Vitiligo: Symptoms, Causes & Treatment

What is Vitiligo?

Vitiligo is a relatively common disease, causing abnormal pigmentation of the skin. Vitiligo disease is manifested by the presence of well-defined bright spots on the skin.

The formation of these spots on the skin is the result of destruction (damage) dysfunction or inactivity of melanocytes.

Melanocytes are cells that produce the skin pigment. Melanocytes are the cells that produce melanin and are found in the lower part of the epidermis. Melanin is the pigment that gives skin its natural color.

The pigment melanin, which is closely associated with vitiligo, is synthesized in the pigment cells in the skin. This pigment protects the underlying tissues of acute and chronic damage to the ultraviolet radiation.

Melanin protects the skin from the damaging effects of free radicals formed upon irradiation.
Some authors associate the function of melanin to the process of skin adaptation to the environment.

This explains the distribution of human races of the globe depending on the intensity of solar radiation.

Vitiligo is a disease in which the main clinical symptom is a change in pigmentation that affects the skin, hair, and eyes and tends to spread.

Vitiligo is not just a cosmetic defect, it is a disease of the whole body; it should be also considered as that the development which could lead to severe psychological damage.

Vitiligo is damaging the pigment cells and yet it is not entirely clear what is the exact mechanism of the induced damage to these cells. Therefore causes of vitiligo are still not fully clarified. It is considered that the development of the disease is a part of complex factors and mechanisms.

Recent studies discovered that vitiligo not only affects the pigment cells but other cells of the superficial layer of the skin – ie. Keratinocytes (these are highly specialized epithelial cells designed to perform a very specific function, separation of the organism from its environment).

Table of Contents

How does vitiligo look like?

The most characteristic feature of vitiligo is the emergence of chalky or milky white patches on the skin that do not occur immediately after birth but years later.

These spots gradually increase in size and also in number. At the beginning, their color is a lighter than the intact skin and subsequently, their color loses pigment. Therefore, especially in the darker skin, it is possible to observe different shades of color.

The size of the spots varies from a few millimeters to large areas affected by vitiligo. Vitiligo spots are oval or round shaped, well limited by the intact skin, and their boundaries have been incorrectly defined. The boundaries of the spots of vitiligo may have the color of normal skin or it may be darker, or even red.

With the increasing of the size of the spots and the appearance of new spots, some of the lesions may merge.

The appearance of vitiligo usually begins during summer and this is due to the fact that the darkening of the intact skin of vitiligo spots is more noticeable.

Vitiligo affects skin symmetrically but may be located in only one area that meets certain skin segment – dermatome (this is an area mainly supplied by a single spinal nerve).

People who have vitiligo usually have no other symptoms (such as itching or pain). These symptoms can occur after sun exposure or sunburn.

Another feature of vitiligo is that stronger pigmented skin areas such as the back of the hands and feet, face, genitals, neck, armpits, areola of the breast. Usually, the first spots appear around the mouth, eyes, and anus.

Hairs growing on areas affected by vitiligo can be normal colored and white colored with advancing vitiligo.
Studies show that about 40 percent of people with vitiligo have pigment defects in the retina, often without having other complaints.

Some patients are also diagnosed with eye uveitis. In others, there is a premature graying hair process. In rare cases, vitiligo may be associated with deafness.

Vitiligo can proceed stably and does not spread to progress slowly and gradually, or in a short period of time to cover large areas of the skin.

The Koebner phenomenon [15] is another condition which could be related to vitiligo. It is the development of isomorphic pathologic lesions in the traumatized uninvolved skin of patients who have cutaneous diseases.

In people with vitiligo which had became traumatized following an injury often developed lesions in the area, including cuts, bruises, burns, bumps, vaccinations, tattoos and other skin conditions.

Types

Vitiligo is a condition that occurs in a specific way in different people, which determines the presence of different types of vitiligo.

Vitiligo can affect different areas and be differently distributed.
Depending on the degree of involvement and areas affected vitiligo is divided into:

Focal vitiligo

Focal vitiligo is manifested by the presence of one or more white spots in an area, but without a segmental distribution.

Focal Vitiligo
Figure 5: (a) Persisting segmental vitiligo lesion (>8 years) with partial repigmentation showing (b) Degenerating follicles, mild fibrosis and absence of eccrine units (H and E, ×20) Credits: https://openi.nlm.nih.gov

 

Segment (one-sided) vitiligo

Segmental vitiligo is located on one side of the body as white spots are arranged along a certain skin segment (dermatome) and terminate abruptly at the middle of the human body.

