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Print version ISSN 0365-0596On-line version ISSN 1806-4841
An. Bras. Dermatol. vol.79 no.1 Rio de Janeiro Jan./Feb. 2004
Cherry hemangioma in the scalp*
José Marcos Pereira
Ex-professor of Dermatology at the College of Medical Sciences, Santa Casa Charitable Hospital, São Paulo
Cherry hemangioma (CH) is an extremely frequent dermatosis with vascular origin involving more than 75% of the population over 70 years of age. Normally they are multiplex spots and focus predominantly on the upper trunk and arms. Clinically they are characterized by pinpoint maculae and papules with up to 5 millimeters in diameter. The most recent lesions can be a strong red color while the older ones are bluish. The etiology of CH is still unknown. From the histologic standpoint, the neoformation of the capillary tube draws attention: they are very dilated and with fenestration along the wall. The basement membranes are thickened and there is abundant collagen stroma between the veins. This work demonstrates the high frequency of CH in the scalp. In a sample of 171 patients (85 men and 86 women) the author noted that 123 (72%) had CH in the scalp. However, according to the literature, CH in the scalp has never been described.
Key-words: scalp; hemangioma.
Cherry hemangioma (CH) [known in the Portuguese language as hemangioma senil, angioma senil, angioma rubi, mancha de Morgan or Mancha de Campbell de Morgan] is also denominated cherry angioma, senile hemangioma, cherry or ruby spots, Campbell de Morgan's spots, Morgan's spots, senile angioma, petechial angioma or capillary angioma.
The disease was described for the first time in 1872 by Campbell de Morgan, surgeon at Middlesex Hospital (1842 to 1875), in England. In his textbook "On the origin of Cancer", he associated CH to the presence of neoplasias and in particular to cancer of the stomach.2
It is an extremely common dermatosis of vascular origin and it is rare for individuals not to present at least one CH. The lesion can be single or multiple, sometimes reaching hundreds dispersed throughout the body, but mainly in the upper trunk and arms.3
Clinically, the initial lesion can be similar to petechiae, being just a macular, flat, red and punctiform lesion. As they develop, they become brilliant-red papules with one to five millimeters in diameter (Figure 1). With time they assume a dark-blue coloration. The lesions are asymptomatic, benign4 and not compressible.5 The lesions bleed on suffering trauma and can form a black clot on the surface, mimicking a malignant melanoma. They grow slowly without involution.
The real incidence of CH is unknown, because few works have covered the subject. Keller6 in a series of 696 volunteers and 583 patients from a clinic in Germany found CH in 34.5% of those under 30 years of age, and in 40.15% of those over 31 years age; Murison et al.2 observed 1,300 patients at a hospital in Glasgow (UK) and found that 5% of the adolescents and 75% of the patients above 70 years had CH. There was no sex bias and CH increased in number and size with age, however the growth index decreased with time. Surprisingly, in a population of soldiers in the air force there was much less CH than in the patients of hospitals. The authors also observed that CH seems to be more frequent in patients with neoplasia than in those without neoplasia.
Although no study has yet clarified the etiopathogenesis of CH, several factors have been related to its onset, as described below.
In diabetics the lesions are more numerous and have a greater volume;7 furthermore, according to Jaimovich,8 they expand under high temperatures.
Epidemic outbreaks of CH have been described. These being patients that within a period of days refer to the emergence of several lesions. Seville et al.9 in 1968 observed that in the Lancaster Moor Hospital (UK) some 1,000 patients were attended with onset of several CH lesions in a few days. The patients presented clinical and histopathological signs of CH, but with no systemic alteration or symptom. Some patients referred to the emergence of the lesions after sun bathing. One patient followed-up for two months showed that the lesions appeared during the hottest days. Honish et al.10 reported an outbreak of CH among patients and workers of a rest clinic, in 1988 in Edmonton (USA). A total of 147 cases were observed in 302 people over a 10-day period. The patients' age varied from 33 to 100 years, and the number of lesions per patient from two to 78, with a mean of 30. The anatomicopathological exam was compatible with CH. The same authors described that in 1985, in Edmonton, three rest clinics and a hospital had an outbreak of CH and in 1987, a similar outbreak occurred at another rest clinic. Although this suggests the possibility of a contagious agent, exhaustive studies attempting to prove this were fruitless.
CH has also been associated with exposure to chemical products. Cohen et al.11 described two cases of CH after exposure to derivatives of bromine. Raymond et al.12 have reported that four months after seven people were exposed to steam of the solvent 2-butoxyethanol, six developed typical CH lesions in the arms, trunk and thighs. Firooz et al.13 observed 250 people that came into contact with mustard gas and after 18 months, approximately 10% presented onset of CH.
