[Overview]

Vitiligo is an acquired, localized or generalized skin depigmentation disease. It is a common skin disease that affects beauty. Easy to diagnose but difficult to treat. Chinese medicine calls it "vitiligo" or "vitiligo".

[Etiology]

The cause of this disease is still unclear. Research in recent years believes that it is related to the following factors:

1. Genetic theory: Some studies believe that vitiligo may be an autosomal dominant skin disease. Foreign authors calculated that 30% of patients had a positive family history and found that both monozygotic twins were affected. Domestic reports of positive family history range from 3 to 12%, which is lower than reported abroad.
2. Autoimmune theory: The relationship between the autoimmune theory and the onset of vitiligo has received increasing attention. Many scholars have noticed that patients and their family members have a higher rate of combined autoimmune diseases. Common ones include thyroiditis, hyperthyroidism or hypothyroidism, food diabetes, chronic adrenal insufficiency, pernicious anemia, wind-dampness arthritis, Malignant melanoma, etc. In the serum of patients with vitiligo, several organ-specific antibodies have been detected, such as anti-thyroid antibodies, anti-gastric parietal cell antibodies, anti-adrenal antibodies, anti-parathyroid antibodies, anti-smooth muscle antibodies, etc., and the detection rate is significantly high. In addition, the incidence of vitiligo in people with autoimmune diseases is 10 to 15 times higher than that in the general population. Recently, it has been discovered that patients with vitiligo have antibodies against melanocyte surface antigens, called vitiligo antibodies. Its titer is related to the degree of depigmentation of the patient's skin. The titer increases with the expansion of the skin lesion area. It has also been found that animals suffering from vitiligo also have similar antibodies. Phenomenon, it is proposed that the disease is an autoimmune disease of melanocytes. Behl (1977) found that monocytes gathered at the edge of white spots in the stage of progress, invaded the junction of the dermis and epidermis, and entered the epidermis through the damaged basal membrane, resulting in a lack of melanocytes and melanin there. He believed that the disease may be a late-stage disease. Autoimmune diseases that cause hypersensitivity reactions. In addition, oral or external corticosteroids are more effective, especially for skin lesions that are not distributed according to dermatomes, which also indirectly proves the immune mechanism of this disease.
3. Psychiatric and neurochemical theory: Many clinicians have found that mental factors are closely related to the onset of vitiligo. It is estimated that about 2/3 of patients suffer from mental trauma, excessive stress, low mood or depression at the onset or development stage of skin lesions. . Stress can increase Black Catechu phenolic amines, such as adrenaline, which can directly affect depigmentation; stress can also increase ACTH secretion, leading to increased corticosteroid secretion, mobilizing sugar and free fatty acids, and stimulating insulin secretion. Insulin indirectly stimulates the increase of L-tryptophan in the brain, which increases the synthesis of 5-hydroxytryptamine in the brain. The metabolite of 5-hydroxytryptamine is melatonin. Excessive activity of pheomelanin receptors plays an important role in the pathogenesis of vitiligo. Excessive activity of melatonin receptors can increase the activity of theophylline enzymes. These enzymes inhibit melanin generation and transformation, but the late stage [third stage] activates their generation, resulting in toxic intermediates of melanin metabolism in melanocytes. Internal accumulation causes melanocytes to die, eventually leading to vitiligo. Some scholars have observed degeneration of nerve endings in white spots, and the degree of change seems to be related to the course of the disease. This phenomenon also supports the neurochemical theory.
4. Self-destruction of melanocytes theory: The basic lesion of vitiligo is the partial or complete loss of function of epidermal melanocytes. Lerner proposed this theory in 1971. It is believed that vitiligo is caused by the hyperfunction of epidermal melanocytes, which promotes their depletion and early decline, and may be caused by the abdominal mass of toxic melanin precursor substances synthesized by the cells themselves. Experiments have shown that certain chemical substances have a selective destructive effect on melanocytes and depigment the skin. Most of these substances are depigmenting agents that replace phenolic chemicals, such as hydroquinone monophenyl ether, hydroquinone, styrolol, hydrogen peroxide, etc. , all have depigmentation effects on skin and hair. The incidence of vitiligo has increased in recent years, which may be related to the development of industry and the increased exposure to such chemicals.
5. Trace element deficiency theory: Some people have suggested that reduced copper levels in the body are related to the onset of vitiligo, but the measured copper levels in the serum and hair of patients do not seem to be significantly different from those of the general population. The trace element theory needs further research.
6. Other factors: Vitiligo can be induced by trauma, surgery, scratching, etc. Certain endocrine diseases, such as hyperthyroidism, diabetes, etc., can be associated with vitiligo. Vitiligo is prone to occur due to sun exposure.

