Halo Nevus

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 Grünwald 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.

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] 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. ^[6] 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. ^[7]

Frequency

The incidence of halo nevi in the population is estimated to be 1%. ^[8] Patients with Turner syndrome have been reported to have an increased incidence of halo nevi. ^[9]

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. ^[10] The average age of onset is 15 years.

Halo nevi are benign. Morbidity is minimal and limited to cosmetic appearance. Because halo nevi are benign, the prognosis for patients is excellent.

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.