A study of Halo naevi, vitiligo and asymptomatic autoimmune thyroiditis (2023)


  Halo Naevus (HN) is a dermatologic condition characterized by a typical whitish rim arround an existing melanocytic congenital or acquired nevus, it was first described in 1916 by Sutton[1]. Halo nævi are common in children and young adults, with a mean age at onset of 15 years. The incidence in general population is estimated to be approximately 1%[2]. Affected individuals frequently have multiple lesions which are usually localized on the back. HN is an autoimmune response and T lymphocytes are considered to play a key role in the progressive destruction of nævus’ cells. Multiple HN is rather rare and this could suggest a higher risk of vitiligo or of autoimmune disease development comparing to solitary HN lesion risks. The mechanism of halo phenomenon is still non completely defined and is suggested to be induced by a destruction of melanocytes by immune response of cytotoxic T cells[3] or due to IgM autoantibodies induction[4].

  We sought to assess the association of Hallo Naevi (HN) or of HN-vitiligo with thyroiditis by screening markers of thyroiditis in patients presenting Hallo Naevi (HN) and HN associated with vitiligo.

Materials and Methods

  In this study were included adults patients with halo nævus and / or vitiligo presented in dermatology outpatient clinic between 2010 and 2016. Clinical and dermoscopy examination were performed. The possible association between vitiligo and thyroiditis was assessed by peripheral blood dosage of Anti-Thyroid Peroxidase (ATPO).

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  Were included 37 patients, 16 female and 21 male. Twenty five patients (67.56%) had one HN, 7 patients(18.91%) had 2 HN and 5(15.31%) of the patients had 3 HN. From 37 patients with halo nevus 10 (27.02%) had associated vitiligo. In all cases vitiligo occurred 3 - 4 years after the onset of HN. In all 10 patients with HN and associated vitiligo, lesions were of non-segmental type: limited, symmetric, small and large lesions of extremities. Among them five had one HN (4 female and 1 male), 2 patients had 2 HN (one male and one female), 3 patients had 3 HN.

  In 27 (72.98%) patients with HN ( and no vitiligo): ATPO peripheral blood levels were normal in 26 patients (96.29%), a 13 years old boy had high ATPO (presented in the discussion) (3.71%).

  In 10 patients with HN and associated vitiligo: 3 had high ATPO results (33.33% of patients,1 male with 2 HN and 2 female with 3 HN) with a 2/1 female/male ratio. One of female with 3 HN had a history of autoimmune thyroiditis and vitiligo - both occurred after the onset of HN (by order thyroiditis, HN then vitiligo). In 2 others cases with high ATPO clinical appearance of the conditions was HN, vitiligo and thyroiditis. Vitiligo features were in all cases of type non-segmental with bilateral hypo-chromic, symmetrical small macules (0.3 - 0.8 cm diameter) and Koebner phenomena or large plaques located on extremities (Figure 1).

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Figure 1: Vitiligo of the hand.


  Thirty eight patients were initially included. One patient was excluded as he presented one lesion that was not a halo naevus but a melanoma with peripheral regression send to surgery and oncology. Vitiligo and halo naevi are both pigmentary disorders of the skin characterized by the acquired loss of functional epidermal melanocytes manifesting as white macules and patches. The cellular mechanisms and biochemical changes that result in the appearance of these two types of achromic lesions and the direct relationship between vitiligo and halo naevi are still subject of discussion. The tendency of different morphologic alterations in mitochondria from perilesional vitiligo skin and from perilesional halo nevi skin reflect heterogeneous backgrounds between the two diseases, revealing that vitiligo and halo naevi may have separate pathogenic mechanisms.

  There is strong evidence that immunological mechanisms are at the base of melanocytic destruction: the presence progressive destruction of of an inflammatory lymphocytic infiltrate that leads to progressive destruction of naevi cells; the presence of antibodies against nevi cells[5]. Recent studies highlighted similarities and differences between events that occur in regression of melanoma, vitiligo and in Sutton’s phenomenon[6-8].