There are many theories on the onset of vitiligo, and all of them have certain basis, but they are all one-sided. It is currently believed that its onset is caused by genetic factors, and under the action of a variety of internal and external factors, immune function, nerve and endocrine function, metabolic function and other functional disorders, resulting in the inhibition of the enzyme system or the destruction of melanocytes or the formation of melanin. disorders, resulting in skin depigmentation.

[Pathological changes]

Vitiligo skin shows a significant reduction or absence of epidermal melanocytes and melanin granules. Dopa-positive melanocytes in the basal layer decrease or disappear.

[Clinical manifestations]

Both men and women of all ethnic groups in the world can suffer from the disease. The incidence varies with region, race and skin color. The darker the skin color, the more the disease occurs. For example, it is less than 1% in the United States and as high as 4% in India. The prevalence in my country is 0.1 to 2%. There is no obvious difference between genders. It can occur in all age groups, but it is more common in teenagers, and about half of the patients are under the age of 20. The disease can occur on the skin of any part of the body. The skin lesions are localized depigmentation spots, which are often milky white or light pink, with a smooth surface and no rash. The white spots have clear boundaries, the edge pigment is increased compared with normal skin, and the hair in the white spots is normal or white. The lesions tend to occur in areas exposed to sunlight and friction injuries, such as the face, upper legs, neck, extensor sides of the forearms and back of the hands, waist and abdomen, sacrococcygeal area, armpits and pubic area, and elbow and knee joints. , the lesions are mostly symmetrically distributed. The white spots are also often arranged in a band-like distribution according to nerve segments (or dermatomes). This type of disease is unilateral. In addition to skin lesions, the lips, labia, glans, and mucous membrane on the inside of the foreskin are also often affected. White spots can occur all over the body, but the melanocytes of the retinal membrane, choroid membrane and pia membrane are not affected. Sometimes, pigmentation may regenerate in the white spots after sun exposure; in winter, there may be hypopigmentation in the center or edges of the white spots. About 20% of patients have white spots that are highly sensitive to ultraviolet rays, and the white spots develop rapidly after sun exposure. Mechanical stimulation, such as acupuncture, scratching, pressure on the skin (tight clothes, hernia supports, etc.) and other local stimulation, such as burns, infection, exposure, frostbite disease, radiation, etc., can cause white spots on the patient's normal skin. It may cause the original white spots to expand, or even cause homomorphic reactions throughout the body. The number of white spots is variable and may change little or disappear on its own, but in most cases, the white spots gradually increase and expand, and adjacent white spots merge into irregular large patches, or even spread all over the body.

This disease usually has no subjective symptoms. A few patients have local cutaneous pruitus sensation in the affected area before or at the same time. Vitiligo is often accompanied by other autoimmune diseases, such as diabetes, thyroid disease, adrenal insufficiency, pernicious anemia, wind-dampness arthritis, scleroderma, atopic dermatitis, alopecia areata, etc.

Based on the shape, location, scope and treatment response of white spots, they are clinically divided into four types: ① localized type, white spots are single or clustered in a certain part; ② sporadic type, white spots are scattered, different sizes and multiple Symmetrical distribution; ③ Generalized type, often developed from the above two types, with the lesion area larger than 1/2 of the body surface; ④ Segmental type, white spots are distributed according to nerve segments or dermatomes. According to the depigmentation of the lesion, the disease can be divided into two types: complete type and incomplete type. The former has negative reaction to dihydroxyphenylalanine (DOPA), melanocytes disappear, and poor response to treatment. The latter reacts positively to DOPA, the number of melanocytes is reduced, and the probability of cure is high.

[Treatment measures]

The treatment of this disease is difficult. Although there are many drugs and methods, the efficacy is not good and the course of treatment is long. It may relapse after recovery.

