Introduction
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. 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.4 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.5
Frequency
United States
The incidence of halo nevi in the population is estimated to be 1%.6 Patients with Turner syndrome have been reported to have an increased incidence of halo nevi.7
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.
Clinical
History
Patients with halo nevi are usually asymptomatic. The central nevus may or may not involute with time. Repigmentation often takes place over months or years; however, it does not always occur. Occasionally, inflammation occurs with crusting in the depigmented zone of a halo nevus. Most commonly, the chief complaint is that of a changing mole (or moles).
Physical
Halo nevi are usually single but may be multiple. They can develop anywhere on the body but are seen most frequently on the trunk. Clinically, they appear as one or more uniformly colored, evenly shaped, round or oval nevi centrally with even peripheral margins of hypopigmentation. The central nevus may be tan, pink, or brown. The width of the halo is variable but is generally of uniform radial distance from the central nevus.
Classic appearance of a halo nevus.
Note the central pink papule (intradermal nevus) and the surrounding halo. The halo is of uniform width at all points, and no inflammatory component can be seen. Note the normal nevus directly inferior.
Causes
The cause is unknown, but halo nevus is believed to be due to an immune response against melanocytes.
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References
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].
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].
Further Reading
Keywords
halo nevus, nevus of Sutton, halo nevi, Sutton nevus, Sutton nevi, melanoma, malignant melanoma