A greater frequency of CH was also observed after liver transplant;14 in graft-versus-host disease;15 after cyclosporin therapy;16 and following argon laser therapy for dermatosis.17
There is considerable controversy regarding the etiopathogenesis of CH. According to Jaimovich,8 it is a non-tumoral self-limiting hyperplasia that is not associated to neoangiogenesis with abnormally increased endothelial proliferation, and the angiogenic growth factors of which, such as TNF-a, FGF-b and VEGF, do not appear to be related to its onset. Hagiwara et al.,18 based on the principal that mastocytes are related to the angiogenesis, counted their number in CH. In normal tissue, the mean number of mastocytes was 6.85±4.9/mm2; while in the presence of CH this was 85.3±45.6/mm2. Tamm et al.19 in immunohistochemical studies demonstrated that the perivascular hyaline tissue observed in CH is composed of collagen IV and VI. The authors established the hypothesis that collagen type VI serves as a platform in the tissues with a high concentration of collagenolytic enzymes and that the increase of collagen type VI in CH is related to its formation. Eichhorn et al.20 observed that most of the blood vessels in CH are fenestrated and have a positive reaction to carbonic anhydrase, which is an enzyme. The authors cogitate the possibility that this enzyme is related to the maintenance of the fenestration. Tuder et al.,21 in immunohistochemical studies using Ki67 markers specific for G2 cells and phase S of the mitoses, concluded that CH is not a true neoplasia, but a composite of mature veins similar to dermal venulae.
The histopathology is very characteristic. In the initial phase CH has the appearance of a capillary hemangioma22 or angioblastoma6 - formed by numerous narrow capillary neoformations and prominent endothelial cells arranged in a lobular form and located exactly between the dermis and the epidermis. With time the capillaries become voluminous and are characteristic of the tubular or spherical dilations of the capillary loops in the papillary dermis.23,24,25 Each dilated vein is connected with one or more neighboring loops by tortuous vascular channels. The veins in the horizontal plexus are not involved.23,24,25 There is little vascular space, and the intercapillary stroma presents edema and homogenization of the collagen. The walls of the capillaries are sometimes hyalinized. Cavernous spaces can also be observed. Important findings are the fenestrated endothelium of the capillaries and the considerably thickened basement membrane.26
Electron microscopy reveals that CH is located immediately under the epidermis and is very different from adjacent tissues. The walls of all the veins are formed by a single layer of endothelial cells, that frequently present the so-called microtubular bodies in the cytoplasm.27 Within the veins one finds blood and fibrin, surrounded by agglomerates of fine collagen fibers. The most characteristic images of CH under electron microscopy are fenestration in the endothelium, that can be intercellular or transcellular,27 as well as a very thickened and multilaminated basal membrane.19,21,27 Furthermore, it is possible to observe villous projections into the lumen of the veins.28
Several observations should be made regarding the differential diagnosis. When CH is surrounded by purpuric halo, one should consider amyloidosis.29 In POEMS syndrome (polyneuropathy, organomegaly and skin changes), the hemangiomas are very similar to CH30. An important differential diagnosis to consider is the histiocytosis X, whose initial lesions are identical to those of CH31. As already mentioned, CH bleeds with trauma, such that the formation of a black clot can simulate malignant melanoma.
Most of the patients are not inconvenienced by CH, however some want to remove it for aesthetic purposes or even because of minor bleeding. Several techniques can be used, including curettage,32 laser33,34 and electrosurgery.35
Although the clinical and histopathological aspects of CH have been very well characterized since it first appeared in the medical literature, its presence in the scalp had not been described previously. The objective of the present work was to clarify the frequency of CH in the scalp.
From September to December 2000, 171 patients were observed at the Dermatological Center of Guarulhos, in the State of São Paulo. The first 85 men and the first 86 women were selected, so that there was uniformity in terms of gender. Each patient was examined while seated in a chair and illuminated by six dichroic lamps, such that the examiner had easy access to all areas of the scalp. The clinical exam was made with the naked eye and the use of a 20X biocular magnifying glass (Naturescope, Nikon).
The patients' age ranged from 18 to 75 years (mean, 40 years). They were all white, since CH is difficult to characterize in black skin. None of the patients examined sought medical attendance due to the CH.
It was observed that 123(72%) of the 171 patients had CH in the scalp, of which 62 were men and 61 women. CH was not present in 48 (28%) patients (23 men and 25 women). The size of the lesions varied from punctiform to five millimeters in diameter, and their number per patient ranged from one to 10, with a mean of five (Figures 2 and 3). There was a higher number of CH, in general over five lesions per patient, in the age group between 30 and 40 years and those with androgenic alopecia above level V, according to the classification of Hamilton/Norwood. All the patients with CH in the scalp also presented it in the trunk and 23 (19%) had facial involvement.
The CH lesions did not present any relationship to diseases of the scalp, such as seborrheic dermatitis, psoriasis and pseudopelade.
