Halo Nevus_1211 Derm Clin Slide
A man aged 26 years presented to the dermatology clinic for a general skin examination. He was specifically concerned about a mole that had been present for a number of years. The mole had recently developed a depigmented halo. No pain or pruritus was reported.The man had not had any trauma to the area. Physical examination revealed a 5-mm melanocytic nevus with regular borders and no color variegation. This nevus was surrounded by a 3-mm depigmented halo. A similar nevus was appreciated on the man’s right lower back. What’s your diagnosis?Submit your answer and read the full explanation below. If you like this activity or have a suggestion, tell us about it in the comment box at the bottom of the page.Do you have related images that you would like to share? Click on the “+Image” link under the comment box to upload your photos. By submitting your photo, you agree that the patient in the photo is not identifiable or has signed a waiver in compliance with HIPAA regulations.
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Halo nevi have been around for centuries, but it was not until 1916 that the condition entered the medical field. The lesion was originally described as “leukoderma acquisita centrifugum.” It has been reported that less than 1% of individuals younger than age 20 years have halo nevi.1
The median age of onset is 15 years; however, there have been cases of patients as old as age 42 years. Halo nevi affect all races and sexes equally. Individuals with halo nevi tend to have an overall increased number of melanocyctic nevi. Approximately 20% of patients with halo nevi will also have vitiligo.1
The path for nevus cell destruction is not well known, but both cellular and humoral immunologic factors have been examined. There are two main theories regarding the basis for the development of the halo of depigmentation in halo nevi. The first — and most widely accepted — posits that a physical, chemical or other event causes a nonspecific change to a nevomelanocyte.2 The body then directly mounts a cell-mediated and/or humoral response to this change. An autoimmune pathogenesis, such as that seen with vitiligo, has also been theorized.2
The second theory suggests that an immunologic response is mounted against an antigenically altered nevus, which shows tumor progression (dysplasia).2 The response is the same as that seen with tumorigenesis.
Copeman et al were the first to show that the human body has antibodies against melanoma cells.2 Individuals with conventional nevi do not have these antibodies; however, people with primary melanoma who have not developed metastases do. On examination of lymphocytes taken from individuals with halo nevi and melanoma, cytotoxicity was shown toward melanoma cells.3 It is not known whether these observations are important in the pathogenesis of halo nevi or whether they are a secondary effect that stems from the underlying pathogenesis.
The central nevus in halo nevi is associated with an infiltrate of scattered macrophages, lymphocytes and CD4 (helper) and CD8 (cytotoxic) T-cells. The peripheral white halo has little infiltrate, and the pathogenesis for its formation is not well known. The destruction of melanocytes in the depigmented zone is secondary to the diffusion of an unknown cytotoxic factor.4
A halo nevus is unique in its appearance. Centrally, it has a melanocytic nevus that may be flat or raised and dark-brown to pink in color. The nevus may be anywhere from 3 to 6 mm in diameter with consistent and well-defined borders.5 The color will also be homogenous across the nevus.
Occasionally, the nevus will have scale or crusting on the surface. Just prior to the development of the halo, the area surrounding the nevus may become erythematous. The halo is appreciated as a well-circumscribed, depigmented area that typically measures a few millimeters in diameter. Its borders are usually symmetric, but may also be in the shape of an oval.6 Use a Wood’s lamp or dermoscope if a more thorough clinical examination of the halo is needed.
Halo nevi may be found anywhere on the body, but most are concentrated on the upper back.2 Individuals with one halo nevus should be carefully examined for more, as anywhere from 25% to 50% will have additional lesions.2
A biopsy of a halo nevus in an early stage will show a dense inflammatory infiltrate penetrating nests of nevus cells in the upper dermis and at the epidermal-dermal junction.7 This correlates clinically with the central nevus. The halo will reveal a noticeable reduction of melanin and will have little to no inflammation. In the later stages of the lesion, nevus cells are decreased and will be absent in some instances.
All melanocytic proliferations associated with halos are in the differential diagnosis, including blue nevi, Spitz nevi, primary melanoma, atypical melanocytic nevi and congenital nevi. Other non-melanocytic lesions that are associated with halos — such as dermatofibromas, flat warts, basal cell carcinoma, lichen planus, psoriasis and seborrheic keratoses — must also be considered in the differential diagnosis.8
Halo nevi have been erroneously confused with melanoma and have been the source of anxiety for clinicians and patients. To differentiate the two, observe the halo. In a halo nevus, the depigmented area is symmetrical and has regular borders. With melanoma, the halo is often asymmetrical with irregular borders. However, this is frequently not enough to diagnose the disease properly. The next step is to examine the central nevi. If the nevus is irregular in color, has notched borders, or is larger than a centimeter, melanoma should be suspected.9
Treatment of halo nevi is not necessary. However, persons with halo nevi should have a full-body skin examination to evaluate for vitiligo and any evidence of dysplastic nevi or melanoma.2 Encourage the patient to proactively monitor the lesion and record any changes within the nevus. If irregularity, bleeding, itching and/or pain develop, the patient should seek a health-care provider to make sure the lesion is not developing into a cutaneous melanoma.9
Halo nevi are asymptomatic and benign in nature. Because they are benign, their prognosis is considered excellent.2 The central nevus may involute over time; if it does not, it is very important to monitor the nevus, as it may start to change. Evolution of the nevus would indicate the possibility of cutaneous melanoma, and the lesion should be removed as soon as possible.
The halo often becomes repigmented, but this process may take months to years. Inflammation may occur with crusting in the depigmented zone. Multiple halo nevi may be a sign of an ocular or cutanous melanoma elsewhere on the body, especially in adults.5 All patients are instructed to have regular skin exams.
A full-body skin exam was performed on this patient, and no suspicious nevi were identified. No further treatment was necessary, and regular skin exams were encouraged.
Kerri Robbins, MD, is a resident in the department of dermatology at Baylor College of Medicine in Houston. The author has no relationships to disclose relating to the content of this article.
1. Herd RM, Hunter JA. Familial halo naevi. Clin Exp Dermatol. 1998;23:68-69.
2. Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology, 2nd ed., St. Louis, Mo.: Elsevier-Mosby; 2008:1725-1726.
3. Zeff RA, Freitag A, Grin CM, Grant-Kels JM. The immune response in halo nevi. J Am Acad Dermatol. 1997;37:620-624.
4. Patrizi A, Neri I, Sabattini E, et al. Unusual inflammatory and hyperkeratotic halo naevus in children. Br J Dermatol. 2005;152:357-360.
5. Paller AS, Mancini AJ. HurwitzClinical Pediatric Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2006:215.
6. Habif, TP. Skin Disease: Diagnosis and Treatment. 2nd ed. St. Louis, Mo: Mosby/Elsevier; 2005. Page 465.
7. Elder DE, Elenitsas R, Johnson BL, et al, eds. Lever’s Histopathology of the Skin. 10th ed., Philadelphia, Pa.: Lippincott Williams & Wilkins; 2009:730-732.
8. Rapini RP. Practical Dermatopathology. Philadelphia, Pa.: Elsevier Mosby; 2005:266.
9. Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology, 5th ed. New York, N.Y.: McGraw-Hill; 2005:170-171.