Causes of Vitiligo

The cause of vitiligo is not known but there is speculation that it is an autoimmune disease which results in the body destroying its own cells, in this case the melanocytes that produce skin pigment. Autoimmune disorders are thought to have a hereditary aspect with certain genes making a person more prone to developing an immune system dysfunction where the body mistakenly attacks itself. Other theories regarding vitiligo causes include the idea that the melanocytes destroy themselves, and that physical trauma (sunburn, for example) or emotional trauma (stress) can trigger vitiligo. There is no substantive evidence to suggest that either hypothesis is correct.

Vitiligo is indiscriminate it seems in terms of who it affects, with one in every hundred people thought to suffer from the skin condition. In the US this equates to between one and two million people with vitiligo, half developing vitiligo before their twentieth birthday, most developing it prior to their fortieth birthday, and with equal rates in both sexes and across all ethnicities. Those with certain autoimmune system disorders, such as hyperthyroidism or Hashimoto’s Thyroiditis, have a higher risk of developing vitiligo, as do those with pernicious anaemia, alopaecia areata, and Addison’s disease (where the body does not produce enough corticosteroid hormone). Most people who suffer from vitiligo do not have an autoimmune disorder however, but many will have a close relative with the condition as vitiligo does run in families.

white rabbit melanin vitiligo

Albinism is a disorder of melanin production like vitiligo

The most likely explanation for vitiligo is that a combination of factors occurs which result in abnormal melanocyte function and the death of these pigment-producing skin cells. It is possible that a neuropeptide may damage melanin and lead to the white skin patches found in vitiligo. The neuropeptide is thought to be released in the skin following physical trauma, or during emotional stress. Emotional stress also affects the hypothalamic-pituitary-adrenal axis (the HPA axis), which also involves the thyroid gland. Chronic stress in this system can lead to a reduced ability to cope with infection, demands for energy, repair, and growth, and lead to abnormal responses in the immune system where autocytotoxicity then arises. Other factors that have been suggested as possible causes of vitiligo range from the use of certain medications over long periods, abrasion from clothes being too tight (on the waist particularly it seems), and the use of rubber gloves or other such protective wear in certain types of employment.

Patients with vitiligo may have a copy of the same gene (NALP1) that is often present in those suffering from hypothyroidism (an under-active thyroid gland). Other skin conditions, and disease affecting the skin as part of their pathology, are also associated with this particular gene on chromosome 17p13, including psoriasis and systemic lupus erythematosus (which can cause a distinctive butterfly rash on the face). As such, it may be that a vitiligo patient’s physician deems it necessary to conduct regular screening of thyroid function. Blood tests to check for the levels of T3, T4, and Thyroid stimulating hormone may be wise for patients with vitiligo.

Researchers at the Laboratory for Investigative Dermatology in New York investigated the connection between cellular immunity and the pathogenesis of vitiligo. Wang, et al (2011), discovered that there were increased numbers of particular types of immune-system cells in the areas of the vitiligo lesions (white skin spots) which may be facilitating the development of vitiligo. Immune system T cells and inflammation-related dermal dendritic cell subsets were elevated in the skin biopsies taken from vitiligo patients. In noting the concentration of Langerhans cells, which then drive Th17 activation in vitiligo, it may be that future research may focus on this immune system activity as a potential target for vitiligo treatment. Elevated tissue mRNA (mitochondrial RNA) levels of interleukin-17A and IL-1Beta mRNA at the leading edge of the vitiligo white patches suggests that specific cellular immune elements play a key role in the inflammation which ultimately destroys the melanocytes in the skin.

A different set of researchers, working in France, have proposed a theory of melanocytorrhagia as the mechanism behind vitiligo (Cario-André , et al, 2007). This hypothesis details the chronic detachment of the the pigment-producing skin cells and, thus, the loss of these cells from the skin due to autoimmune, neural, and impaired redox mechanisms following physical trauma and free-radical damage. Essentially, the melanocytes are unable to ‘stick’ in the skin and the depigmentation occurs, leading to the symptoms of vitiligo. Although the melanocytorrhagic hypothesis does not fully explain the cause of vitiligo in terms of the reason for the defect in the skin cells, it may offer a target for future vitiligo treatment.

Continue Reading —> Vitiligo Treatment


N Engl J Med. 2007 Mar 22;356(12):1216-25.
NALP1 in vitiligo-associated multiple autoimmune disease.
Jin Y, Mailloux CM, Gowan K, Riccardi SL, LaBerge G, Bennett DC, Fain PR, Spritz RA.

PLoS One. 2011 Apr 25;6(4):e18907.
Th17 cells and activated dendritic cells are increased in vitiligo lesions.
Wang CQ, Cruz-Inigo AE, Fuentes-Duculan J, Moussai D, Gulati N, Sullivan-Whalen M, Gilleaudeau P, Cohen JA, Krueger JG.

Pigment Cell Res. 2007 Oct;20(5):385-93.
The melanocytorrhagic hypothesis of vitiligo tested on pigmented, stressed, reconstructed epidermis.
Cario-André M, Pain C, Gauthier Y, Taïeb A.

‘Vitiligo on legs’ picture courtesy of Grook Da Oger, 2009.

‘White Rabbit’ picture courtesy of TJ Blackwell, 2010.

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