Segment Vitiligo
f02: Segmental Vitiligo. Unilateral lesions that respect, almost completely, the bodymidline, characterize segmental vitiligo. There are rare cases of bilateralsegmental vitiligo Credits: https://openi.nlm.nih.gov

Segmental vitiligo is characterized by the stability of the course and rarely spreads beyond the affected areas. This form is rare and usually, begins in childhood.

More than half of the people who have segmental vitiligo have polyose. Polyose is a condition in where there is a white hair strand.

Mucosal vitiligo

Mucosal Vitiligo only affects mucous membranes and is extremely rare. This form of vitiligo should be restricted from other diseases that are more common and where there are white patches on the mucous membranes.

Mucosal Vitiligo
Figure 7: Depigmentation in buccal mucosa, the spreading of vitiligo affect symmetrically both sides of the body. Credits: https://openi.nlm.nih.gov

Generalized vitiligo

In generalized vitiligo the spreading of vitiligo affect symmetrically both sides of the body.

Generalized Vitiligo
Figure 1: A patient with generalized vitiligo. Note the typical pattern of bilateral, multifocal depigmentation of hands and periorbital regions. Credits: https://openi.nlm.nih.gov

Vitiligo Vulgaris – ordinary vitiligo

Vitiligo Vulgaris is characterized by disseminated spreading of the white spots all over the body without the typical affecting of some sections.

Acrofacial vitiligo

AcrofacialVitiligo is characterized by the affected skin of the face, fingers, hands and feet. This is the most common form of vitiligo.

This is a condition in which there is a loss of pigment from areas of the skin resulting in irregular white or light pink spots or patches. The skin has normal texture.

Acrofacial Vitiligo
Figure 4: Acrofacial Vitiligo (a, b and d) with lips showing thick milky white depigmentation and typical histopathological features (c) of progressive LS. Hematoxylin and eosin (H and E, ×20) Credits: https://openi.nlm.nih.gov

Mixed vitiligo

Vitiligo is mixed when it has signs of both vitiligo Vulgaris and Acrofacial vitiligo.

Universal vitiligo

Universal Vitiligo is characterized by the almost complete loss of pigmentation of the skin.
Universal vitiligo is most often combined with multiple endocrine disorders. This is a rare type of vitiligo in which more than 80% of the skin is depigmented.

Universal Vitiligo
Figure: Universal Vitiligo Credits: https://th.wikipedia.org/

Causes

The main theories about the appearance of vitiligo are:

Genetic factors

The involvement of genetic factors [1] in the occurrence of vitiligo is supported by the higher incidence of vitiligo in the family.

However, there are many families in which one of the members is diagnosed with vitiligo, as there are other families where vitiligo appeared in a generation or is more common in more distant relatives.

All these factors suggest that for the vitiligo occurrence genetical factors are involved, and can be combined with other mechanisms. This is the reason why vitiligo is a multifactorial and polygenetic disease.

This, in turn, means that the children of people with vitiligo are not necessarily affected by the disease.

People with vitiligo often have combined symptoms with a specific genetic polymorphism: HLA-DR4, -Dw7, -DR7, -DR1, -B13, -Cw6, -DR53, -A19.

Mutations and signals are found in different chromosomes – 1st, 2nd, 7th, 8th, 11th, 17th, 19th, 22nd.

People with vitiligo usually inherit a set of genes with the impact of various triggers such as stress, trauma, burns and other unlocks disease.

The genetic theory is supported by the fact that in some families there is an increased incidence of autoimmune diseases because what is considered to be the so-called inherited increased susceptibility to autoimmune diseases.

Autoimmune theory and the role of the immunity

The autoimmune theory [2] is supported by the frequent combination of vitiligo with other autoimmune diseases such as Hashimoto’s thyroiditis, Graves’ disease, pernicious anemia, diabetes, gastritis, alopecia areata, psoriasis, Addison’s disease, systemic lupus erythematosus, inflammatory bowel disease, rheumatoid arthritis, autoimmune polyglandular syndrome and others.

Studies about vitiligo confirmed the roles of both cellular and the humoral immunity.
Another supporting data for the autoimmune theory is the discovery of anti-melanocytes antibodies – these are antibodies fighting against their own cells that form the skin pigment.

In support of the autoimmune theory is also the fact that in the process of treatment of melanoma – malignant tumors of the skin, which is formed of pigment cells in the skin – can appear white spots.

