CASE #1: Cherry angioma

Cherry angiomas (also known as Campbell De Morgan spots, senile angiomas, and cherry hemangiomas) are red, blue, purple or black vascular papules or macules that blanch under pressure and may be surrounded by a pallid halo.

Cherry angiomas vary in size and contour, from a small, red macule that resemble petechiae to larger, dome-shaped papules and polypoid plaques (polypoid angiomas). Cherry angiomas, the most common vascular proliferation in the skin, are usually found on the trunk and limbs and less frequently on the face and scalp.6


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Age, pale skin, pregnancy, malignancy, and certain chemicals and medications are associated with the appearance of these lesions. Cherry angiomas are most common in whites and usually first appear in the third decade; most pale-skinned individuals have a few by their sixth decade. In women, cherry angiomas often develop during pregnancy and may involute during the postpartum period, which suggests that hormonal factors influence development.

The sudden appearance of such benign lesions as cherry angiomas can portend systemic disease. Sudden presentation of many angiomas may be a sign of internal malignancy. Chemicals and compounds that have been reported to cause cherry angiomas include mustard gas, 2-butoxyethanol, bromides, and cyclosporine.

Cutaneous angiomas can be skin findings in the POEMS (Polyneuropathy, Organomegaly, Endocrinopathies, M-protein, and Skin changes) syndrome. Familial nevus flammeus associated with early onset cherry angiomas has been noted.7

The histology of cherry angiomas is well defined. In small, early growths, one or more thin-walled vascular channels that are dilated and interconnected are present in the dermal papillae. More mature cherry angiomas demonstrate a loss of the rete ridges and gradual atrophy of the superficial epidermis. Polypoid cherry angiomas show networks of dilated communicating channels with scant intervening connective tissue.

Cherry angiomas can demonstrate a collarette at the periphery of the angioma. There can be an increase in the density of mast cells in cherry angiomas compared with normal skin. Ultrastructural studies show that cherry angiomas have reduplicated basement membranes and fenestrations of the endothelium. The non-replicating nature of the endothelial cells compromising cherry angiomas suggests that they are not true neoplasms.

The differential diagnosis includes: glomeruloid hemangioma, angiokeratoma circumscriptum, Kaposi’s sarcoma, angiokeratoma corporis diffusum (Fabry syndrome), angio­keratoma of the scrotum, bacillary angiomatosis, blue rubber bleb nevus syndrome, strawberry hemangioma, angiokeratoma of Mibelli, angiokeratoma of the vulva, petechiae, and pyogenic granulomas.

The molecular and genetic mechanisms of cherry angiomas have recently been defined. Researchers found that the level of microRNA-424 (miR-424) was substantially decreased in cherry angiomas vs. normal skin, resulting in increased protein expression of MEK1 and cyclin E1.8 Inhibiting miR-424 in normal endothelial cells led to a similar increased protein expression of MEK1 and cyclin E1, which induced proliferation of the endothelial cells, an action important for the development of cherry angiomas. Targeting MEK1 and cyclin E1 with small interfering RNA decreased the number of endothelial cells.

Cherry angiomas are a cosmetic problem, and treatment is not required. There are surgical treatments if desired for enhanced cosmesis, but no medical therapy exists. Surgical options include such purely destructive treatments as shave excision, electrodesiccation and curettage, intense pulsed light sources (i.e., nonablative high-intensity pulses of visible light to cause tissue remodeling) and cryotherapy, as well as such targeted treatments as lasers.

As vascular skin proliferations, cherry angiomas contain oxygenated hemoglobin, which strongly absorbs visible light at 418, 542, and 577 nm.9,10 Lasers used to treat cherry angiomas produce light around this spectrum. Hemoglobin exposed to light in this spectrum is vaporized, the vascular lumen obliterated, and the cherry angioma destroyed.

The three types of lasers that are effective in this regard are: (1) quasi-continuous wave (CW) lasers, which shutter the CW beam into short segments, producing interrupted emissions of constant laser energy; (2) pulsed lasers, which emit high-energy laser light in ultra-short pulse durations with relatively long time periods between each pulse; and (3) V-beam pulsed lasers, which provide ultra-long pulse durations. The lasers most commonly used include pulsed dye lasers, quasi-CW copper bromide lasers, quasi-CW Krypton lasers, quasi-CW potassium-titanyl-phosphate (KTP) lasers, and argon-pumped tunable dye lasers.

The pulsed dye laser is the optimal tool for destroying vascular lesions because it possesses superior clinical efficacy and a low risk profile. The laser’s large spot size (5 mm to 10 mm) allows bigger lesions to be treated quickly. Side effects include postoperative bruising that may last one to two weeks and transient pigmentary changes. Crusting, textural changes, and scarring rarely occur with use of a pulsed dye laser.

Quasi-CW lasers are effective but more commonly cause scarring. V-beam pulsed dye lasers furnish ultra-long pulse durations, so greater is energy directed at the target blood vessels over a longer period of time, resulting in more uniform blood-vessel damage than older pulsed dye lasers. The dynamic cooling found in newer pulsed dye lasers increases comfort during treatment, enabling higher fluencies (energy) to be delivered safely and effectively with fewer treatments.

Dr. Scheinfeld is assistant clinical professor of dermatology at Columbia University in New York City, where he has a private practice. The author has no relationships to disclose relating to the content of this article.


References

1. Mulliken JB. Update on vascular anomalies. In: Proceedings of the international workshop on vascular anomalies. Boston, Mass: June 21-24, 2008.

2. Tanner JL, Dechert MP, Frieden IJ. Growing up with a facial hemangioma: parent and child coping and adaptation. Pediatrics. 1998;101:446-452.

3. Suh KY, Frieden IJ. Infantile hemangiomas with minimal or arrested growth: a retrospective case series. Arch Dermatol. 2010;146:971-976.

4. Metry D, Heyer G, Hess C, et al. Consensus statement on diagnostic criteria for PHACE syndrome. Pediatrics. 2009;124:1447-1456.

5. Girard C, Bigorre M, Guillot B, Bessis D. PELVIS syndrome. Arch Dermatol. 2006;142:884-888.

6. Kim JH, Park HY, Ahn SK. Cherry angiomas on the scalp. Case Rep Dermatol. 2009;1:82-86. 

7. Gao XH, Wang LL, Zhang L, et al. Familial nevus flammeus associated with early-onset cherry angiomas. Int J Dermatol. 2008;47:1284-1286.

8. Nakashima T, Jinnin M, Etoh T, et al. Down-regulation of mir-424 contributes to the abnormal angiogenesis via MEK1 and cyclin E1 in senile hemangioma: its implications to therapy. PLoS One. 2010;5:e14334. 

9. Gupta G, Bilsland D. A prospective study of the impact of laser treatment on vascular lesions. Br J Dermatol. 2000;143:356-359.

10. Dawn G, Gupta G. Comparison of potassium titanyl phosphate vascular laser and hyfrecator in the treatment of vascular spiders and cherry angiomas. Clin Exp Dermatol. 2003;28:581-583.

All electronic documents accessed June 15, 2011.