What are the risk factors that can exacerbate vitiligo?

Vitiligo is a condition characterised by depigmentation in certain areas of the body, which can be more or less visible. Its development is primarily influenced by genetic and immune factors. In this condition, the immune system attacks the body's own cells: the epidermis sends danger signals, activating T lymphocytes, which release inflammatory cytokines responsible for the destruction of melanocytes. While genetic predispositions favour its onset, certain environmental factors such as UV exposure, exposure to mites, contact with certain chemicals, and stress, could also exacerbate vitiligo.

• Exposure to dust mites suspected in the origin of vitiligo.

  Exposure to dust mites is suspected to induce vitiligo in some patients. Dust mites are microscopic organisms that sometimes cause allergies and produce proteases, enzymes that break down proteins. The detachment of melanocytes involved in vitiligo is induced by the destruction of certain proteins that allow them to adhere to each other, known as E-cadherins.

  A research group from INSERM wanted to test this hypothesis on skin samples from patients with vitiligo and others not affected, exposed to mites. The results of the molecular analyses highlighted that the protease produced by the mites is responsible for the destruction of E-cadherins. Therefore, mites appear to be capable of indirectly inducing the detachment of melanocytes. This phenomenon was found on the skin of all patients but was a hundred times more significant on the skin of patients with vitiligo, indicating a heightened sensitivity to mites and a more reactive immune system.

• The Koebner phenomenon, a factor involved in skin depigmentation in individuals already affected by or predisposed to the condition of vitiligo.

  The Koebner phenomenon is also involved in the spread of vitiligo patches. This refers to the preferential distribution of depigmentation in areas frequently subjected to friction or micro-traumas. The implicated trauma triggers an inflammatory response that activates T lymphocytes. These induce the production of cytokines and the generation of reactive oxygen species, involved in oxidative stress, by skin cells. In individuals predisposed to vitiligo, melanocytes are more sensitive to oxidative damage and autoimmune attacks. The destruction of melanocytes results in localised depigmentation, marking the emergence of new vitiligo areas in the traumatised region.

• Contact with chemical products, associated with vitiligo.

  Contact with chemical substances, particularly phenol derivatives such as 4-TBP and MBEH, triggers a oxidative stress in melanocytes, disrupting the endoplasmic reticulum (ER), the cell compartment where protein and lipid synthesis occurs, leading to the accumulation of misfolded proteins. This situation activates a cellular response, which releases inflammatory signals (DAMP, IL-6, IL-8), promoting the activation of the immune system and contributing to the destruction of melanocytes in vitiligo.

• Can sun exposure exacerbate or trigger the onset of vitiligo?

  When skin is exposed to UV rays, it undergoes cellular stress that triggers the production of heat shock proteins, such as HSP70i. An overexpression of this protein has been linked to an autoimmune depigmenting response, which can lead to the attack of melanocytes by the immune system. Severe burns caused by prolonged sun exposure could thus initiate a chain reaction involving HSP70i, promoting an autoimmune response and oxidative stress, which exacerbates cellular damage. UV rays could therefore contribute to the onset of vitiligo.

In summary, although vitiligo is primarily caused by genetic and immune factors, environmental factors such as UV exposure can also contribute to its exacerbation.