Successful treatment of vitiligo is usually performed using medicines that modify the immune response such as corticosteroids, ultraviolet light, cytotoxic drugs.

According to the US National Library of Medicine, about 15 to 25 percent of people with vitiligo are also affected by at least one other autoimmune disorder, particularly autoimmune thyroid disease, rheumatoid arthritis, type 1 diabetes, psoriasis, pernicious anemia, Addison disease, or systemic lupus erythematosus.

Oxidative stress

Some studies suggest that oxidative stress [3] is at the root causes of the destruction of the cells that form the skin pigment.

Studies based on the role of oxidative stress are supported by a number of changes in the skin and in the blood test results of vitiligo patients.

There are increased levels of hydrogen peroxide and decreased levels of catalase, but the results also indicate low levels of catalase, and glutathione and elevated levels of superoxide dismutase and xanthine oxidase.

Autotoxic theory

The autotoxic theory is also known as the theory of self-destruction of cells that form pigment.

According to this theory, vitiligo occurs when melanocytes form large amounts of cytotoxic aldehydes – compounds that are precursors of melanin. This leads to autodestruction- self-destruction of cells that form the pigment.

Autotoxic theory can be explained by the way vitiligo affects industrial workers who are facing impact with catechol, phenols and sulfhydryl groups – substances contained in the chemical and cleaning agents.

Neural theory

Melanocytes – cells that form the pigment are in contact with the endings of the nerve fibers. According to the neural theory [4], some melanocytes are damaged by mediators that are released by nerve endings.

In these areas where the connection is impaired, increased sweating is indicated, which is a sign of autonomic dysfunction.

The existence of neural theory is supported by the presence of segmental vitiligo. In this form of vitiligo, changes are localized in certain skin segments.

Virus infections

There is a confirmed presence of the cytomegalovirus (CMV) in the skin of vitiligo patients. This virus can be detected in the healthy skin and in the places where white spots are available [5].

People who are not affected by vitiligo do not have the virus cytomegalovirus.

There is evidence of the involvement of another virus – herpes simplex virus (HSV).
Based on these data is created and hypothesis to the participation of virus infection to onset of vitiligo.

Can vitiligo be combined with other diseases?

Vitiligo is a disease which frequently occurs in association with other diseases. It is, therefore, necessary to test whether other diseases are present.

These diseases may occur after the appearance of vitiligo or may precede vitiligo symptoms.

The most common combination is vitiligo and autoimmune diseases. Since autoimmune diseases are primarily thyroid diseases – up to 40%, usually there is a reduced function of the gland.
Vitiligo most often can be combined with the following diseases:

Endocrine diseases

From endocrine disorders the most common autoimmune is the thyroid disease:

  • Hashimoto’s thyroiditis
  • Graves’ disease

Usually, the symptoms of vitiligo disease precede the symptoms of thyroid gland disease.
Furthermore, vitiligo may take place simultaneously with other endocrine diseases such as:

  • Addison’s disease
  • Type 1 diabetes
  • Hypoparathyroidism
  • Polyglandular autoimmune (PGA) syndrome

Autoimmune or systemic diseases

Vitiligo can be combined with other autoimmune or systematic diseases such as:

  • Pernicious anemia
  • Gastritis
  • Myasthenia gravis
  • Lichen sclerosis
  • Systemic lupus erythematosus
  • Inflammatory bowel disease
  • Rheumatoid arthritis

Other skin diseases

Vitiligo can be combined with other skin diseases. The reason for such combination is due to various factors, which include the autoimmune mechanisms.

Vitiligo can flow together with the following skin diseases:

  • psoriasis
  • alopecia areata
  • halo nevus
  • malignant melanoma

The occurrence of vitiligo in malignant melanoma or during treatment of such disease is considered a good sign for the prognosis of the disease and the effect of the therapy.

Engaging melanocytes outside the skin

Vitiligo is a disorder affecting melanocytes (cells which form the pigment) and therefore, in addition to the skin, the condition can also affect the hair, eyes, inner ear and the meninges of the brain.

Therefore, vitiligo can pe present in combination with:

  • Polyose – presence of white hair strand
  • Premature graying of hair
  • Hearing violation or eyesight violation
  • Pigment disorders of the iris and the retina
  • Choroiditis
  • Uveitis
  • Aseptic meningitis

Vitiligo and rare syndromes

Although it is very rare, vitiligo can be part of the so-called. syndromes, or a combination of different disabilities.

Syndromes that include vitiligo usually have characteristic manifestations and diagnosis ca be made early.