1. Psoralea (psoralen) and its derivatives As early as the 13th century, some people in Egypt used a plant called Daami to treat vitiligo. After 1947, three crystalline substances were proposed: ① δ-methoxypsoralen (δ-MOP, ammoidin); ② δ-isoamylenoxypsoralen (ammidin); ③ 5-methoxypsoralea (δ-isoamylenoxypsoralen, ammidin) Psoralea element (5-methoxypsoralen, majudin). Among them, δ-MOP has the best effect on pigment production. The above-mentioned uniform photosensitive compounds need to be supplemented by sunlight or ultraviolet irradiation. Its mechanism for treating vitiligo may be to act on not yet completely destroyed or normal melanocytes adjacent to damaged cells in the epidermis, stimulating their functions, causing tyrosinase to catalyze melanin synthesis, promoting the division and movement of melanocytes, and restoring skin color. normal.

(1) δ-MOP oral method is suitable for patients with multiple and wide white spots. Take 10 to 20 mg daily, divided into 2 times after meals, and 2 hours after taking the medicine, expose it to sunlight and long-wave ultraviolet rays (UVA), which is called photochemotherapy (PUVA). Generally, it is advisable to expose yourself to the sun for no more than 5 minutes. Generally, pigment appears only after 16 to 24 treatments, and the best effect can be achieved after 10 or more treatments. If continuous treatment for 6 to 12 months is still ineffective, it can be considered ineffective. Drug side effects include loss of appetite, anemia, leukopenia and toxic hepatitis. Therefore, it should not be used by people with diabetes, SLE, porphyria and poor liver function. When outdoor activities take a long time, stop taking it internally 3 days before the activity. During the treatment period, avoid eating limes, wildcelery herb, mustard greens, carrots, etc.

(2) External use of δ-MOP: Apply 0.2% to 0.5% δ-MOP solution to the affected area, and perform phototherapy after 1 to 2 hours. You can also apply 0.1% δ-MOP lotion or tincture to the affected area and expose it to sunlight or ultraviolet light after 1 to 2 hours.

(3) Trimethylpsoralen (δ-trimethylpsoralen, trisoralen, TMP) is artificially synthesized and has lower toxic reaction than δ-MOP. Its oral dosage is 10 to 50 mg per day, once a day, 2 days after taking it. ~4 hours of exposure to sunlight or long-wave ultraviolet rays, children should reduce the dosage as appropriate. There is no obvious side effect, but the efficacy is unreliable, and the regenerated pigment is not lasting and requires long-term treatment.

When taking photosensitive drugs, you should protect your eyes from ultraviolet damage. For this reason, wear UV-resistant great yang glasses within 24 hours after taking the medicine, and take the medicine in the evening.

(4) Psoralea is a Chinese materia medica commonly used to treat vitiligo. Contains Psoralea. Grind it finely and soak 30g of the crude drug in 100mL in 95% alcohol. After 5 to 6 days, take the filtrate and apply it to the affected area, and then irradiate it with sunlight or long-wave ultraviolet rays.

2. Corticosteroids Corticosteroids may inhibit melanocyte antibodies and prevent melanocytes from being destroyed.

(1) Systemic medication: Take prednisone as an example, take 5 mg orally three times a day for 1.5 to 2 months. After taking effect, reduce it by 1 tablet 2 to 4 weeks later, to 1 tablet every other day, and maintain it for 3 to 6 months. If the medication is ineffective for 3 months, discontinue treatment. This method is more effective for exposed parts and generalized damage, especially for those with rapid development of skin damage under stress and those with autoimmune diseases. Sometimes, if Psoralea is ineffective, adding hormones can be effective.

(2) Topical application ① Cream or solution containing corticosteroids can be applied to the white spots. Commonly used drugs include triamcinolone cream, clofluxazone cream, Enfu cream, etc. In recent years, the Shide cream has been used better. Efficacy. Such drugs can cause telangiectasia and skin atrophy. Therefore, white spots on the face should be used with caution; ② For facial injections, triamcinolone suspension (10 mg/mL) should be injected into the white spots, usually once a week, and no more than 10mg, to prevent skin atrophy, do not use more than 6 times.

3. Copper and zinc preparations It has been determined that some patients are deficient in certain trace elements, such as copper and zinc. After supplementing the deficient elements, their condition improves or even recovers. Commonly used is 10mL of 0.5% copper sulfate solution, diluted with water or milk, 3 times a day, and the dosage may be reduced for children. Copper sulfate solution can also be used to induce ions into the affected area, once a day. People with zinc deficiency in the body can take Liquorice Root zinc 0.25g, 2 to 3 times a day; or zinc gluconate 0.14g, 2 to 3 times a day.

4. Immunomodulators: Applied drugs include levamisole, transfer factor, thymosin, etc. Levamisole 50mg, 3 times a day, 3 days every two weeks. Transfer factor is injected subcutaneously at 1 to 2 U each time, twice a week. Thymosin, 5 to 10 mg each time, twice a week.

