vitiligo
Introduction
Introduction to vitiligo Vitiligo is a common and frequent pigmented skin disease. The disease is characterized by local or generalized pigmentation to form leukoplakia. It is an acquired localized or generalized skin pigmentation disorder. It is a common skin disease affecting beauty, easy to diagnose and difficult to treat. Traditional Chinese medicine is called white barge and vitiligo. Vitiligo is a confined white patch that occurs due to skin pigmentation, making the local skin white spotted. This disease is usually called depigmentation in medicine. The disease has occurred all over the world. The incidence rate in India is the highest. There are about 10,000 people in China, which can affect all races. There is no significant difference between men and women. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: Diabetes
Cause
Cause of vitiligo
Genetic theory (20%):
Some studies suggest that vitiligo may be an autosomal dominant hereditary skin disease. Foreign authors have a positive family history of 30% of patients, and two of the monozygotic twins have been found. The domestic family history of positive family is 3% to 12%. , lower than foreign reports.
Autoimmune theory (15%):
The relationship between autoimmune theory and the pathogenesis of vitiligo has received increasing attention. Many scholars have noticed a high rate of autoimmune diseases among patients and their family members. Common thyroiditis, hyperthyroidism or diminished, diabetes, chronic adrenal insufficiency, Pernicious anemia, rheumatoid arthritis, malignant melanoma, etc., and in the serum of patients with vitiligo, specific antibodies such as anti-thyroid antibodies, anti-thyroid cell antibodies, anti-adrenal antibodies, anti-parathyroid antibodies are detected. Anti-smooth muscle antibodies, etc., and the detection rate is significantly higher. In addition, in patients with autoimmune diseases, the incidence of vitiligo is 10 to 15 times higher than that of the general population. Recently, patients with vitiligo have anti-melanocyte surface antigen antibodies. Vitiligo antibodies, the titer is related to the degree of skin pigmentation in patients, the titer increases with the expansion of the lesion area, and it is also found that animals suffering from vitiligo have a similar phenomenon, suggesting that the disease is an autoimmune disease of melanocytes, Behl (Behl ( 1977) found mononuclear cell aggregation at the edge of the white spot, invading the dermal epidermis At the boundary, the damaged basement membrane enters the epidermis, making the melanocytes and melanin absent. The disease may be an autoimmune disease with delayed hypersensitivity reaction. In addition, oral or topical corticosteroids, especially The skin lesions that are not distributed according to the dermatome have better curative effect, and indirectly prove the immune mechanism of the disease.
Spiritual and neurochemical theory (20%):
Many clinicians have found that mental factors are closely related to the onset of vitiligo. It is estimated that about two-thirds of patients have mental trauma, excessive tension, low mood or depression during the onset of disease or skin lesions, and tension can cause catecholamines to increase. Adrenalin can directly affect discoloration; stress can also increase the secretion of ACTH, leading to increased secretion of corticosteroids, and mobilize sugar and free fatty acids, stimulate insulin secretion, insulin indirectly stimulates the increase of L-tryptophan in the brain, making the brain serotonin The synthesis is increased, and the metabolite of serotonin is melatonin. The hyperactivity of brown melanin receptor plays an important role in the pathogenesis of vitiligo. Excessive hyperactivity of melatonin receptor can increase the activity of theophylline. These enzymes inhibit black. Biochemical, but later activated its generation, causing melanin metabolism of toxic intermediates to accumulate in melanocytes, causing melanocytes to die, eventually leading to vitiligo, some scholars have observed that the nerve endings at the leukoplakia have degenerative changes, And the degree of change seems to be related to the course of the disease, and this phenomenon also supports the theory of neurochemistry.
