Practice Essentials
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. They are entirely benign lesions and of only cosmetic significance.
Because melanoma that has undergone regression may appear gray or white, halo nevi have been erroneously confused with melanoma and can be the source of much anxiety among both clinicians and patients. [1]
Pathophysiology
The etiology is unknown, but halo nevus is believed to be due to an immune response against melanocytes. 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]
A distinct relationship seems exist that distinguishes halo nevus in patients without vitiligo and halo nevus in patients with vitiligo, although definitive features have not been determined. Multiple halo nevi, the presence of Koebner phenomenon, and a family history of vitiligo have been identified as possibly increasing the risk of vitiligo in patients with halo nevi. [5]
Nevus excision may prevent progression to vitiligo vulgaris. In a study of 54 patients with excised halo nevus, the presence or absence of vitiligo vulgaris was associated with improvement in the surrounding vitiligo following excision. [6]
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. [7] 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. [8]
Cases of halo nevi developing following intermittent intense sun exposure have been reported suggesting ultraviolet exposure may have a role in the etiology. [9]
Epidemiology
Frequency
The incidence of halo nevi in the population is estimated to be 1%. [10] Patients with Turner syndrome have been reported to have an increased incidence of halo nevi. [11]
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. [12] The average age of onset is 15 years.
Prognosis
Halo nevi are benign. Morbidity is minimal and limited to cosmetic appearance. Because halo nevi are benign, the prognosis for patients is excellent. The course of halo nevi is normally uncomplicated. Problems arise in those instances where the lesions have been misdiagnosed or when the lesion is excised and wound complications develop postoperatively.
Patient Education
Patients should be instructed to monitor the lesion. If changes occur that suggest irregularity or if such symptoms as bleeding, itching, pain, or ulceration develop, the patient should be reevaluated promptly to exclude the possibility of cutaneous melanoma. For patient education resources, see the patient education article Mole Removal.
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Classic appearance of a halo nevus.
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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.
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At low magnification, a dome-shaped papular lesion reveals a dense infiltrate of lymphocytes in the dermis (hematoxylin and eosin, original magnification X40).
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Higher magnification reveals nests of nevus cells with numerous lymphocytes surrounding them and in the interstitium (hematoxylin and eosin, original magnification X40).
Tables
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 |
