A healthy adolescent boy is dragged by his concerned mother to your office for evaluation of several moles with surrounding white rings (figure1) . She noticed the asymptomatic lesions on her son’s back several days ago following a trip to the beach. What's the diagnosis?
Diagnosis and Clinical Presentation
Diagnosis: Halo nevi Halo nevi were recognized as early as the 16th century, as illustrated by Mattias Grunewald’s painting The Temptation of Saint Anthony. The nevi were first medically described in 1916 by Richard Lightburn Sutton who labeled the phenomenon leukoderma acquisita centrifugum. Since then the names Sutton nevi and perinevoid vitiligo have been synonymously applied. In recent decades halo nevi have been studied extensively in vivo as a model for regression in melanoma (1, 2). Halo nevi appear as one or more moles with sharply demarcated rings of depigmentation. The halo generally forms around an acquired intradermal nevus, but halos surrounding epidermal, junctional, congenital and Spitz nevi also have been described (3,4). The onset of the ring of depigmentation is thought to occur over a period of days to weeks. The central pigmented lesion may persist or completely disappear and repigmentation of the skin occurs over months to years. Generally, the diagnosis of halo nevi is based on clinical presentation. However, a retrospective study of 142 patients with halo nevi revealed that 76 cases were diagnosed on histological grounds alone, indicating that a large number of halo nevi may go unrecognized clinically (4).
Epidemiology and pathogenesis
Halo nevi generally affect individuals in the first two decades of life, with a mean age of diagnosis at 15 years and an overall incidence of less than 1%. Men and women are affected equally with no racial predilection. Evidence points to an association between vitiligo and halo nevi with some individuals experiencing both conditions concurrently (2). Vitiligo and halo nevi demonstrate a complete absence of melanocytes in the depigmented epidermis and lymphocytic infiltration of the surrounding skin suggesting a similar immunologic trigger for both conditions. Although no precipitating factor for the formation of halo nevi has been identified, this phenomenon is characterized histologically by mainly CD8+ T lymphocytes, which form a dense band-like lymphocytic infiltrate in the papillary and reticular dermis with nests of nevus cells located centrally. These CD8+ cells may have a direct cytotoxic affect against melanocytes.5 The presence of antibodies that react with melanocytic cells in vitro in these patients supports a humoral component in the pathogenesis as well (5).
The presence of a halo around an innocent nevus may occasionally lead to the misdiagnosis of melanoma because the inflammatory cells can obscure the architectural features of the underlying nevus (3). There are only rare reports of melanoma developing within a halo nevus. However, the differential diagnosis of halo nevus should include the halo phenomenon surrounding a regressing melanoma which results in the disappearance of the cutaneous tumor and eventual superficial fibrosis (6). Regressing melanomas are characterized by asymmetric and patchy areas of hypopigmentation and depigmentation which appear within and around the melanoma (6). Halo nevi are innocent moles and should be monitored like other innocent acquired nevi. Only atypical appearing lesions require biopsy .
In the patient in the vignette the halos were noted by his mother following a sunburn after a visit to the beach. The subsequent tanning of the normal skin resulted in a dramatic increase in the contrast between the nevus, normal skin, and the depigmented halos. The pigmented nevi have similar symmetric features with uniform borders and texture. The round depigmented macule on the right mid back probably represents an area of complete regression of a pigmented nevus. A photograph was obtained for baseline documentation and a followup visit was scheduled for one year.
Well demarcated symmetric halo nevi in healthy children are innocent and require only monitoring.
- 1. Musette P, Bachelez H, Flageul B, Delarbre C, Kourilsky P, Dubertret L, Gachelin G. Immune-mediated destruction of melanocytes in halo nevi is associated with the local expansion of a limited number of T cell clones. J Immunol. 1999;162:1789–1794.
- 2. Suh JC, Yeum JS, Shin DJ, Seo SK, Na GY, Suh MK. Clinical study of halo nevi. Korean J Dermatol. 2001 Jun;39(6):648-653.
- 3. Suh JC, Yeum JS, Shin DJ, Seo SK, Na GY, Suh MK. Clinical study of halo nevi. Korean J Dermatol. 2001 Jun;39(6):648-653.
- 4. Harvell JD, Meehan SA, LeBoit PE. Spitz nevi with halo reaction: a histopathological study of 17 cases. J Cutan Pathol. 1997 Nov; 24(10):611-9.
- 5. Mooney MA, Barr RJ, Buxton MG. Halo nevus or halo phenomenon: a study of 142 cases. J Cutan Pathol. 1995; 22(4):342-8.
- 6. Zeff RA, Freitag A, Grin CM, Grant-Kels JM. The immune response in halo nevi. J Am Acad Dermatol 1997 Oct; 37(4): 620-4.
- 7. Moretti S, Spallanzani A, Pinzi C et al. Fibrosis in regressing melanoma versus nonfibrosis in halo nevus upon melanocyte disappearance. J Cutan Pathol 2007; 34: 301-308.