The theory of self-destruction of melanocytes (20%):
The basic pathological condition of vitiligo is partial or complete loss of function of epidermal melanocytes. Lerner proposed this theory in 1971, suggesting that vitiligo is due to its epidermal melanocyte hyperfunction, which promotes early loss of depletion and may be due to the toxicity of the cell itself. Due to the accumulation of melanin precursors, experiments have shown that certain chemicals have selective destructive effects on melanocytes and decolorize the skin. These substances are mostly decolorizing agents that replace phenolic chemicals, such as hydroquinone monophenyl ether. Hydroquinone, succinol, hydrogen peroxide, etc. all have decolorization 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 chance of exposure to such chemicals.
Trace element deficiency theory (10%):
It has been suggested that the reduction of copper content in the body is related to the pathogenesis of vitiligo, but the determination of copper content in serum and hair of patients seems to have no significant difference with the general population. The relevant trace element theory needs further study.
Other factors (10%):
Trauma including trauma, surgery, scratching, etc. can induce vitiligo, some endocrine diseases, such as hyperthyroidism, diabetes, etc., may be associated with vitiligo, sun exposure is prone to vitiligo.
There are many episodes of vitiligo, and they all have certain basis, but they all have certain one-sidedness. At present, it is believed that the pathogenesis is genetic, and under various internal and external factors, immune function, nerve and endocrine, and metabolic function. In many ways, the function is disordered, resulting in inhibition of the enzyme system or destruction of melanocytes or melanin formation, resulting in skin pigmentation loss.
When the spirit is too tight, the consumption of adrenaline increases, and Dopa mainly synthesizes adrenaline, thus reducing melanin synthesis.
The level of copper or ceruloplasmin in the blood and skin of patients with vitiligo is reduced, resulting in decreased tyrosinase activity, thus affecting the metabolism of melanin.
In addition, certain chemicals and photosensitivity drugs can also induce the disease.
Pathogenesis
The pathogenesis of vitiligo may be the loss of tyrosinase function in melanocytes at the local epidermal dermal junction, which oxidizes tyrosine to dopa, which hinders the formation of melanin.
Chinese medicine believes that emotional internal injuries, liver qi stagnation, poor air movement, re-feeling wind evil, fighting in the skin, resulting in local qi and blood loss and the occurrence of this disease.
Prevention
Vitiligo prevention
Vitiligo has always been the focus of attention. Now with the improvement of people's living standards, the incidence of vitiligo is also rising. If the incidence of vitiligo is reduced, then it is necessary to prevent vitiligo. Prevention is very important. How can it be done? Good prevention of white hurricanes. Home to do the following:
1. Reduce the intake of contaminated food, correct partial eclipse, adhere to dinner, formulate scientific dietary recipes, and maintain the supply of nutrients is especially important for children.
At the same time, vegetables and fruits should be washed repeatedly and eaten. Allow time to soak for 15~30 minutes with clean water, then rinse and eat. Peeled fruits should be peeled.
2, reduce the inhalation of harmful gases, choose fresh air in the morning exercise or exercise.
3. Pay attention to labor protection. Do a good job in labor protection and reduce direct contact with chemical raw materials, paints and heavy metals and harmful substances.
4. Pay attention to the pollution caused by the decoration of the house. The decoration materials contain formaldehyde, ammonia, benzene and other series of toxic substances, and the ground bricks and marbles also contain radioactive substances, which can cause damage to multiple organs and organs in the human body. After the house is renovated, it should be relocated after three months of ventilation. After the house is relocated, it should be kept in constant ventilation. If conditions permit, it should be monitored by the environment.
Adhere to treatment, consolidate for a period of time to help prevent recurrence, use irritating drugs with caution, do not damage the skin, avoid mechanical friction, clothes should be wide and fit, pay attention to work and rest, feel comfortable, actively cooperate with treatment, usually Try to eat vitamin C as little as possible, because vitamin C can reduce the formed DOPA to DOPA, thus interrupting the biosynthesis of melanin. On the other hand, vitamin C can reduce the absorption of copper ions in the intestine and lower the blood. Serum copper oxidase activity, which affects tyrosinase activity, usually eat more beans and their products, pay attention to outdoor exercise, moderate sunbathing.