The most common syndromes with vitiligo are:

  • Syndrome Alezandrini (Alezzandrini) Syndrome

Syndrome Alezandrini includes vitiligo on the face, polyose, deafness, unilateral retinal degeneration.

  • Vogt-Koyanadzhi-Harada (Vogt-Koyanagi-Harada) syndrome

Syndrome, Vogt-Koyanadzhi-Harada includes a combination of vitiligo uveitis, aseptic meningitis, diakuzis, tinnitus, polyose, and alopecia.

What are the risk factors leading to the occurrence of vitiligo?

Usually, people with vitiligo share various factors which are thought to have a connection with the onset of the disease. Preventing your skin from the risks of various factors can delay and even prevent the occurrence of white spots.

People with vitiligo are born with normal pigment. Vitiligo is not a disease such as albinism, which is congenital. At a certain point, the cells that produce the skin pigment stop doing it and the on the skin start appearing white spots.

The appearance of white spots requires consultation with a dermatologist. This will provide with easier individual treatment for each patient based on the factors that have triggered the initial symptoms.

The most frequently reported risk factors in vitiligo are:

Stress

Stress is a factor that is most often discussed as provocative for the appearance of vitiligo.
Almost everyone with vitiligo reported prior psycho-emotional trauma of various origin.

Psychological discomfort is additionally distorted by the cosmetic effect of vitiligo.

Each person with vitiligo is advised to take steps to reduce the stress levels because it has a favorable influence on the course of the disease.

Sun exposure

Very often people with vitiligo claim to have noticed its appearance after summer vacation or after an active sun exposure. The reasons for this may be different.

If the disease is already active the sun exposure usually makes more obvious the difference between the affected and the unaffected skin. Do not exclude the role of the influence of oxidative stress after sun exposure.

People with vitiligo are subjected to deliberate sunbathing because it is a widespread perception that sun exposure may reduce the symptoms. According to Genetic and Rare Diseases Informational Center: Up to 30% of vitiligo patients report some spontaneous repigmentation, particularly in areas of the body that receive a lot of sun exposure.

People with vitiligo are advised to be extremely careful while taking sunbaths. If you do not take the necessary measures such as the application of sunscreen or wearing appropriate clothing, the affected areas may increase their sizes.

To adequately protect the skin, it is necessary to use sunscreen with a high protection factor (SPF> 30) and the exposure should be limited to one hour or less.

Skin injuries

Traumas of various kinds of injuries are also commonly cited as risk factors for the appearance of vitiligo. Scratches, puncture, thermal or chemical burns, contact with various chemicals also can provoke the occurrence of vitiligo, especially in places where the injurious factor is available.

Some chemicals such as phenols, industrial substances, and even photographic chemicals may trigger the onset of vitiligo in people who are predisposed to the disease. People who already have vitiligo should avoid such chemicals and strive to reduce all injuries on the skin.

Family history

It is believed that there is a greater risk for people have a family history related to vitiligo, early graying of hair or other autoimmune diseases.

Vitiligo is polygenetic disease and its appearance depends on many other factors. Therefore, if a family member has vitiligo it does not necessarily mean that the disease will spread to other family members.

The age groups between 10 and 30 years of age are considered the riskiest.

Some autoimmune diseases

Often people with vitiligo are suffering from various autoimmune diseases.
Of all autoimmune diseases, the usual combination of vitiligo is with autoimmune thyroid disease.

Vitiligo may be both preceding the disease and appearing after the emergence of another autoimmune disease.

From which diseases should vitiligo be distinguished?

Vitiligo diagnosis is usually not difficult to be placed by a dermatologist. The most common problem challenge is to exclude or confirm the diseases associated with vitiligo.

Although the diagnosis of vitiligo can be easily placed by a dermatologist, it may still be possible to discuss other diseases in the differential diagnosis plan before the final diagnosis is made. In the case of such doubts, some research needs to be done.

The most common diseases which could be associated with vitiligo are:

Pityriasis Versicolor

The most common differential diagnosis of vitiligo is made with the Pityriasis Versicolor.

One of the manifestations of the Pityriasis Versicolor is white spots on the skin of the chest and the back. These spots are usually covered with fine flakes and are accompanied by pruritus.

It can be very easy to distinguish these disease using a native preparation that is reviewed under the microscope – threads and spores can be easily distinguished by a Wood Lamp [6].

Postinflammatory hypopigmentation

Postinflammatory hypopigmentation is a process that is characterized by discoloration of the skin at the areas, where various damaging factors are destroying the skin pigmentation:

  • Traumas;
  • An inflammatory or other disease processes;
  • Chemical effects.

