What is Vitiligo?

Vitiligo is a common acquired localized or generalized skin depigmentation disorder. Caused by the disappearance of melanocyte function in the skin, but the mechanism is still unclear. It can occur in all parts of the body, and is common in the back of the fingers, wrists, forearms, face, neck, and around the genitals. Female vulva can also occur, mostly young women.

Basic Information

English name: vitiligo
Visiting department: dermatology
Multiple groups: teens
Common locations: Back, wrist, forearm, face, neck

Common causes: unknown
Common symptoms: The skin lesion is milky white, the surface is smooth without rash, and the white spots are clear
Contagious: no

Causes of Vitiligo

The cause of the disease is unknown. In recent years, research has suggested that it is related to the following factors:

Genetic theory

Vitiligo can appear in twins and families, indicating that heredity plays an important role in the pathogenesis of vitiligo. Studies have suggested that vitiligo has incomplete penetrance and that there are multiple pathogenic sites on the gene.

2. Autoimmune theory

Vitiligo can be combined with autoimmune diseases such as thyroid disease, diabetes, chronic adrenal insufficiency, malignant anemia, rheumatoid arthritis, and malignant melanoma. Antibodies specific to various organs can also be detected in the serum, such as anti-thyroid antibodies, anti-gastric wall cell antibodies, anti-adrenal antibodies, anti-parathyroid antibodies, anti-smooth muscle antibodies, anti-melanocyte antibodies, etc.

3. Spiritual and neurochemical theory

Psychological factors are closely related to the onset of vitiligo. Most patients have trauma, excessive tension, depression or depression during the onset or development of skin lesions. There are degenerative changes in the nerve endings at the leukoplakia, which also supports the neurochemical theory.

4. Melanocyte self-destruction theory

Vitiligo patients can produce antibodies and T lymphocytes, indicating that the immune response may cause destruction of melanocytes. Toxic melanin precursors synthesized by cells and certain chemicals that cause skin discoloration may also selectively destroy melanocytes.

5. Trace element deficiency theory

Patients with vitiligo have reduced levels of copper or ceruloplasmin in their blood and skin, resulting in reduced tyrosinase activity, which affects melanin metabolism.

6. Other factors

Trauma, sun exposure, and some light-sensitive drugs can also induce vitiligo.

Clinical manifestations of vitiligo

There is no significant difference in gender, and the disease can occur in all age groups, but it is more common in adolescents. The skin lesions are depigmented pigmentation, often milky white or light pink, with a smooth surface and no rash. The condition of white spots is clear, the pigment on the edges is increased compared with normal skin, and the hair inside the white spots is normal or white. Lesions are more likely to occur in areas exposed to sunlight and friction, and the lesions are more symmetrically distributed. White spots are often arranged in bands according to the distribution of nerve segments. In addition to skin damage, the mucous membranes of the lips, labia, glans and medial foreskin are also frequently affected.

Most of the patients have no conscious symptoms, and a small number of patients have local itching before or at the same time. Vitiligo is often accompanied by other autoimmune diseases, such as diabetes, thyroid disease, adrenal insufficiency, scleroderma, atopic dermatitis, and alopecia areata. The specific types are as follows:

Limited type

(1) Focal type One or more white spots are confined to one area, but are not distributed in segments;

(2) Unilateral type (segmental type) One or more white spots are distributed in segments and disappear suddenly at the midline;

(3) Mucosal type Only the mucosa is involved.

2. scattered

(1) Vulgaris widely and scattered white spots;

(2) Facial extremities are distributed on the face and limbs;

(3) Mixed type Segmented type, facial acral type and / or common type mixed distribution.

3. Pan hairstyle

Total or almost all pigment loss.

More than 90% of the vitiligo is scattered, and the remaining vitiligo is more localized than pan-type.

According to the loss of pigmentation at the lesion, the disease can be divided into two types: complete and incomplete. The former had a negative response to dihydroxyphenylalanine (DOPA), melanocytes disappeared, and the response to treatment was poor. The latter responds positively to DOPA. The number of melanocytes does not disappear, but the number is reduced, and the chance of cure is high.

Differential diagnosis of vitiligo

Anemia mole

Symptoms since childhood, more common in the face, are light-colored spots, irritation friction does not locally red, and the surrounding skin red.

2. White pityriasis

It may be related to dry skin and sun, showing hypopigmented spots, unclear edges, and a few white scales on the surface.

3. Pigmentless mole

Onset or shortly after birth, skin lesions are localized pale spots with jagged edges.

4. Tinea versicolor

The damage occurred in the trunk and upper limbs, with pale white round or oval spots, unclear borders, fine scales on the surface, and positive fungal examination.

5. Albinism

It is a congenital non-progressive disease and often has a family history. The skin and hair of the whole body lack pigment, the iris is transparent in both eyes, the choroid pigment disappears, and it is easy to identify with vitiligo.

6. Leprosy white spot

For incomplete hypopigmentation spots, unclear borders, disappearance of surface sensation, and other symptoms of leprosy.

7. White spots of syphilis

Occurs in the neck, is not pure white, and is seropositive for syphilis.

8. Other

It should also be distinguished from discoid lupus erythematosus and leukoplakia.

Vitiligo complications

The common complications are uveitis, severe uveitis is seen in Vogt-Koyanagi-Harada (VKH) syndrome, and rare complications are Alezzandrini syndrome (eye-skin-ear syndrome).

Vitiligo Treatment

Hormone therapy

(1) Systemic treatment is mainly applicable to patients with pancreatic advanced vitiligo. Oral or intramuscular injection of hormones can stabilize advanced vitiligo as quickly as possible.

(2) Topical treatment of topical glucocorticoids is effective for the treatment of localized vitiligo, but attention should be paid to the adverse reactions caused by long-term topical glucocorticoids. The commonly used drugs in clinical practice include Halomethasone ointment, Mometasone furoate cream, and the like.

2. Phototherapy and photochemotherapy

(1) Light therapy with narrow-wave ultraviolet (NB-UVB) has a certain effect on localized or generalized vitiligo.

(2) Photochemotherapy (PUVA) For localized application of furan coumarins (8-MOP, psoralen) + sun exposure in localized vitiligo is a better treatment option, and can be used for adults and 5 years old Children above.

3. Transplantation

It is suitable for those with stable skin, few skin lesions and few scars. Common methods include autologous epidermal transplantation, microdermal grafting, and autologous melanocyte transplantation.

4. Immunosuppressive

For sites that are not suitable for hormone use, or to avoid long-term adverse effects of hormone application, topical calcineurin inhibitors (tacrolimus, pimecrolimus) have certain effects.

5. Vitamin D ₃ derivatives

Vitamin D ₃ derivatives can be combined with NB-UVB, PUVA and other treatments. It can also be combined with topical hormones and calcineurin inhibitors.