1 Enhance physical fitness. Mental relaxation: long-term anxiety, nervousness, unpleasant mood, etc. can all stimulate the disease, so patients should be cheerful and open-minded.
2 Attention to the environment: dampness, rain, cold, exposure, friction, etc. may induce vitiligo.
3 to prevent infection: frostbite, burns and other trauma can lead to vitiligo.
4 Consolidation treatment: After the clinical recovery of vitiligo patients, their immune ability and microcirculatory disorders have not returned to normal, so after the clinical recovery, that is, after the white spots completely disappear, a course of treatment should be consolidated.
Complication
Vitiligo complications Complications diabetes
Often complicated by diabetes, pernicious anemia, autoimmune disease, thyroid disease, primary adrenal insufficiency and so on.
In clinical manifestations, a variety of diseases can be complicated or secondary. There are many cases of vitiligo combined with some autoimmune and endocrine diseases, such as hyperthyroidism or hypothyroidism, diabetes, chronic adrenal insufficiency and chronic Active hepatitis, in addition, there are reports that vitiligo and pernicious anemia, syncope, alopecia areata or alopecia areata, psoriasis, scleroderma, morphea, malignant tumor, drug eruption, herpes zoster, bronchial asthma, Position dermatitis, rheumatoid arthritis, myasthenia gravis, chronic subcutaneous tissue candidiasis and eye disease, and concomitant with herpes-like dermatitis, acromegaly, parapsoriasis, chronic persistent erythema, late Hair dermatophytosis, sclerosing atrophic moss and other diseases have recently been reported in people with HIV infection and myelodysplastic syndrome.
Symptom
Vitiligo symptoms common symptoms tinnitus facial leukoplakia pruritus alopecia areata stagnation of the liver stagnation of the small blisters pigmented lesions
[clinical manifestations]
Men and women can be affected in all ethnic groups in the world. The incidence varies with the region and the color of the human race. The deeper the skin color, the more the disease occurs. For example, the United States is less than 1%, while India is as high as 4%. The prevalence rate in China is 0.1% to 2%. There is no significant difference in gender, all age groups can be ill, but adolescents are good, the age of onset is less than 20 years old, the skin of all parts of the body can be affected, the skin lesions are local pigmentation spots, often milky white It can also be light pink, smooth surface without rash, clear white spot, thicker edge pigment than normal skin, normal or white hair in white spot, lesions occur in sun exposure and friction damage parts, such as face, upper leg , neck, forearm extension and hand back, waist and abdomen, armpit and genital area, elbow and knee joints are all good sites, lesions are more symmetric distribution, white spots are often according to nerve segments (or dermatomes) Distribution and banding, this type of unilateral disease, in addition to skin damage, lips, labia, glans and foreskin inner mucosa are also often affected, leukoplakia can be generalized, but the retina, choroid and pia mater melanocytes are not Affected, there is After sun exposure, there may be pigment regeneration in the white spot area; in winter, there is hypopigmentation in the center or edge of the white spot, and about 20% of the white spot is highly sensitive to ultraviolet light. After sun exposure, white spots develop rapidly, and mechanical stimulation, such as acupuncture, sputum Grab, pressure on the skin (tights, squats, etc.) and other local stimuli, such as burns, infections, sunburns, frostbite, radiation, etc., can cause white spots on the patient's normal skin, or enlarge the original white spots, or even pan The homomorphic response of the whole body, the number of white spots is uncertain, can rarely change or self-resolved, but in most cases, the white spots gradually increase and expand, and the adjacent white spots merge into irregular large slices and even generalized the whole body.
There are many symptoms of this disease. 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, pernicious anemia, rheumatoid arthritis, and hard skin. Disease, atopic dermatitis, alopecia areata, etc.