Postinflammatory hypopigmentation is more typical for people with a darker skin color and tends to improve over time and restore normal pigmentation to the affected areas.

Postinflammatory hypopigmentation enters the differential diagnosis of vitiligo when the hands are affected, as well as the palms and the face.

White lichen

White lichen or pityriasis alba most often comes into consideration when affecting the face or the upper limb.

A characteristic feature of the white lichen is that it usually affects children, especially the cheeks area. Pityriasis alba has not well-defined borders and swelling. These peculiarities distinguish the condition from vitiligo.

Pityriasis
Figure 1: Lesions involving the face and orientated along lines of skin cleavage. Source: www.openi.nlm.nih.gov

Usually, white lichen can be confused with vitiligo. For people with darker skin, the most common manifestations come together with atopic dermatitis. The white lichen undergoes a reversal of the symptoms.

Lichen sclerosis et atrophic

When affecting the anogenital area (ie, the area around the anus and intimate parts), the most frequent differential diagnosis is lichen sclerosis et atrophic.

Lichen sclerosis et atrophic
Figure 1: (A) Well-demarcated hypopigmented patches without surface changes on the right abdomen. (B) Multiple hypopigmented papules and plaques occurring with atrophic surface change and hardening on the left abdomen. The lesions shown in both (A) and (B) had occurred spontaneously 3 years ago. (C) Histology demonstrates marked fibrosis with edema in the upper dermis, suggesting lichen sclerosus et atrophicus (H&E, ×40). (D) Higher magnification shows epidermal hyperkeratosis, superficial perivascular lymphohistiocytic infiltrate, and homogenization of the dermal collagen in the superficial dermis (H&E, ×100). Credits: www.openi.nlm.nih.gov

In a case of suspected lichen sclerosis et atrophic necrosis, it is necessary to carefully assess the density of the stained areas and to take a skin biopsy.

Lichen sclerosis et atrophic is a disease that occurs more often in women in the 5th and 6th decades, unlike vitiligo that occurs earlier. In men, lichen sclerosis et atrophic is very often the cause of onset phimosis over time.

Congenital diseases

Some congenital illnesses also come under the differential diagnosis of vitiligo. Such diseases are:

  • Piebald – the presence of white hair in combination with depigmentation of the skin.
  • Nevus depigmentosus – causing the presence of white blotch from birth resulting from impaired transport of pigment granules.
  • Nevus anemicus – the presence of a white spot resulting from narrowing of the blood vessels.

A characteristic feature of congenital illness is their manifestation at birth or early childhood. In addition, these innate diseases have no tendency for progression. Vitiligo occurs later and has a tendency for progression.

Leprosy

Leprosy is a disease that can be found in particular regions, but there are countries where this disease is considered in the differential diagnosis of vitiligo.

In leprosy, the affected skin areas are also characterized by defecation. In addition, leprosy is characterized by many other changes depending on the type of disease.

Cutaneous lupus erythematosus

Discoid lupus erythematosus is a chronic form of cutaneous lupus erythematosus, which can be localized or generalized. Women are more prone to developing the disease. Discoid lupus erythematosus is usually diagnosed in people between 20 and 40 years of age.

Lupus Erythematosus
fig5: Subacute cutaneous lupus erythematosus Source: www.openi.nlm.nih.gov

Clinically, it appears with red flaking papules or plaques that leave pigmentation, atrophic and white scars. Lesions are usually asymptomatic but may be manifested with mild itching or pain.

Discoid lupus erythematosus primarily affects areas exposed to sunlight such as cheeks, nose, ears, upper back, neck and the back of the palms.

The scalp can also be affected and this leads to permanent alopecia with scars. It can rarely appear on the palms or feet.

Differentiating signs of vitiligo discoid lupus erythematosus include a hyperpigmented, infiltrated ring around the leukoderma, follicular channel obstruction (follicular hyperkeratosis), scarring and alopecia.

The lesion biopsy is positive for direct immunofluorescence (e.g., basal membrane). Hyperkeratosis with perivascular lymphocyte infiltrate in the dermis is established.

Progressive macular hypomelanosis

Progressive macular hypomelanosis is characterized by the presence of areas with reduced pigmentation on the back, chest, and abdomen of younger patients.

Progressive Macular Hypomelanosis
fig1: (a) Disseminated whitish macules on the front and the back of the trunk. (b) Nonscaly macules in detail on the back. Source: www.openi.nlm.nih.gov

The skin biopsy shows a reduced amount of pigment in the epidermis, but there is also the presence of melanocytes and skin with normal appearance.