Recently, it was reported that six patients were treated with cyclosporine A and achieved good results. There are also reports of the use of isoprinosine.

5. Depigmentation therapy: When the skin lesion area is greater than 50% and does not respond to drug treatment; generalized skin lesions, especially those with only small patches of normal skin in exposed areas, and patients are unwilling to undergo pigment regeneration treatment, depigmentation therapy is feasible for cosmetic reasons . The commonly used drug is hydroquinone monophenyl ether (MBEH), which can cause irreversible destruction of melanocytes. In order to prevent its irritation, the initial stage [first stage] concentration is 10%, and it is used externally twice a day. If there is no irritation, the concentration can be increased to 20% within 2 to 3 months. It takes 6 to 24 months for all depigmentation to occur. Its side effects are dermatitis, cutaneous pruitus, and in severe cases, dry skin, alopecia areata, premature graying of hair, etc. Avoid close contact with other people's skin for at least 2 to 3 hours after taking the medication.

6. Covering therapy: When white spots affect beauty, covering agents made of artificial pigments can be applied to the affected area to make it close to normal skin. Such as commercially available Tianzi covering cream. We have applied 0.2 to 5% dihydroxyacetone alcohol solution to the affected area to achieve better results.

7. Surgical treatment: Surgical treatment can be considered for those who are ineffective with drug therapy. Its contraindications are hypertrophic scars and keloid constitution. ① Autologous suction blister epidermal transplantation, use (26.66kPa ~ 39.99kPa 200 ~ 300mmHg) negative pressure to aspirate and blister, cut off the top epidermis of the blister containing melanocytes, transplant it into the blister induced by liquid nitrogen or topical PUVA, and remove the epidermis of skin lesions. The success of this treatment depends on the type of vitiligo, its location and how the blisters are formed. Autologous suction epidermal transplantation does not leave scars, but the operation is complex and requires special equipment. ②Autologous micro-transplantation, also called drilling skin grafting method, drills holes into the normal skin on the outside of the thigh or the inside of the upper arm to take skin grafts; drills and peels the affected area using the same method, and transplants the normal skin grafts to the peeled area of ​​the affected area , the diameter of the drill hole is 1.5~2mm, the distance between the transplanted skins is 4~5mm, a small amount of topical antibiotics are applied, and then fixed with microporous tape, and the dressing is removed after 7 days. Pigment regeneration takes 3 to 4 weeks after surgery. ③Autologous melanocyte transplantation, melanocytes are isolated from the patient's normal epidermis and cultured. After vacuuming the blister at the white spot on the skin, use a 25-gauge needle to suck out the blister fluid, and then inject the cultured melanocyte suspension into the blister cavity. After four weeks, it can be There is pigment regeneration.

8. Other surgical methods ①5-FU/dermabrasion, Tsuji et al. used 5-FU cream externally to treat grinded vitiligo lesions in 28 cases, twice a day, for a total of 7 to 10 days, 64 % achieved complete pigment regeneration, but the mechanism of action is unclear. Infection and isoform reactions are side effects. ②Micro-pigmentation method (tattoo method), Halder et al. used microsurgery technology to implant iron oxide pigment into the dermis. The short-term effect was good, but obvious loss of pigment occurred soon after. side effect Same as above. ③Reactive pigments (vitadye) can be used for dyeing and can cover obvious damage. Covermark is a cosmetic that can produce a variety of shades and also has a good covering effect.

[Identification]

It is easy to diagnose based on the characteristics of the lesions and needs to be differentiated from the following diseases:

1. Pityriasis alba: Small patches of vitiligo on the face should be differentiated from pityriasis alba. Pityriasis alba white spots have unclear boundaries, no increase in peripheral skin pigment, and a gray-white bran-like scale on the surface.
2. Pityriasis versicolor: The damage occurs on the posterior hairline, forebrain, back, and upper limbs. It is a pale white round or oval spot with unclear boundaries and fine scales on the surface. The fungal test is positive.
3. Poor vascular nevus: It is present at birth. Due to the lack of local capillaries, the surrounding skin becomes red when the affected area is rubbed, and the white spots do not change.
4. Albinism: It is a congenital non-progressive disease that often has a family history. The skin and hair all over the body lack pigment. The iris membrane of both eyes is transparent, and the pigment of the choroid membrane disappears, making it easy to distinguish.