  The association of vitiligo with autoimmune thyroid diseases and the increased prevalence of autoantibodies including thyroid autoantibodies in vitiligo had been proven by several recent studies[9-11]. In Sutton’s nevi was usually described an inflammatory cellular infiltrate surrounding symmetrically the naevus, consisting mainly of T-lymphocytes. B-lymphocytes, Langerhans cells and macrophages are absent or rarely observed[3]. Thyroiditis is defined histologically by the presence of a diffuse lymphocytic infiltrate in the thyroid gland, with the formation of lymphoid follicles. Cell mediated and antibody mediated immune responses lead to the destruction of thyroid cells[10]. In patients with multiple HN, the risk of vitiligo and other autoimmune diseases seems to be higher than in pediatric patients with a single HN. The female/male ratio is 5 - 10/1 in autoimmune thyroiditis and the onset of disorder usually takes place between the third and sixth decade of life. Due the fact that halo naevus’ onset is usually be earlier than vitiligo, clinicians should pay particular attention even to patients presenting children/boys with one or several HN. The follow-up of HN is clinical and by dermoscopy, very high photo-protection is necessary (SPF 50+) for HN of photo exposed areas. Non-segmental, stable, limited vitiligo management is most frequently made by potent topical steroid therapy, topical calcineurin inhibitors, or narrow-band UVB 311 nm or associations phototherapy by UVA and psoralen (PUVA) (phototherapy is contraindicated in areas where vitiligo is associated with HN), excimer laser 308 nm.

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  A 13 years old boy with congenital melanocitic naevi that was referred to dermatology presented a recent white patch arround one naevus. Clinical evaluation revealed a whitish rim arround an congenital melanocitic nevus from the lumbar area, without cutaneous induration, resembling a halo nevus (Figure 2).

Figure 2: Halo nevus. Clinical image.

  Dermoscopy revealed a mixed pattern composed of a central network, structureless light brown-gray area and some small brown globules in periphery (Figure 3)[12]. There was no family or personal history of vitiligo or autoimune diseases.Anti-Thyroid Peroxidase (ATPO) levels were 107.6UI/mL (normal values 0 - 34UI/mL), Thyroid Stimulating Hormone (TSH) was 3,2 uUI/mL (normal values 0,4 - 4 uUI/mL), free thyroxine (fT4) was 1,14 ng/dL (normal values 0,98 - 1,63 ng/dL). Thyroid ultrasound showed heterogeneous thyroid echotexture. Anti-thyroglobulin and fT4 were not performed but the patient was reffered to the endocrinologist for specialty investigations and monitoring.

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Figure 3: Halo nevus. Dermoscopy 10 x magnification.


  In a series of 37 halo naevi, ten cases (27, 2%) had an associated vitiligo, among them 3 (33.33%) had peripheral blood levels of Anti-Thyroid Peroxydase (ATPO). One case from 27 patients with HN without vitiligo (3.70%) had high levels of ATPO and ultrasound sign of thyroiditis. In patients with one or several HN, a systematic dermatoscopy and endocrine assessments can reveal associated autoimmune diseases as vitiligo and thyroiditis but halo naevi and vitiligo patients have more frequent high levels of ATPO (33.33%) than those with just halo naevi without vitiligo (3.70%).