According to the morphology, location, extent and treatment response of leukoplakia, it is clinically divided into four types:
1 limited type, white spot single or clustered in a certain part;
2 loose hair, white spots scattered, different sizes, more symmetrical distribution;
3 general hair style, often developed from the above two types, the lesion area is larger than 1/2 of the body surface;
4 segment type, leukoplakia is distributed according to the nerve segment or dermatome. According to the pigmentation loss at the lesion, the disease can be divided into two types: complete type and incomplete type. The former is negative for dihydroxyphenylalanine (DOPA). The melanocytes disappeared and the treatment response was poor. The latter responded positively to DOPA, the number of melanocytes decreased, and the chance of cure was large.
The disease occurs on the day after tomorrow, and it can be ill at all ages. There are reports of neonatal morbidity. After delay, it can also develop sexually. Children with early onset can self-heal.
The surface temperature of the skin lesions can be increased, sweat is increased, often complicated by diabetes, pernicious anemia, autoimmune disease, thyroid disease, primary adrenal insufficiency and so on.
Examine
Vitiligo examination
Laboratory inspection
In the large amount of research work on vitiligo, it has been found that vitiligo patients have a variety of laboratory abnormalities, although most of these abnormalities are non-specific, but have a certain reference significance for the diagnosis and treatment of this disease and pathogenesis.
1. Blood test Vitiligo is necessary to do some blood tests before or during treatment. It can be found abnormal or find potential visceral lesions. Identifying the cause can improve the cure rate and help the recovery of vitiligo.
(1) Blood gas analysis: The pH value was determined. Compared with 100 normal subjects, 100 patients with vitiligo had an average of 7.3650 for vitiligo and 7.3888 for normal people. The blood pH of patients with vitiligo was slightly lower than that of normal people.
(2) Blood routine: Most patients with vitiligo have anemia, white blood cells and thrombocytopenia.
(3) Immune abnormalities: It has been found that there are various autoantibodies in the serum of patients with vitiligo, including thyroglobulin, anti-thyroid microsomes, anti-stomach cells, anti-adrenalin, anti-smooth muscle, anti-myocardial, anti-insulin, anti-platelet and anti- For nuclear antibodies, the positive rate ranges from 8.2% to 50%. The detection of anti-melanocyte surface protein antibodies in serum of patients with vitiligo is important for this disease, but the positive rate is determined by indirect immunofluorescence using normal skin as a substrate. Low, using cultured melanocytes as a substrate, using improved indirect immunofluorescence or immunofluorescence complement fixation, immunoprecipitation, the positive rate of immunoblotting is greatly improved, up to 50% to 80%, reported Immunoglobulin G, immunoglobulin M and immunoglobulin A in patients' serum were higher than normal, complement (C3), serum total complement activity (CH50) decreased, and helper T cells (TH) decreased or increased. The ratio of T cells to inhibitory T cells was changed. The patients were tested for tuberculin intradermal test, and the phytohemagglutinin (PHA) intradermal test and lymphocyte transformation test showed a low phenomenon. Reports of elevated levels of soluble interleukin-2 receptor (SIL-2R) in patients' serum indicate that it is necessary to perform some blood tests before or during treatment to detect abnormal or potential in vivo lesions. Further investigation of possible causes for symptomatic treatment can improve the cure rate and help the recovery of vitiligo.
2. The trace elements were compared with 100 cases of hair and elemental human hair in 100 cases of vitiligo. The mean value of vitiligo patients was 8.6898 g/g, and the normal person was 10.0703 /g. The P value was less than 0.05 by t test. Patients with vitiligo are closely related to low copper. There is no significant difference between zinc, tin and manganese in normal people. Other activities include decreased serum copper oxidase activity, increased serum monoamine oxidase, increased serum ceruloplasmin, and chromosomal aberrations. Report of patients with microcirculatory disorders.
