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Halo Nevus

  • Author: Edward J Zabawski, Jr, DO; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Apr 21, 2014
 

Background

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 Gr ü nwald 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.

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Pathophysiology

The etiology of halo nevi is unknown. 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] 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.[5] 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.[6]

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Epidemiology

Frequency

United States

The incidence of halo nevi in the population is estimated to be 1%.[7] Patients with Turner syndrome have been reported to have an increased incidence of halo nevi.[8]

Mortality/Morbidity

Halo nevi are benign. Morbidity is minimal and limited to cosmetic appearance.

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. The average age of onset is 15 years.

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Contributor Information and Disclosures
Author

Edward J Zabawski, Jr, DO Medical and Surgical Dermatology

Edward J Zabawski, Jr, DO is a member of the following medical societies: American Osteopathic Association, New England Dermatological Society

Disclosure: Nothing to disclose.

Coauthor(s)

Clay J Cockerell, MD Director, Clinical Professor, Department of Dermatology, Division of Dermatopathology, University of Texas Southwestern Medical Center

Clay J Cockerell, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, International AIDS Society, International Academy of Pathology, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, Society for Investigative Dermatology, Southern Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Susan M Swetter, MD Director, Pigmented Lesion and Melanoma Program, Professor, Department of Dermatology, Stanford University Medical Center and Cancer Institute, Veterans Affairs Palo Alto Health Care System

Susan M Swetter, MD is a member of the following medical societies: American Academy of Dermatology, Women's Dermatologic Society, American Society of Clinical Oncology, Society for Melanoma Research, Eastern Cooperative Oncology Group, American Medical Association, Pacific Dermatologic Association, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

References
  1. Happle R. [Grunewald nevus]. Hautarzt. 1994 Dec. 45(12):882-3. [Medline].

  2. 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. [Medline].

  3. Patrizi A, Neri I, Sabattini E, Rizzoli L, Misciali C. Unusual inflammatory and hyperkeratotic halo naevus in children. Br J Dermatol. 2005 Feb. 152(2):357-60. [Medline].

  4. van Geel N, Vandenhaute S, Speeckaert R, et al. Prognostic value and clinical significance of halo naevi regarding vitiligo. Br J Dermatol. 2011 Apr. 164(4):743-9. [Medline].

  5. Fishman HC. Letter: Malignant melanoma arising with two halo nevi. Arch Dermatol. 1976 Mar. 112(3):407-8. [Medline].

  6. Jacobs JB, Edelstein LM, Snyder LM, Fortier N. Ultrastructural evidence for destruction in the halo nevus. Cancer Res. 1975 Feb. 35(2):352-7. [Medline].

  7. Herd RM, Hunter JA. Familial halo naevi. Clin Exp Dermatol. 1998 Mar. 23(2):68-9. [Medline].

  8. Brazzelli V, Larizza D, Martinetti M, et al. Halo nevus, rather than vitiligo, is a typical dermatologic finding of turner's syndrome: clinical, genetic, and immunogenetic study in 72 patients. J Am Acad Dermatol. 2004 Sep. 51(3):354-8. [Medline].

  9. Zalaudek I, Moscarella E, Argenziano G. Artifactual "pseudo-halo nevi" secondary to sunscreen application. J Am Acad Dermatol. 2006 Jun. 54(6):1106-7. [Medline].

  10. Berg P, Lindelof B. Differences in malignant melanoma between children and adolescents. A 35-year epidemiological study. Arch Dermatol. 1997 Mar. 133(3):295-7. [Medline].

 
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Classic appearance of a halo nevus.
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.
At low magnification, a dome-shaped papular lesion reveals a dense infiltrate of lymphocytes in the dermis (hematoxylin and eosin, original magnification X40).
Higher magnification reveals nests of nevus cells with numerous lymphocytes surrounding them and in the interstitium (hematoxylin and eosin, original magnification X40).
Table. Distinguishing Features of Halo Nevus and Melanoma
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
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