Background
Halo nevi are common benign skin lesions that represent melanocytic nevi in which an inflammatory infiltrate develops, resulting in a zone of depigmentation surrounding the nevus. Although Sutton originally described the lesion in 1916 as leukoderma acquisita centrifugum, the lesions were noted earlier, as evidenced by their depiction in the painting The Temptation of Saint Anthony by Matthias Gr ü nwald circa 1512-1516.[1]
Because melanoma that has undergone regression may appear gray or white, halo nevi have been erroneously confused with melanoma and have been the source of much anxiety among both clinicians and patients. Nevertheless, they are entirely benign lesions and of only cosmetic significance.
Pathophysiology
The etiology of halo nevi is unknown. Numerous studies have attempted to unravel the immunologic mechanisms by which an immune response develops to existing aggregates of nevus cells.[2] The infiltrating cells are predominantly T-lymphocytes, and cytotoxic (CD8) lymphocytes outnumber helper (CD4) lymphocytes by a ratio of approximately 4:1. These, as well as scattered macrophages, comprise most inflammatory cells in halo nevi.[3] As seen in vitiligo, melanocytes in the epidermis in the halo component of the nevus are completely absent, suggesting a similar etiologic mechanism.[4] The exact role that the lymphocytes play in the regression of halo nevi has not been fully determined, although a theory of direct cytotoxic effects on melanocytes seems plausible.
Of interest, circulating antibodies to the cytoplasm of melanoma cells have been detected in patients with halo nevi.[5] Because these antibodies have disappeared after removal of the halo nevus, they were thought to be related. Subsequent investigation failed to reveal a temporal relation between the appearance of these antibodies and the regression of nevus cells, and these antibodies are now believed to appear as a consequence of the release of cytoplasmic proteins of halo nevus melanocytes secondary to cell damage.
Ultrastructurally, advanced lesions of halo nevus show dermal macrophages containing portions of nevus cells. While it is clear that an immunologic mechanism results in the demise of melanocytes in halo nevi, the precipitating cause and the exact role of the lymphocytes remain unknown.[6]
Epidemiology
Frequency
United States
The incidence of halo nevi in the population is estimated to be 1%.[7] Patients with Turner syndrome have been reported to have an increased incidence of halo nevi.[8]
Mortality/Morbidity
Halo nevi are benign. Morbidity is minimal and limited to cosmetic appearance.
Race
All races are susceptible to the development of these lesions. A familial tendency for halo nevi has been reported.
Sex
No sexual predilection is reported.
Age
Halo nevi are found most commonly in children. The average age of onset is 15 years.
Happle R. [Grunewald nevus]. Hautarzt. Dec 1994;45(12):882-3. [Medline].
Zeff RA, Freitag A, Grin CM, Grant-Kels JM. The immune response in halo nevi. J Am Acad Dermatol. Oct 1997;37(4):620-4. [Medline].
Patrizi A, Neri I, Sabattini E, Rizzoli L, Misciali C. Unusual inflammatory and hyperkeratotic halo naevus in children. Br J Dermatol. Feb 2005;152(2):357-60. [Medline].
van Geel N, Vandenhaute S, Speeckaert R, et al. Prognostic value and clinical significance of halo naevi regarding vitiligo. Br J Dermatol. Apr 2011;164(4):743-9. [Medline].
Fishman HC. Letter: Malignant melanoma arising with two halo nevi. Arch Dermatol. Mar 1976;112(3):407-8. [Medline].
Jacobs JB, Edelstein LM, Snyder LM, Fortier N. Ultrastructural evidence for destruction in the halo nevus. Cancer Res. Feb 1975;35(2):352-7. [Medline].
Herd RM, Hunter JA. Familial halo naevi. Clin Exp Dermatol. Mar 1998;23(2):68-9. [Medline].
Brazzelli V, Larizza D, Martinetti M, et al. Halo nevus, rather than vitiligo, is a typical dermatologic finding of turner's syndrome: clinical, genetic, and immunogenetic study in 72 patients. J Am Acad Dermatol. Sep 2004;51(3):354-8. [Medline].
Zalaudek I, Moscarella E, Argenziano G. Artifactual "pseudo-halo nevi" secondary to sunscreen application. J Am Acad Dermatol. Jun 2006;54(6):1106-7. [Medline].
Berg P, Lindelof B. Differences in malignant melanoma between children and adolescents. A 35-year epidemiological study. Arch Dermatol. Mar 1997;133(3):295-7. [Medline].
| Halo Nevus | Melanoma |
| Nevus cells in nests | Single atypical melanocytes at all levels of the epidermis and aggregates of atypical melanocytes in the dermis |
| Lesion symmetrical | Lesion asymmetrical |
| Maturation of nevus cells | Lack of maturation |
| Mitotic figures rare or absent | Mitotic figures present |
| Lymphocytic infiltrate present diffusely throughout lesion | Lymphocytic infiltrate tends to be at be concentrated at periphery |
Print