3.Wood lamp inspection Wood lamp is very helpful to judge the subtle difference of pigmentation. Melanin absorbs the whole band of ultraviolet light. If the melanin is reduced, the refraction is strong and the light color is light, while the melanin is increased, the light is weak and the color is dark. Wood lamp can be used to check the depth of melanin in the skin, such as checking the pigment damage of the epidermis (such as freckles), the pigment can be deepened when irradiated, and the pigment in the dermis has no such reaction, so that the position of melanin can be determined. Under the Wood lamp, the change in pigmentation of the vitiligo epidermis is much more pronounced under visible light, while the change in dermal pigmentation is not apparent under the Wood light.
Auxiliary inspection
Vitiligo histopathology in addition to basal layer melanocytes, and the number of melanin particles decreased or disappeared, generally no inflammatory reaction, basal cell layer vasosome and melanocytes in vitiligo patients decreased or lacked, in the active period of damage, the center There is an abnormally enlarged melanocyte around the density of melanocytes, which is 2 to 3 times higher than that in the normal area of the marginal zone. Epidermal edema and sponge formation at the edge of the so-called vitiligo bulge can be observed in the early inflammatory phase. The infiltration of lymphocytes and histiocytes can be seen. The main change of the formed vitiligo damage is the reduction or even disappearance of melanocytes in melanocytes. It is reported that Langerhans cells can be increased, normalized or redistributed. The entire epidermis-melanin unit is damaged, and there are no melanocytes in the late decolorized skin lesions. It is also treated with special staining and electron microscopy. Reactive keratin hyperplasia can be seen in the ultraviolet-irradiated skin, and phagocytic cells are also seen in the initial dermis. Increased melanosomes in the epidermal melanocytes at the pigmented margin of the lesion, silver staining and electron microscopic observation of lesions Nerve degenerative changes, Dopa-responsive examination, complete white almost invisible type melanocytes, without completely Only a few type melanocytes, and the reaction is weak, the following points will be described later relevant circumstances.
1. Histopathology In the absence of concurrent skin inflammation, no pathological biopsy is generally required, and may be considered as appropriate in the following cases.
(1) For pigmented epilepsy suspected of vitiligo, it can not be diagnosed after long-term follow-up observation, or when there is a malignant change.
(2) For leukoplakia that is ineffective for a long time, it is not clear that it is a complete leukoplakia. When patients are eager to treat, they can do histopathological examination to determine whether melanocytes are present, especially for dihydroxyphenylalanine (dopa). Reactive melanocytes are used as a reference for efficacy estimation.
2. Immunopathology At present, there are few materials in this area, most of which are positive. Only a few individuals have found that some patients have immunoglobulin G or (C3) deposition in the basement membrane and immunoglobulin in keratinocytes by direct immunofluorescence. Protein G or complement (C3) deposition.
3. Ultrastructural electron microscopy changes similar to light microscopy, that is, the ultrastructural changes of the edge of white spot are most significant. The three main cells in the epidermis: keratinocytes, melanocytes and Langerhans cells (LC) are abnormal. There is a lack of melanocytes in the leukoplakia, vacuoles appear in the melanocyte cytoplasm at the edge of the leukoplakia, the nucleus is pyknotic, the rough endoplasmic reticulum is highly expanded or even ruptured, the membrane ribosome can partially shed, and the expansion pool contains flocs, mitochondria. Atrophy or swelling, melanin bodies are significantly reduced, III, IV grade is less, there may be melanin small body aggregation, the interior is fine granular, and melanin deposition is uneven, residual melanin particles can be seen in lysosomes, white spot A small number of keratinocytes may have a slight expansion of the rough endoplasmic reticulum, mitochondrial structure is unclear, intracellular edema, keratinocytes in the margins of the leukoplakia are disordered, edema inside and outside the cell, tension microfilament disorder, desmosome rupture, decrease or even disappear, Especially, the keratinocytes in the vicinity of melanocytes are most obviously changed. The melanosomes in the keratinocytes are abnormally structured, the mitochondria and the rough endoplasmic reticulum are degenerated, and the Langerhans cells in the leukoplakia are obviously degraded. Change, the nuclear notch deepens, the nucleus is huge, the perinuclear space is unevenly enlarged, the rough endoplasmic reticulum increases, the expansion, the mitochondria swell, the intracellular vacuoles increase, the characteristic Birbeck particles decrease significantly, the cell body becomes round, and the cell processes mostly disappear. The Langerhans cell changes at the edge of the white spot are lighter. It is worth noting that the skin with normal clinical appearance away from the leukoplakia also has ultrastructural changes:
(1) Melanocytes have inflammatory changes, but are lighter than the margins of white spots.