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  1. 1. Sutton, R.L. An unusual variety of vitiligo (leukoderma acquisitum centrifugum). (1916) J Cutan Dis 34: 797-800.
  2. 2. Stierman, S.C., Tierney, E.P., Shwayder, T.A. Halo congenital nevocellular nevi associated with extralesional vitiligo: a case series with review of the literature. (2009) Pediatr Dermatol 26(4): 414-424.
    Pubmed || Crossref
  3. 3. Zeff, R.A., Freitag, A., Grin, C.M., et al. The immune response in halo nevi. (1997) J Am Acad Dermatol 37(4): 620-624.
    Pubmed || Crossref
  4. 4. Patrizi, A., Bentivogli, M., Raone, B., et al. Association of halo nevus/i and vitiligo in childhood: a retrospective observational study. (2013) JEADV 27(2): e148-e152.
    Pubmed || Crossref || Others
  5. 5. Frank, S.B., Cohen, H.J. The halo nevus. (1964) Arch Dermatol 89(3): 367–373.
  6. 6. Moretti, S., Spallanzani, A., Pinzi, C., et al. Fibrosis in regressing melanoma versus nonfibrosis in halo nevus upon melanocyte disappearance: could it be related to a different cytokine microenvironment? (2007) J Cutan Pathol 34(4): 301-308.
    Pubmed || Crossref || Others
  7. 7. de Vijlder, H.C., Westerhof, W., Schreuder, G.M., et al. Difference in pathogenesis between vitiligo vulgaris and halo nevi associated with vitiligo is supported by an HLA association study. (2004) Pigment Cell Res 17(3): 270-274.
    Pubmed || Crossref || Others
  8. 8. Nedelcu, R.I., Zurac, S.A., Brinzea, A., et al. Morphological features of melanocytic tumors with depigmented halo: review of the literature and personal results. (2015) Rom J Morphol Embryol 56(2 Suppl): 659-663.
    Pubmed || Others
  9. 9. Zabawski, E.J. Jr, Cockerell, C.J. Halo nevus. (2012).
  10. 10. Bumbacea, R.S., Popa, L.G., Orzan, O.A., et al. Clinical and therapeutic implications of the association between chronic urticaria and autoimmune thyroiditis. (2014) Acta Endocrinologica (Buc) 10(4): 595-604.
    Crossref || Others
  11. 11. Tatu, A.L., Ionescu, M.A. Multiple autoimmune syndrome type III- thyroiditis,vitiligo and alopecia areata. (2017) Acta Endo (Buc) 13 (1): 124-125.
  12. 12. Tatu, A.L. Topical Steroid Induced Facial Rosaceiform Dermatitis. (2016) Acta Endo (Buc) 12(2): 232-233.
    Crossref || Others


Can halo nevi cause vitiligo? ›

Halo nevus (HN) has been shown to be associated with vitiligo, but no standard signs are currently available to identify HN patients at risk of vitiligo, and the relevant data obtained in previous studies are somewhat conflicting. This study aimed to identify factors affecting the presence of vitiligo in HN patients.

Is halo nevus and autoimmune disease? ›

The etiology of halo nevi is unknown. It is an autoimmune response and T lymphocytes are considered to play a key role in the progressive destruction of nevus cells.

Are halo nevi cancerous? ›

Can they be cancerous? Halo nevi are almost always benign. In rare cases, however, a halo nevus can indicate the presence of melanoma, a form of skin cancer, somewhere else on the body. This is more likely to be the case in older adults and those with halo nevi that are irregularly shaped or colored.

Is halo mole vitiligo? ›

Background: Halo nevus (HN) is a rare dermatologic disorder characterized by typical whitish rim surrounding an existing melanocytic nevus resembling halo. It is a cosmetic problem that may be linked to vitiligo, and it is advised to remove these nevi in order to avoid development of vitiligo.

How do you treat halo nevus? ›

Halo nevi are usually benign. No treatment is necessary if they have a typical appearance, other than reassuring the patient that they are not a concern for skin cancer. The white skin around a halo ​nevus may be more prone to sunburn, so the use of sunscreen is a good idea to protect the skin.

What causes vitiligo? ›

Vitiligo is caused by the lack of a pigment called melanin in the skin. Melanin is produced by skin cells called melanocytes, and it gives your skin its colour. In vitiligo, there are not enough working melanocytes to produce enough melanin in your skin. This causes white patches to develop on your skin or hair.

How long does it take for a halo nevus to go away? ›

Observations have showed that the halo nevi last for 10 years or more, but a large subgroup passes through various stages to finally regress completely. The process takes approximately 8 years on average.

How common are halo nevus? ›

Halo naevi (US plural, nevi) are not uncommon, with an estimated prevalence of 1% of the white-skinned population. They are usually seen in healthy children or young adults of either sex. They can occur at an older age too.

Does vitiligo affect moles? ›

Upper extremity moles were associated with a 37% increase in the likelihood of vitiligo among white women, according to an analysis of the prospective Nurses' Health Study.

What causes halo nevi? ›

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.