Wood Lamp Study shows orange fluorescence due to the presence of Propionibacterium acnes.
Electronic microscopy shows a change from large melanosomes in the normal-looking skin to small, joined, membrane-bound melanosomes in the hypopigmented skin.

Leukoderma associated with melanoma

Leukoderma associated with melanoma may be unrecognizable to vitiligo. The review found a history of melanoma, leukoderma at the site of excision, melanoma or metastasis.

The biopsy of melanocytic lesions may indicate a loss of pigmentation in primary lesions and a non-concentrating hypopigmented macule.

Tuberculous sclerosis

Tuberous sclerosis is characterized by hypopigmented leaf-shaped macules, convulsions, angiofibromas and mental retardation. Lesions are usually affecting the chest and legs.

After a Wood Lamp study, hypopigmentation and incomplete pigment loss could be detected.

Corticosteroid-induced dermatopathy

In corticosteroid-induced dermatopathy, an undetermined hypopigmentation, localized in the field of topical corticosteroid therapy, associated dermal and epidermal atrophy, telangiectasia, purpura, is observed. Diagnosis is clinical.

Diagnosis

Vitiligo diagnosis is usually not a challenge for a skin specialist.
Several studies are required to confirm or exclude the diagnosis.

Vitiligo is a disease that can be combined with other illnesses, and therefore, sometimes, additional research is needed to define the diagnosis.

Routine physical examination

The routine examination conducted with vitiligo include a review with a detailed history of:

  • The onset of the disease;
  • Data about the deterioration with progress and engagement of new areas;
  • Risk factors that have triggered the onset of the disease or its deterioration;
  • Vitiligo affecting other members of the family;
  • Type of skin;
  • The presence of other white spot areas;
  • Photosensitivity data;
  • Emotional impact;
  • The existence of other complaints except for the presence of white spots;
  • Is treatment being carried out and was it effective?
  • Medication intake;
  • Exposure to household chemicals or occupational conditions causing damaging of the skin

Diagnosis of vitiligo can only be done with a clinical examination by a specialist. During the physical examination, the rate of skin involvement is observed, whether it affects the hair, whether there is early hair coloring or changes in some moles.

The recommended routine tests that are performed include sediment study, blood count, differential blood count, biochemical tests for blood sugar, liver function as well as autoantibody testing – antinuclear antibodies, antithyroglobulin antibodies, parietal cell antibodies.

The Wood Light Study is a study where the surface of the skin is examined with an ultraviolet light.
When testing for vitiligo, mucous membranes should also be examined.

The Wood Lamp study with vitiligo is very important because it allows to better assess the extent of skin involvement, especially in people with lighter skin. Not all white stains stand out well from the intact skin when examining people with lighter skins.

Skin biopsy

The skin biopsy is a manipulation that takes a small piece of skin, and then this piece of skin is examined under a microscope.

The skin biopsy taken from a white plaque is done to confirm vitiligo and/or to exclude another disease where skin changes may be resembling white patches.

Thyroid gland exam

Thyroid exam is part of vitiligo screening.
The association of vitiligo with thyroid disease is very common and is present in up to 40% of all people who have vitiligo.

The thyroid test screen enters the THD (thyroid stimulating hormone) test. In addition to THD, thyroid hormone Thyroxine and triiodothyronine (T3 and T4) are also examined. When thyroid abnormalities are detected, the treatment of the thyroid gland is performed by an endocrinologist.

Eye tests

Eye tests are not usually performed for people who have vitiligo. However, it is estimated that about 40% of vitiligo people have subclinical pigmentary retinal abnormalities.

The human eye contains pigment cells – melanocytes.Because of that reason that it is possible for people with vitiligo to have eye damage.

What is the prognosis for Vitiligo?

Vitiligo is a disease that leads to psychological discomfort. The prognosis for the course of the vitiligo disease is unpredictable. The initial appearance of changes in the skin cannot predict the further course of the disease.

Depending on the course of the disease, vitiligo may be:

Stable – no new spots appear on the skin over time;
Progressive – there is a continuous appearance of new skin spots over time.

Depending on the course of vitiligo, different treatment is needed.
Spontaneous recovery of skin pigmentation is unlikely to occur.

When vitiligo affects large areas of the body, then there is a risk of skin damage from the sun’s rays and the appearance of actinic keratoses or other types of damage.

