A condition that affects 2% of the population. Between 20% and 30% of cases appear during childhood. Vitiligo causes depigmented patches to appear because immune system is destroying the melanocytes in the skin.

What is vitiligo?

A chronic skin pigmentation condition characterised by selective melanocyte loss.1 2

It is generally thought of as an autoimmune disease associated with genetic and environmental factors coupled with metabolic changes and oxidative stress2. However, none of these theories have fully explained the specific characteristics of this disorder.

There are two types of vitiligo: symmetrical or non-segmental vitiligo (NSV) and focal or segmental vitiligo (SV)2 3. The former is more common and is characterised by white macules, which are often symmetrical and often get larger in time. They tend to appear on the face, hands, elbows, knees, underarms and hips, but can develop anywhere on the body. Segmental vitiligo has a unilateral (asymmetric) distribution that may coincide with a whole or part of the skin segment (similar to a dermatome)3. Typical for this type of vitiligo is its rapid onset and the involvement of the pigment system of the hair follicle3.

Three in four patients with vitiligo start developing it before the age of 30 years2

25% before the age of 10 25 %
25% before the age of 10
50% before the age of 20 50 %
50% before the age of 20
70% - 80% before the age of 30 70 80 % %
70% - 80% before the age of 30

Who does it affect?

Vitiligo is the most common skin depigmentation disorder. It is estimated that between 0.5% and 2% of the global population (children and adults combined)2 suffer from this condition.

154 million people affected in the world

There are no differences with respect to ethnicity or sex, although women are more likely to consult a dermatologist, probably because of the significant negative impact on social relationships and physical appearance2.

What causes vitiligo?

The pathogenesis of vitiligo is not entirely clear, although it is known that several factors are responsible for the loss of melanocytes in the epidermis of the affected area2. Several factors influence the appearance of vitiligo, but no one hypothesis has explained the characteristics of the condition to date.

There is evidence of a genetic factor in vitiligo. In fact, it is estimated that approximately 20% of patients with vitiligo have a first-degree relative with the condition. The relative risk of presenting the disease in case of having a first-degree relative with vitiligo is seven to ten times higher2. These data aside, people affected by vitiligo are often the first in their families, showing that the mode of genetic transmission of the disease is still unclear and probably involves different genes that have not yet been specifically identified.

There is sufficient evidence to indicate that oxidative stress can contribute to melanocyte deterioration2. In fact, melanocytes release reactive oxygen species (ROS) in response to stress, interfering with pro-and antioxidants substance balance, which eventually leads to a pre-senescent antiageing cell state) 2. Oxidative stress has also been seen to reduce melanocyte adhesion to the basal membrane of the epidermis2. Added to this, cell damage caused by persistent stress can interfere with the vitality and functionality of vitiligo melanocytes, which starts the process of disappearance 4.

For many years it was thought that the role of immunity in vitiligo is mainly due to the fact that approximately one third of patients affected by vitiligo will develop thyroid disease during their lifetime. For decades it has been assumed that different components of the immune system were key factors in the development of vitiligo, such as auto-antibodies, cellular immunity and others. So far, however, none of these mechanisms has actually been proven to be the main driver of the disease. Since autoimmunity has never explained the lack of clinical evidence of inflammation in lesions or the poor response to immunosuppressive therapy, it is reasonable to consider that the role of the immune system is of secondary importance in the development of vitiligo compared to other factors.

04MIA protein:
A new cause

Researcher and dermatologist Dr Matteo Bordignon discovered a new molecule with an important role in the development of vitiligo in 2013: MIA protein 5. MIA protein interferes with the melanocytes, causing them to detach from the basal membrane and move toward the stratum corneum where they are exfoliated, along with their surrounding keratinocytes, leaving behind depigmented macules. According to this hypothesis, these melanocytes are not destroyed by the immune system, rather they are simply swept away, without any effect other than leaving a white patch, as has been observed habitually in clinical practice5.

Psychological consequences

Vitiligo has an enormous impact on quality of life

It is an asymptomatic skin condition that has extremely detrimental effects on patient quality of life, affecting primarily psychological aspects and causing low self-confidence, body image concerns and sometimes hindering social relations4. That is why people with vitiligo constantly search for ways to correct their skin pigmentation, at any age and whatever the form of the disease.

“I have been doing research into vitiligo for 15 years to be able to offer my patients an effective treatment. At last, there’s a solution to this condition,”

- Dr. Matteo Bordignon -

Since the discovery of MIA protein, Dr Matteo Bordignon has been working on this new approach. In collaboration with Laboratorios Bella Aurora, he has succeeded in developing the first efficient treatment for blocking the development of vitiligo and repigmenting white macules.

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1. Bordignon M, Luisetto R, Valente ML, Fedrigo M, Castellani C, Angelini A, et al. Melanoma Inhibitory Activity (MIA) Is Able to Induce Vitiligo-Like Depigmentation in an in vivo Mouse Model by Direct Injection in the Tail. Front Med (Lausanne). 2020 Aug 21;7:430.

2. Bergqvist C, Ezzedine K. Vitiligo: A Review. Dermatology. 2020;236(6):571-592.

3.Taieb A, Alomar A, Böhm M, Dell’anna ML, De Pase A, Eleftheriadou V, et al; Vitiligo European Task Force (VETF); European Academy of Dermatology and Venereology (EADV); Union Europeenne des Medecins Specialistes (UEMS). Guidelines for the management of vitiligo: the European Dermatology Forum consensus. Br J Dermatol. 2013 Jan;168(1):5-19. 4

4. Bellei B, Picardo M. Premature cell senescence in human skin: Dual face in chronic acquired pigmentary disorders. Ageing Res Rev. 2020 Jan;57:100981..

5. Bordignon M, Castellani C, Fedrigo M, Thiene G, Peserico A, Alaibac M, et al. Role of alpha5beta1 integrin and MIA (melanoma inhibitory activity) in the pathogenesis of vitiligo. J Dermatol Sci. 2013 Aug;71(2):142-5.

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