with normal skin.[13]



These lesions generally do not require treatment. If they are cosmetically unappealing or are subject to bleeding angiomas may be removed by electrocautery, a process of destroying the tissue by use of a small probe with an electric current running through it.[14] Removal may cause scarring. More recently pulsed dye laser or intense pulsed light (IPL) treatment has also been used.[15][16]

Future treatment based on a locally acting inhibitor of MEK1 and Cyclin E1 could possibly be an option. A natural MEK1 inhibitor is myricetin[17][18]


In most patients, the number and size of cherry angiomas increases with advancing age. They are harmless, having no relation to cancer at all.[19]


Cherry angiomas occur in all races, ethnic backgrounds, and sexes.


  1. ^ James, William; Berger, Timothy; Elston, Dirk (2006). Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Philadelphia: Saunders. p. 595. ISBN 978-0-7216-2921-6. OCLC 62736861. 
  2. ^ "cherry angioma" at Dorland's Medical Dictionary
  3. ^ Eichhorn, M; Jungkunz, W; Wörl, J; Marsch, WC (1994). "Carbonic anhydrase is abundant in fenestrated capillaries of cherry hemangioma". Acta dermato-venereologica. 74 (1): 51–3. PMID 7908484. 
  4. ^ Kishimoto,, Saburo; Hideya Takenaka; Hideya Takenaka; Hideya Takenaka; Hirokazu Yasuno (2000). "Glomeruloid hemangioma in POEMS syndrome shows two different immunophenotypic endothelial cells". Cutaneous Pathology. 
  5. ^ Nakashima, T; Jinnin, M; Etoh, T; Fukushima, S; Masuguchi, S; Maruo, K; Inoue, Y; Ishihara, T; Ihn, H (2010). Egles, Christophe, ed. "Down-regulation of mir-424 contributes to the abnormal angiogenesis via MEK1 and cyclin E1 in senile hemangioma: its implications to therapy". PLoS ONE. 5 (12): e14334. doi:10.1371/journal.pone.0014334. PMC 3001869Freely accessible. PMID 21179471. 
  6. ^ Firooz, Alireza; Komeili, Ali; Dowlati, Yahya (1999). "Eruptive melanocytic nevi and cherry angiomas secondary to exposureto sulfur mustard gas". Journal of the American Academy of Dermatology. 40 (4): 646–7. doi:10.1016/S0190-9622(99)70460-3. PMID 10188695. 
  7. ^ Hefazi, Mehrdad; Maleki, Masoud; Mahmoudi, Mahmoud; Tabatabaee, Abbas; Balali-Mood, Mahdi (2006). "Delayed complications of sulfur mustard poisoning in the skin and the immune system of Iranian veterans 16–20 years after exposure". International Journal of Dermatology. 45 (9): 1025–31. doi:10.1111/j.1365-4632.2006.03020.x. PMID 16961503. 
  8. ^ Ma, Hui-Jun; Zhao, Guang; Shi, Fei; Wang, Yi-Xia (2006). "Eruptive cherry angiomas associated with vitiligo: Provoked by topical nitrogen mustard?". The Journal of Dermatology. 33 (12): 877–9. doi:10.1111/j.1346-8138.2006.00200.x. PMID 17169094. 
  9. ^ Emadi, Seyed Naser; Hosseini-Khalili, Alireza; Soroush, Mohammad Reza; Davoodi, Seyed Masoud; Aghamiri, Seyed Samad (2008). "Mustard gas scarring with specific pigmentary, trophic and vascular characteristics (case report, 16-year post-exposure)". Ecotoxicology and Environmental Safety. 69 (3): 574–6. doi:10.1016/j.ecoenv.2007.01.003. PMID 17382390. 
  10. ^ Raymond, Lawrence W.; Williford, Linda S.; Burke, William A. (1998). "Eruptive Cherry Angiomas and Irritant Symptoms After One Acute Exposure to the Glycol Ether Solvent 2-Butoxyethanol". Journal of Occupational & Environmental Medicine: 1059–64. doi:10.1097/00043764-199812000-00005. 
  11. ^ Cohen, Arnon D.; Cagnano, Emanuela; Vardy, Daniel A. (2001). "Cherry Angiomas Associated with Exposure to Bromides". Dermatology. 202 (1): 52–3. doi:10.1159/000051587. PMID 11244231. 
  12. ^ De Felipe, I.; Redondo, P (1998). "Eruptive Angiomas After Treatment With Cyclosporine in a Patient With Psoriasis". Archives of Dermatology. 134 (11): 1487–8. doi:10.1001/archderm.134.11.1487. PMID 9828895. 
  13. ^ Hagiwara, K; Khaskhely, NM; Uezato, H; Nonaka, S (1999). "Mast cell "densities" in vascular proliferations: a preliminary study of pyogenic granuloma, portwine stain, cavernous hemangioma, cherry angioma, Kaposi's sarcoma, and malignant hemangioendothelioma". The Journal of dermatology. 26 (9): 577–86. PMID 10535252. 
  14. ^ Aversa, AJ; Miller Of, 3rd (1983). "Cryo-curettage of cherry angiomas". The Journal of dermatologic surgery and oncology. 9 (11): 930–1. doi:10.1111/j.1524-4725.1983.tb01042.x. PMID 6630708. 
  15. ^ Dawn, G.; Gupta, G. (2003). "Comparison of potassium titanyl phosphate vascular laser and hyfrecator in the treatment of vascular spiders and cherry angiomas". Clinical and Experimental Dermatology. 28 (6): 581–3. doi:10.1046/j.1365-2230.2003.01352.x. PMID 14616818. 
  16. ^ Fodor, Lucian; Ramon, Ytzhack; Fodor, Adriana; Carmi, Nurit; Peled, Isaac J.; Ullmann, Yehuda (2006). "A Side-by-Side Prospective Study of Intense Pulsed Light and Nd:YAG Laser Treatment for Vascular Lesions". Annals of Plastic Surgery. 56 (2): 164–70. doi:10.1097/ PMID 16432325. 
  17. ^ Lee, KW; Kang, NJ; Rogozin, EA; Kim, HG; Cho, YY; Bode, AM; Lee, HJ; Surh, YJ; et al. (2007). "Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1". Carcinogenesis. 28 (9): 1918–27. doi:10.1093/carcin/bgm110. PMID 17693661. 
  18. ^ Kim, JE; Kwon, JY; Lee, DE; Kang, NJ; Heo, YS; Lee, KW; Lee, HJ (2009). "MKK4 is a novel target for the inhibition of tumor necrosis factor-alpha-induced vascular endothelial growth factor expression by myricetin". Biochemical pharmacology. 77 (3): 412–21. doi:10.1016/j.bcp.2008.10.027. PMID 19026990. 
  19. ^

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