Derm Dx: White patch around a mole


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A 16-year-old patient presented with complaints of a whitish patch that had developed around one of her moles.

A halo nevus is a nevus surrounded by a ring of depigmentation or "halo." Halo nevi are typically found in both male and female patients aged younger than 20 years. Those who develop halo nevus also have an increased number...

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A halo nevus is a nevus surrounded by a ring of depigmentation or “halo.” Halo nevi are typically found in both male and female patients aged younger than 20 years. Those who develop halo nevus also have an increased number of melanocytic nevi (the common mole). About 20% of patients diagnosed with halo nevi have vitiligo.

Halo nevi are characterized by a melanocytic nevus surrounded by a well-circumscribed ring of hypopigmentation or depigmented skin. The melanocytic nevus is flat or raised and dark-brown to pink in color with possible scaling or crusting. Most commonly, the central nevus measures between 3mm-6mm in diameter, has smooth and well-defined borders and has a homogenous color.

Halo nevi may be found anywhere on the body, though these lesions occur most frequently on the trunk. Erythema sometimes precedes the depigmented halo, which appears over a period of weeks to months. The halo is usually symmetric with a uniform width, which varies from a few millimeters up to several centimeters, but it can also be asymmetric.

Halo nevi pathogenesis is unclear. The most commonly accepted theory is that lesions result from an immune response against an altered melanocytic nevus due to autoimmune, physical or chemical insults. Multiple halo nevi may then occur from the cross-reactivity of the immune response at melanocytic nevi at distant sites.

Patients with regressing halo nevi present further evidence of an autoimmune response.. Antibodies and lymphocytes directed against melanoma cells have been isolated from patients with halo nevi that are cytotoxic to melanoma cells in culture.

It is unclear whether these antibodies are actually important in the pathogenesis of halo nevus. Concomitant vitiligo presents in a decent proportion of patients, providing further support for an autoimmune pathogenesis.

Histologically, in fully evolved stages the central nevus of a halo nevus demonstrates a band-like infiltrate of lymphocytes and histiocytes, which occupy the papillary dermis and can penetrate nests of nevus cells.

The course is variable after development of halo nevi.. Rarely, the central nevus can persists indefinitely and the halo may repigment. Most commonly, the nevus gradually loses its pigmentation, turns pink and irregular, and then disappears leaving a white macule — a round-to-oval area of depigmentation.

Complete repigmentation of the skin is subsequently seen in most patients, but may take years. In rare cases, the central nevus may darken rather than lighten. Rapid onset of a large number of halo nevi in an older adult can be a sign of ocular or cutaneous melanoma elsewhere.

The most important task of a clinician is to distinguish the halo nevi from a melanoma. Asymmetric irregular halo may be seen with melanoma, compared with the symmetry usually found in a halo nevus, but asymmetry does not mean malignancy.

Most often, the decision to perform a biopsy is based on the clinical characteristics of the central lesion. Keep in mind that halo nevi are much more common than primary melanomas with halos, especially in adolescents.

The clinical setting should be taken into account when deciding an approach to halo nevi. All patients should be asked about a history of melanoma, atypical nevi and vitiligo. Each lesion should be examined for atypical features that might be suspicious for atypical melanocytic nevus or melanoma. In the absence of atypia, periodic skin examinations are sufficient.

Atypical halo nevi should be biopsied, especially in individuals aged older than 40 years with new-onset halo nevi. A complete physical exam to rule out cutaneous or ocular melanoma may be warranted. 

Other answer choices:

Nevus anemicus is a congenital vascular anomaly that results in pale areas of the skin. These lesions present as macules of varying size and shape that are paler than the surrounding skin. They are most commonly found on the upper to mid trunk.

The nevus may resemble vitiligo, but there is a normal amount of melanin in the lesion. On physical exam, Wood’s light does not accentuate the lesion, and diascopy or application of pressure causes the borders and extent of the lesion to become imperceptible due to blanching of surrounding skin.

Applying heat or ice will accentuate the lesion by creating an increasingly hyperemic border, whereas the lesion will remain pale. The underlying pathogenesis is an increased sensitivity of blood vessels to catecholamines with permanent vasoconstriction.

Nevus anemicus is differentiated from vitiligo by the pale appearance of the lesion, as opposed to the absence of pigmentation, and by using the physical exam signs noted previously. Nevus anemicus does not require treatment and no treatment is effective.

Nevus depigmentosus is a hypopigmented skin condition that is thought to reflect cutaneous pigmentary mosaicism. The most common presentation of nevus depigmentosus is a localized hypopigmented patch.

Although lesions of nevus depigmentosus are classically present at birth, they may sometime become apparent later in childhood in individuals with lighter skin.

Christopher Chu is medical student at Baylor College of Medicine.

Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine also in Houston.


  1. Bolognia J, Jorizzo J, Rapini R. 2008. “Chapter 62 – Mosaicism and Linear Lesions.” Dermatology. St. Louis, MO: Mosby/Elsevier. Print.
  2. Bolognia J, Jorizzo J, Rapini R. 2008. “Chapter 106 – Other Vascular Disorders.” Dermatology. St. Louis, MO: Mosby/Elsevier. Print.
  3. Bolognia J, Jorizzo J, Rapini R. 2008. “Chapter 112 – Benign Melanocytic Neoplasms.” Dermatology.  St. Louis, MO: Mosby/Elsevier. Print.
  4. William J, Berger T, Elston D, Odom R. 2006. “Chapter 28 – Dermal and Subcutaneous Tumors.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunder Elsevier. Print.
  5. William J, Berger T, Elston D, Odom R. 2006. “Chapter 30 – Melanocytic Nevi and Neoplasms.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunder Elsevier. Print.
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