I. Etiology
The cause of disease pathogenesis is not clear. In recent years, studies have concluded that the following factors are involved.
1, genetic theory
The most important thing is that you can get a good idea of what you want to do. The study believes that vitiligo has an incomplete epiphenomenon rate and there are multiple pathogenic loci on the gene.
2, autoimmune theory
The most important thing is that you can find the best way to get the most out of your vitiligo. The serum can also detect many organ-specific antibodies, 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, mental and neurochemical theory
The psychological factors are closely related to the development of vitiligo, most patients have trauma, excessive tension, depression or frustration at the stage of initiation or lesion development. The nerve endings at the white spots have degenerative changes, which also support the neurochemical theory.
4, melanocyte self-destruction theory
Vitiligo patients can produce antibodies and T lymphocytes in their bodies, indicating that the immune response may lead to the destruction of melanocytes. The toxic melanin predecessors and certain chemicals that cause skin depigmentation may also have selective destructive effects on melanocytes.
5, trace element deficiency theory
The level of copper or copper blue protein in the blood and skin of vitiligo patients is reduced, resulting in lower tyrosinase activity, thus affecting the metabolism of melanin.
6, other factors
Second, clinical performance
The actual fact is that there is no significant difference in gender, all age groups can develop, but the adolescents are more likely to occur. The skin lesions are pigment loss spots, often milky white, can also be light pink, smooth surface without rash. The white patches are well-defined, with increased pigmentation at the edges compared to normal skin, and normal or whitened hair within the patches. The lesions tend to occur in areas exposed to sunlight and abrasive damage, and are mostly symmetrically distributed. The lesions are often symmetrically distributed and often arranged in bands according to the distribution of nerve segments. In addition to skin lesions, the lips, labia, glans and inner mucosa of the foreskin are often involved.
The disease has no conscious symptoms, but a few 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, baldness, etc. The specific subtypes are as follows.
1.Limited type
(1) Focal type One or more white spots are confined to one area, but not in segmental distribution;
(2) Unilateral type (segmental type) One or more white spots are segmentally distributed and suddenly disappear at the midline;
(3) Mucous membrane type Only the mucous membrane is involved.
2.Dispersed type
(1) Common type Extensive and scattered white spots;
(2)Facial and limb type
(3) Mixed type with mixed distribution of segmental type, facial limb type and/or common type.
3. Pancytopenia
Total or almost total depigmentation.
More than 90% of vitiligo is scattered type, and the remaining vitiligo is more limited type than generalized type.
The most important thing is that it is not only the most common type of disease, but also the most common type of disease. The former reacts negatively to DOPA, melanocytes are lost, and treatment response is poor. The latter is positive for DOPA and the melanocytes are not lost but only reduced in number, which has a high chance of cure.
Differential diagnosis
1.Anemic nevus
It is a light-colored spot with no local reddening by stimulation and friction, but the surrounding skin is red.
2.White furuncle
It may be related to dry skin and sun exposure, and it shows hypopigmented spots with unclear edges and a small amount of white scales on the surface.
3.Non-pigmented nevus
It develops at birth or soon after birth, and the lesion is a limited pale white spot with jagged edges.
4.Plaque ringworm
The damage occurs on the trunk and upper limbs, and is a pale white round or oval patch with unclear borders and fine scales on the surface, with positive fungal examination.
5.Albinism
It is a congenital non-progressive disease, often with family history, lack of pigmentation of the circumferential skin and hair, transparent iris of both eyes, and loss of choroidal pigmentation, easily distinguished from vitiligo.
6, lepromatous leukoplakia
Incomplete hypopigmented spots with unclear borders and loss of surface sensation, with other symptoms of leprosy.
7.Phase II syphilis white spots
Occurs in the neck, not pure white, syphilis seropositive.
8.Other
It should also be distinguished from discoid lupus erythematosus and mucosal leukoplakia.
Complications
It is often complicated by diabetes, pernicious anemia, baldness, atopic dermatitis, thyroid disease, primary adrenal cortical insufficiency, scleroderma, malignant tumor, etc.
V. Treatment
1.Drug treatment
(1) Psoralen and its derivatives such as methoxsalen orally followed by ultraviolet radiation.
(2) Large doses of vitamins such as vitamin B, vitamin C, vitamin P long-term use.
(3) Useful treatment such as drugs containing copper Such as 0.5% copper sulfate solution taken orally.
(4) Immunomodulators Levamisole orally, lyophilized BCG vaccine (BCG) intramuscularly, oral bovine placenta, etc.
(5) skin stimulants local rubbing make the skin inflammatory reaction, promote pigmentation, commonly used are 30% tincture of bone marrow, nitrogen mustard alcohol, phenol (pure carbolic acid), 25% to 50% trichloroacetic acid, spotted tincture, etc.. This method is only applicable to small lesions, and large blisters can appear at the lesions after application.
(6) Corticosteroids Various corticosteroids such as beclomethasone propionate ointment, halometasone cream, deinflammatory pine urea ointment and other local sealing package treatment.
2.Surgical treatment
Autologous epidermal transplantation is feasible for patients with stable lesions without progress.
3.Depigmentation therapy
It is suitable for those with large skin lesions, more than half of the body surface area, and can be applied externally with 3%-20% hydroquinone monoanisole cream.
4.Physical therapy
Narrow-wave ultraviolet light, long-wave ultraviolet light or 308nm excimer laser treatment.
Sixth, prevention
1, reduce the intake of contaminated food, correct partial diet, develop scientific dietary recipes.
2, reduce the inhalation of harmful gases, choose a place with fresh air for morning exercise or sports.
3, pay attention to labor protection.
4.Pay attention to the pollution caused by housing decoration.
5.Keep a happy mood.