People with vitiligo who have a visual impairment may experience poor quality of life.
Long-term vitiligo symptoms do not suggest a possibility of spontaneous recovery of skin pigmentation and the potential effect of applied therapy is small.

People who have atopic dermatitis usually have a heavier flow of vitiligo.
In the summer months, vitiligo symptoms usually improve.

The most common restoration of skin pigmentation in vitiligo begins around the hair follicles.

Treatment of vitiligo

Various means can be chosen for the treatment of vitiligo. The choice of treatment is determined by the areas and extent of involvement, the duration of the disease, and the age of the patient.

It is also important whether the disease has a progressive stroke or whether it is stable. The natural skin color is also important.

In cases where vitiligo is combined with other diseases, it is also necessary to treat the accompanying diseases.

The various treatment methods have their advantages and disadvantages. There is no universal approach and universal treatment.

The main approaches to treatment can be divided into the following groups:

Daily application of cosmetic products

Medical corrective makeup

The purpose of medical corrective makeup is to cover the imperfections. Medical corrective makeup [7] can be applied to both women and men to the face and body. The specifications required for a medical makeup are: not to leave stains on clothes and have a safe formula – hypoallergenic and non-comedogenic.

Applying medical make-up is very appropriate for people who are unwilling to receive treatment.
The application of such cosmetics has the advantages that it is cheap, almost no side effects and is easy to apply.

Autobronzants can also be used to achieve artificial tanning.

Sun protection

The use of sun protection products helps to avoid burning of the skin affected by vitiligo.
The use of sunscreen prevents the appearance of cancer, as well as any damage that can cause the sun.

The application of sunscreen reduces the contrast between the affected and the normally pigmented skin can be avoided.

Restore skin pigmentation

Restoration of pigmentation of the skin [8] with vitiligo can be done using different local and systemic means.

Corticosteroids

In the treatment of vitiligo, corticosteroids may be applied.
The use of systemic corticosteroids is not recommended.

Generally, they could be used in particular cases with strict indications, such as the occurrence of a rapidly progressive vitiligo, and it is necessary to stabilize the condition.

The use of topical corticosteroids [9] is widespread in people who have single and limited lesions.
People with darker skin should expect better effect from the application of topical corticosteroids.

Treatment with topical corticosteroids usually takes 4 to 6 months. Unfortunately, after stopping such treatment, there is a risk of relapse, as well as side effects.

Local immunomodulators

Local immunomodulators used to treat vitiligo are calcineurin inhibitors – pixelrolimus and tacrolimus.
Their effectiveness is considered to be higher when combined with UVB or Excimer laser.

The use of calcineurin inhibitors in children is safer than corticosteroids. The course of treatment with calcineurin inhibitors is also long – of about 6 months.

Another advantage of the calcineurin inhibitors is that they are safe to use for long-term treatment compared to topical corticosteroids.

Local calcipotriol

Local calcipotriol may be used in vitiligo at a concentration of 0.005%. Local calcipotriol is a synthetic analog of vitamin D3.

Topical treatment with calcipotriol may also have a good effect on vitiligo.
To achieve a faster effect, it is recommended to combine with topical corticosteroids or UV therapy.

Pseudocatalase

Catalase is an enzyme that can be detected normally in the skin. This enzyme reduces skin damage caused by free radicals. There is a scientific evidence that in the skin of people with vitiligo the enzyme catalase is lowered.

Pseudocatalase [10] is administered for the treatment and the aim is to replace the normal enzyme. Pseudocatalase is used in combination with UVB 311. Pigmentation can be restored and disease progression prevented.

UVB therapy

The most commonly used therapy for minimizing the symptoms of generalized vitiligo is the phototherapy with UVB 311 nm narrowband phototherapy.

It is believed that the effect of this type of therapy is due to local immunosuppression, stimulation of melanocyte-stimulating hormone formation, increased melanocyte proliferation and acceleration of the pigment formation process.

The advantages of narrow-band UVB phototherapy are due to the safety way of use for both adults and children. This therapy is not toxic, no additional eye protection is required during the procedure.

UVB phototherapy [11] shows greater effectiveness than PUVA treatment and is also less likely to have side effects.

Excimer Laser

In the treatment of localized vitiligo, usually, an excimer laser [11] is the most proper therapy. The Excimer Laser is a device that generates UVB rays with a wavelength of 308 nm.

Treatment with an excimer laser can be combined with calcineurin inhibitors and is very appropriate in acro pharyngeal vitiligo. A better effect is achieved on the facial area comparing to the palms and soles.