How do I know if my mole is cancerous? ›

Border – melanomas usually have a notched or ragged border. Colours – melanomas will usually be a mix of 2 or more colours. Diameter – most melanomas are usually larger than 6mm in diameter. Enlargement or elevation – a mole that changes size over time is more likely to be a melanoma.

How do cancerous moles start? ›

The first sign of melanoma is often a mole that changes size, shape or color. This melanoma shows color variations and an irregular border, both of which are melanoma warning signs. Melanomas can develop anywhere on your body.

Is a white mole cancerous? ›

It is also important to make note of any blue or white colours that may be present in your moles, as this is a sign that the mole may be cancerous. If your mole has multiple colours or shades, you should speak with your doctor. The mole in the left image is monotone and is healthy.

What is halo disease? ›

Halo blight caused by Pseudomonas syringae pv. phaseolicola is a major disease of beans throughout the world. The pathogen attacks both foliage and pods. The disease is most destructive where temperatures are moderate and abundant inoculum is available.

Why do I have so many moles on my body? ›

It's thought to be an interaction of genetic factors and sun damage in most cases. Moles usually emerge in childhood and adolescence, and change in size and color as you grow. New moles commonly appear at times when your hormone levels change, such as during pregnancy.

Is vitiligo a serious disease? ›

Vitiligo does not pose a serious threat to one's health, but it can result in physical complications, such as eye issues, hearing problems, and sunburn. People with vitiligo also tend to be more likely to have another autoimmune disease (like thyroid disorders and some types of anemia).

Which food causes vitiligo? ›

Some food items like juicy fruits rich in vitamin C or ascorbic acid such as oranges and lemon, other fermented food items as curd, alcohol, Fish, red meat are to be avoided as they have harmful effect on vitiligo and can give rise to spreading of patches.

Can Vitamin B12 deficiency cause vitiligo? ›

Skin lesions associated with vitamin B12 deficiency are skin hyperpigmentation, vitiligo, angular stomatitis, and hair changes. Cutaneous lesions that do not respond to conventional therapy can be an indication of vitamin B12 deficiency.

What are white looking moles on skin? ›

Amelanotic melanomas are missing the dark pigment melanin, which gives most moles their color. They can appear pinkish, white, red, or even essentially clear.

When should I be worried about a mole? ›

It's important to get a new or existing mole checked out if it: changes shape or looks uneven. changes colour, gets darker or has more than 2 colours. starts itching, crusting, flaking or bleeding.

What virus can cause vitiligo? ›

Viruses such as Cytomegalovirus (CMV) and Epstein Barr virus were detected in the epidermis of vitiligo patients [16,24]. The Herpes Zoster Virus was found in patients affected with segmental vitiligo [20]. The vitiligo was found to be associated with the Herpes Simplex Labialis Virus as well [22].

Can vitiligo become cancerous? ›

It's believed to be an autoimmune disease. Skin cancer treatment may contribute to the development of vitiligo. But research shows vitiligo doesn't cause skin cancer and may even offer some protection against it and several other types of cancer, possibly due to genetics.

What autoimmune causes vitiligo? ›

What they learned was that vitiligo was “very highly associated” with a number of other autoimmune diseases, mostly thyroid disease, but also pernicious anemia, rheumatoid arthritis, psoriasis, lupus, Addison's disease, and adult-onset autoimmune diabetes.

Does vitiligo affect moles? ›

Upper extremity moles were associated with a 37% increase in the likelihood of vitiligo among white women, according to an analysis of the prospective Nurses' Health Study.

How long does a halo nevus last? ›

Observations have showed that the halo nevi last for 10 years or more, but a large subgroup passes through various stages to finally regress completely. The process takes approximately 8 years on average.

How common are halo nevus? ›

Halo naevi (US plural, nevi) are not uncommon, with an estimated prevalence of 1% of the white-skinned population. They are usually seen in healthy children or young adults of either sex. They can occur at an older age too.

What is non segmental vitiligo? ›

Nonsegmental vitiligo is a depigmented skin disorder showing acquired, progressive, and depigmented lesions of the skin, mucosa, and hair. It is believed to be caused mainly by the autoimmune loss of melanocytes from the involved areas.


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