Cherry hemangioma

Cherry hemangioma
Cherry angioma
Classification and external resources

A cherry angioma.
ICD-9 448.1
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.



Cherry angiomas are made up of clusters of capillaries at the surface of the skin, forming a small round dome ("papule"), which may be flat topped. 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. 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.


Cherry angiomas appear spontaneously in many people in middle age but can also, although less common, 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, much because of a lack of interest in the subject. This is probably because they rarely are caused by an internal malignancy.

The first study trying to bring light to the molecular and genetic mechanisms behind cherry/senile hemangioma was recently published.[3] 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,[4][5][6][7] 2-butoxyethanol,[8] bromides[9] and cyclosporine.[10] A correlation has been seen between cherry hemangiomas and activity of the enzyme carbonic anhydrase[11] as well as a significant increase in the density of mast cells in cherry hemangiomas compared with normal skin.[12]

A recent study[13] suggests that Prichard's structures are the cardiac equivalent of cutaneous senile angioma. The study describes Prichard's structures in the heart as "adult, fully differentiated, postmitotic-type endothelial cells with virtually no turnover." and that these cells are senescent cells that "arrest growth and cannot be stimulated to re-enter the cell cycle by physiological mitogens; they become resistant to apoptotic cell death; and they acquire altered functions.". The study concludes that Prichard's structures are formed by "infolding of the endothelial lining of the endocardium of the fossa ovalis as an irritational response to altered blood flow, eddies or turbulence."


On the rare occasions that they require removal, traditionally cryosurgery or electrosurgery have been used.[14] 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, except in very rare cases that involve a sudden appearance of many angiomas, which can be a sign of a developing internal malignancy.


Cherry angiomas occur in all races, ethnic backgrounds, and both 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. ^ Nakashima, T; Jinnin, M; Etoh, T; Fukushima, S; Masuguchi, S; Maruo, K; Inoue, Y; Ishihara, T et al. (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 3001869. PMID 21179471. 
  4. ^ 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. 
  5. ^ 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. 
  6. ^ 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. 
  7. ^ 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 charactristics (case report, 16-year post-exposure)". Ecotoxicology and Environmental Safety 69 (3): 574–6. doi:10.1016/j.ecoenv.2007.01.003. PMID 17382390. 
  8. ^ 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. 
  9. ^ 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. 
  10. ^ 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. 
  11. ^ 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. 
  12. ^ 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. 
  13. ^ Val-Bernal, J. Fernando; Martino, MARÍA; Mayorga, Marta; Garijo, M. Francisca (2007). "Prichard's structures of the fossa ovalis are age-related phenomena composed of nonreplicating endothelial cells: the cardiac equivalent of cutaneous senile angioma". APMIS 115 (11): 1234–40. doi:10.1111/j.1600-0643.2007.00756.x. PMID 18092955. 
  14. ^ Aversa, AJ; Miller Of, 3rd (1983). "Cryo-curettage of cherry angiomas". The Journal of dermatologic surgery and oncology 9 (11): 930–1. 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. 

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