Although an extremely frequent dermatosis, there is little reference to CH in the classic textbooks of dermatology, while in books specifically about trichology, the disease is not mentioned at all. Although in widespread use, the expression hemangioma or senile angioma is not appropriate for this dermatosis, since it is found in five percent of adolescents2 and in 40.15% of the subjects examined aged up to 31 years,6 or that is, a very young population. Incidences have been described of up to 75% in people over 70 years of age.2 These values, however, could be much larger, mainly in the trunk and arms of those with clear skin and aged around 30 years, irrespective of their gender. Careful examination in a well illuminated local and with the use of a dermatoscope, could identify miniscule punctiform lesions of CH. The largest, already well formed and characteristic lesions are found in individuals with a more advanced age.
The etiology of CH is unknown, however epidemic outbreaks call attention9,10 as well as its appearance after exposure to chemical products.11,12,13 There is no plausible justification for its greater incidence in the upper trunk and arms. In his observations the author has noticed a great incidence of CH in the scalp, even though no textbook or work in all of the literature researched mentions its presence in this region. Keller6 in a series of 1279 individuals, found a high occurrence of CH in individuals over 30 years of age. A model was drawn, on which the location was marked of all the CH found - of the hundreds of points marked, only two were in the scalp, although no reference was made in the text to this fact. The present work has the purpose of showing that CH is very frequent in the scalp. Of 171 patients examined, 123 (72%) presented it in this location, an incidence high enough to justify this publication. The lesions observed were asymptomatic, with no sex bias and were more frequent and larger in patients over thirty years of age and in those with advanced androgenetic alopecia, in other words, beyond degree V of Hamilton/Norwood (Figure 4). This fact may be explained by the solar action on the scalp, as described, in the report of an increased incidence of CH after solar exposure.9 No patient sought consultation due to CH in the scalp; however, once informed of its presence many wanted to have it removed for aesthetic reasons or because the lesions bleed with ease.
CH is the most frequent dermatosis of vascular origin in the human being. Its incidence in the scalp is very high, involving men and women equally and it is more frequent in adults from 30 to 40 years of age. Advanced androgenetic alopecia seems to be related to a higher incidence of CH. Although most of the people are not aware of its presence in the scalp, many patients, once notified manifest interest in having it removed for aesthetic reasons, or because they can easily bleed following minimal traumatism.
1. Brannen M, Nixon RK, Doucette JW. Petechial angiomata. Arch Dermatol 1961; 83:386-390. [ Links ]
2. Murison AR, Sutherland JW, Williamson AM. De Morgan spots. Brit M J 1947; 1:634-636. [ Links ]
3. Odom RB, James WD, Beger TG. Dermal and subcutaneous tumors. In; Andrews. Disease of the skin. Saunders Company, USA. 2000 pp: 733-799. [ Links ]
4. Johnson WC. Tumores Vasculares. In: Bondi EE, Jegsothy BV, Lazarus GS. Dermatologia, Diagnóstico e tratamento. Ed. Artes Médicas, Brasil; 1993; pp.214-226. [ Links ]
5. Reed RJ, O'Quinn SE. Vascular neoplasms. In: Fitzpatrick TB, Arndt KA, Clark WH, Eisen AZ, Van Scott EJ, Vaughan JH. Dermatology in general medicine.McCraw-Hill Inc. USA, 1971; pp: 533-556. [ Links ]
6. Keller VR. Zur klinik und histologie der senilen angiome. Dermatologica 1957; 114:345-359. [ Links ]
7. Shah K, Shah AC, Shah PC. Campbell de Morgan's spots in diabetes mellitus. Brit J Dermat 1966; 78:493-494. [ Links ]
8. Jaimovich L. Por qué se multiplican los "pontos rubí" con la edad ? Act Terap Dermatol 1999; 22:233-240. [ Links ]
9. Seville RH, Rao PS, Hutchinson DN, Birchal G. Outbreak of Campbell de Morgan Spots. Brit Med J 1970; 1:408-409. [ Links ]
10. Honish A, Grimsrud K, Miedzinski L, Gold E, Cherry RR. Outbreak of Campbell de Morgan spots in a nursing home Alberta. Can Dis Wkly Rep 1988; 14:211-212. [ Links ]