(2) There are also mild abnormalities in organelles in keratinocytes, such as rough endoplasmic reticulum expansion and mitochondrial swelling.
(3) Only Langhans cells (LC) are normal.
In addition to the above three kinds of cell changes, the basement membrane changes are also significant, especially at the edge of the white spot, the base plate is blurred, thickened, and there may be basal plate rupture, visible multi-layer replication of the basement membrane, and superficial capillary endothelial cell proliferation. , interstitial edema, lymphocytes around the blood vessels, tissue cell infiltration, abnormal nerve structure at the edge of the leukoplakia, including axonal swelling, axonal disruption, Schwann cell basement membrane replication or multi-layer replication, Schwann cell nucleoprotein glycoprotein granules , rough endoplasmic reticulum and mitochondria increased significantly.
4. There are few data on immunological changes under electron microscope. Some doctors have observed clear positive particles deposition under the basement membrane and collagen fibers of the leukoplakia. Immunoglobulin G and complement (C3) are shown by PAP method under light microscope. The deposition sites were consistent, and immunofluorescence was about half of the patient's basement membrane with immunoglobulin G deposition.
Diagnosis
Vitiligo diagnosis
diagnosis
Typical vitiligo is easy to diagnose.
TCM pathogenesis and syndrome differentiation
1. Chinese medicine believes that emotional internal injuries, liver qi stagnation, poor air qi, resilience of wind and evil, fighting in the skin, resulting in local qi and blood loss, the occurrence of this disease, or due to liver and kidney yin deficiency, lack of blood and other reasons Caused.
2. TCM syndrome differentiation
(1) stagnation type:
Main card: white patches on the head and torso, irregular shape, no inflammation and dander. Mental depression or impatience, pale tongue or bruises, thin white fur, slow pulse.
Dialectical: the wind evil attacked, the blood and blood lost.
(2) Kidney yin deficiency type:
Main card: no fixed part of the hair, can be limited or generalized, white spot boundary is clear, white hair inside the white spot, white hair, dizziness, tinnitus, waist and knees, faceless, thin tongue, thin tongue, tooth marks, weak pulse.
Dialectical syndrome: liver and kidney yin deficiency, wind evil chaos in the skin.
Differential diagnosis
For early incomplete decolorization, edge blurred damage needs to be identified with the following diseases:
1. Anemia occurs from childhood, more common in the face, for light spots, irritating friction does not red, and the surrounding skin is red.
2. White pity is caused by fungal infection. White spots may appear after treatment, but the number is small, small in shape and not pure white.
3. The body rash is mostly scaly stains, and there is no halo around the pigment.
4 The tinea versicolor lesion occurred in the posterior hairline, forebrain, back, upper limbs, pale white or elliptical spots, unclear borders, fine scales on the surface, positive for fungal examination.
5. Albinism is a congenital non-progressive disease, often with a family history, skin around the body, hair lacks pigmentation, the iris of both eyes is transparent, and the choroid pigment disappears easily.
6. Leprosy leukoplakia is not deformed, it is incomplete hypopigmentation, the boundary is unclear, the feeling disappears, and other symptoms of leprosy.
7. The second stage syphilis leukoplakia occurs in the neck, the color is not pure white, and the syphilis serum is positive.
8. Others should also be differentiated from tinea versicolor, discoid lupus erythematosus, and mucous membrane leukoplakia.