The excimer laser treatment course is three times a week for at least 12 weeks.

PUVA therapy

PUVA therapy [12] can be done with systemic or local means. PUVA treatment uses substances called psoralens. Oral psoralens can be orally or locally administrated (by spraying).

Psoralens are photosensitizing substances which should be combined with the use of UVA rays – ultraviolet rays with a wavelength of 320 nm to 400 nm.

PUVA therapy is performed 2-3 times a week. Conducting PUVA therapy is associated with side effects and is therefore no longer one of the commonly used vitiligo treatment methods.

Beta-carotene

The use of beta-carotene [13] can cause pigmentation of the skin (yellow-orange shade). This is due to the accumulation of vitamin in the stratum corneum.

Beta-carotene therapy starts with a dose of 25 mg 3 to 5 times a day, and after 4-5 weeks the dose is reduced twice daily.

The use of beta-carotene is contraindicated in the presence of kidney or liver disease. Beta-carotene treatment is suitable for people with light skin and is pointless for people with dark skin.

Note that obtaining a yellow-orange nuance of the skin is not always a cosmetically acceptable result.

Combined treatment methods

Increasingly popular treatment of vitiligo is the simultaneous use of different treatment methods. Combination therapy [14] can achieve a better effect and reduce the risk of relapse after cessation of treatment.

Each of the therapeutic approaches is applied over an extended period of time. The most commonly used combined treatment methods include the use of various lubricants with any of the methods of treatment with UV rays.

The choice of combination therapy depends on the area of concern, the area of involvement, age, disease progression and natural skin color.

Pigment cell transplantation

One of the newest approaches to vitiligo treatment is the transplantation of pigment cells.

There are various techniques for cultivating and transferring pigment cells which may be applied, and pigmentation restoration occur at the areas affected by vitiligo.

Pigment cell transplantation [15] is a suitable treatment method for vitiligo that is stable in the course and there is no formation of new plaques. In addition, transplantation can be performed on a skin that does not tend to form hypertrophic scars and keloids (rough and enlarged scars).

Depigmentation of the skin

Depigmentation of the skin affected by vitiligo is only applicable to certain indications such as generalized vitiligo involvement – at least 50% of the skin surface, especially in combination with a naturally dark skin color.

The choice for such treatment should be left as the last therapeutic option.
The agent used to depigment the skin all over the world is hydroquinone mono benzyl ether. This drug achieves a permanent depigmentation of the skin as a result of the destruction of skin pigment cells – melanocytes.

There is a risk of itching, allergic or irritant reactions.
For depigmentation, a laser could be used as a ruby Q-switched laser.

References

  1. The genetics of Vitiligo
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3513341/
  2. Understanding Autoimmune Diseases
    https://www.niams.nih.gov///Health_Info/Autoimmune/default.asp
  3. Study of Oxidative Stress in Vitiligo
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068765/
  4. Highlights in pathogenesis of vitiligo
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360494/
  5. Hepatitis C Virus Antibodies and Vitiligo Disease
    http://ijph.tums.ac.ir/index.php/ijph/article/viewFile/1875/1856
  6. Wood’s lamp examination
    http://www.floridahealthfinder.gov/healthencyclopedia/Health%20Illustrated%20Encyclopedia/1/003386.aspx
  7. Interest of corrective makeup in the management of patients in dermatology
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3459545/
  8. Vitiligo Skin Transplantation (MKTP)
    https://clinicaltrials.gov/ct2/show/NCT00830713
  9. The treatment of vitiligo with topical corticosteroids. Light and electronmicroscopic studies
    https://www.ncbi.nlm.nih.gov/pubmed/773413
  10. The effect of pseudocatalase/superoxide dismutase in the treatment of vitiligo: A pilot study
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076862/
  11. The efficacy of excimer laser (308 nm) for vitiligo at different body sites.
    https://www.ncbi.nlm.nih.gov/pubmed/16684284
  12. Topical PUVA therapy for vitiligo.
    https://www.ncbi.nlm.nih.gov/pubmed/1828681
  13. Beta-carotene
    https://medlineplus.gov/druginfo/natural/999.html
  14. Topical treatment and combination approaches for vitiligo: new insights, new developments.
    https://www.ncbi.nlm.nih.gov/pubmed/20197746/
  15. Vitiligo and the Koebner Phenomenon (Model of Vitiligo Induction and Therapy: a Clinical and Immunological Analysis) (Koebner)
    https://clinicaltrials.gov/ct2/show/NCT01082393

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