11. Cohen AD, Cagnano E, Vardy DA. Cherry angiomas associated with exposure to bromides. Dermatology 2001; 202:52-53. [ Links ]
12. Raymond LW, Williford LS, Burke WA. Eruptive cherry angiomas and irritant symptoms after one acute exposure to the glycol ether solvente 2-butoxyethanol. J Occup Environ Med 1998; 12:1059-1064. [ Links ]
13. Firooz A, Komeili A, Dowlati Y. Eruptive melanocytic and cherry angiomas secondary to exposure to sulfur mustard gas. J Am Acad Dermatol 1999; 40:646-647. [ Links ]
14. Chu P, Le Boit PE. An eruptive vascular proliferation resembling acquired tufted angioma in the recipient of a liver transplant. J Am Acad Dermatol 1992; 26:322-325. [ Links ]
15. Garnis S, Billick RC, Srolovitz H. Eruptive vascular tumors associated with chronic graft-versus-host disease. J Am Acad Dermatol 1984; 10:918-921. [ Links ]
16. De Felipe I, Redondo P. Eruptive angiomas after treatment with cyclosporine in a patient with psoriasis. Arch Dermatol 1998; 134:1487-1488. [ Links ]
17. Wollina U, Zielinski M, Knopf B, Hipler C. Eruptives kapilläres hämangiom nach argon-laser-therapie eines naevus flammeus. Hautarzt 1989; 40:212-214. [ Links ]
18. Hagiwara K, Khaskhely NM, Uezato H, Nonaka S. Mast cell "densities" in vascular proliferations: A preliminary study of pyogenic granuloma, portwine stain, cavernous hemangioma, cherry angioma, Kaposi's sarcoma, and malignant hemangioendothelioma. J Dermatol 1999; 26:577-586. [ Links ]
19. Tamm E, Jungkunz W, Marsch WC, Lutjen-Drecoll E. Increase in types IV and VI collagen in cherry haemangiomas. Arch Dermatol Res 1992; 284:275-282. [ Links ]
20. Eichhorn M, Jungkunz W, Worl J, Marsch WC. Carbonic anhydrase is abundant in fenestrated capillaries of cherry hemangioma. Acta Derm Venereol(Stockh) 1994; 74:51-53. [ Links ]
21. Tuder RM, Young R, Karasek M, Bensch K. Adult cutaneous hemangiomas are composed of nonreplicating endotelial cell. J Investg Dermatol 1987; 89:594-597. [ Links ]
22. Lever WF, Lever GS - Tumors of vascular tissue. In: Lever WF, Lever GS. Histopathology of the skin. JB Lippincott USA 1975 pp: 591- 617. [ Links ]
23. Braverman IM. Cutaneous microvasculature. In. Freedberg IM, Eisen AZ, Wolf K, Austen KF, Goldsmith LA, Katz SI, Fitzpatrick TB. Dermatology in general medicine. McGraw-Hill USA, fifth edition, USA 1999; pp: 299-305. [ Links ]
24. Braverman MS, Braverman IM. Three-dimensional reconstructions of objects from serial sections using a microcomputer graphics system. J Invest Dermatol 1986; 86:290-294. [ Links ]
25. Braverman IM, Keh-Yen A. Ultrastructure and three-dimensional reconstruction of serveral macular and papular telangiectases. J Invest Dermatol 1983;81:489-497. [ Links ]
26. Calonje E, Wilson-Jones E. Vascular Tumors. In; Lever's Histopathology of the skin. Lippincott-Raven USA. 1997. pp: 889-953. [ Links ]
27. Stehbens WE, Ludatscher RM. Fine structure of senile angiomas of human skin. Angiology 1968; 19:581-592. [ Links ]
28. Sala E, Crosti C, Menni S, Piccino R. Cherry hemangioma: na SEM study. J Cutan Path 1984; 11:531-533. [ Links ]
29. Schmidt CP. Purpuric halos around hemangiomas in systemic amyloidosis. Cutis 1991; 48:141-143. [ Links ]
30. Kanitakis J, Roger H, Soubrier M, Dubost JJ, Chouvet B, Souteyrand P. Cutaneous angiomas in POEMS syndrome.Arch Dermatol 1988; 124:695-698. [ Links ]
31. Messenger GG, Kamei R, Honig PJ. Histiocytosis X resembling cherry angiomas. Ped Dermatol 1985; 3:75-78. [ Links ]
32. Aversa AJ, Miller III OF. Cryo-curettage of cherry angiomas. J Dermatol Surg Oncol 1983; 9:930-931. [ Links ]
33. Landthaler M, Haina D, Waidelich W, Braun-Falco O. A three-year experience with the Argon LASER in dermatotherapy. J Dermatol Surg Oncol 1984; 10:456-461. [ Links ]
34. Aghassi D, Anderson RR, Gonzalez S. Time-sequence histologic imaging of laser-treated cherry angiomas with in vivo concofocal microscopy. J Am Acad Dermatol 2000; 43:37-41. [ Links ]
35. Spiller FS, Spiller RF. Cryoanesthesia and electrosurgical treatment of benign skin tumors. Cutis 1985; 35:551-552. [ Links ]
José Marcos Pereira
Rua Sílvio Rodini, 611 apto 101
São Paulo SP 02241-000
Tel.: (11) 6452-8727
in August, 17th of 2001
Approved by the Consultive Council and accepted for publication in June, 10th of 2002
* Work done at private clinic of the author