permanent baldness
Introduction
Introduction Cicatricial alopecia is a localized alopecia that occurs suddenly in any long-haired part of the body. It refers to the destruction of hair follicles caused by various causes to form scars, resulting in permanent alopecia. The disease is called "Ghosts" and "oily winds".
Cause
Cause
The cause of permanent alopecia:
(1) Causes of the disease: There are many causes of hair follicle destruction, which are roughly divided into the following five categories:
1. Developmental defects, such as skin dysplasia, Conrdi's disease, epidermal sputum, sweat ductalization, ichthyosis, and keratinization.
2. Physical factors such as curly hair, burns, and radiation dermatitis.
3. Infection such as jaundice, purulent sputum, sputum, sputum, folliculitis, lupus vulgaris, leprosy, etc.
4. Tumors such as sweat duct tumors.
5. Unexplained skin diseases such as lichen planus, lupus erythematosus, scleroderma, sarcoidosis, follicular mucin deposition disease.
(B) pathogenesis: the pathogenesis is still not very clear. A number of causes of hair follicle damage form scars, resulting in permanent alopecia. In recent years, alopecia areata is more likely to be an autoimmune disease. Changes in humoral immunity include non-organ specific autoantibodies and organ-specific autoantibodies. Anti-smooth muscle antibodies, anti-nuclear antibodies (mainly spotted), anti-mitochondrial antibodies, anti-basement membrane antibodies and rheumatoid factor have been reported. Organ-specific autoantibodies have been reported to have anti-thyroid antibodies, anti-gastric cell antibodies, anti-adrenal antibodies, and the like. The positive rate of autoantibodies is related to the patient's gender, age, and severity of illness. The change in cellular immunity is a large amount of lymphocyte infiltration around the blood vessels and hair bulbs of the alopecia areata lesions. The study also found that hair follicles in the alopecia areata have strong HLAI, class II immunoreactivity, and adhesion molecules involved in hematopoietic cell migration are abnormally expressed. These changes may be caused by the release of cytokines by certain stimulating factors such as trauma, neuroinflammation or infection. Cytokines can be involved in the development of a variety of immune response processes leading to the development of unique antigenic immune responses to hair follicles. In recent years, studies on a variety of cytokines involved in immune regulation in alopecia areata have been remarkable. Although the above mechanisms are more prevalent, the exact etiology is still unclear and does not confirm the exact autoantigen and pathogenic genes. The genetic type of hair loss is still unclear. Multi-gene inheritance patterns with different out-of-date rates and performance seem reasonable, but are still affected by additional hormones and immunity.
Examine
an examination
Related inspection
Hair hair mineral inspection
Examination of permanent alopecia:
There are scars on the affected area, hair follicle damage, and permanent alopecia. The corresponding clinical manifestations of various causes can also be seen. Other skin manifestations and histopathology, laboratory changes, etc. of visible lupus erythematosus caused by lupus erythematosus. Multiple alopecia areata occur suddenly, with round or oval hair loss on the scalp. Because there is no self-consciousness, it is often found inadvertently and by others. It is also noticed that a large amount of hair is lost when combing the hair, and the flaky hair loss area is found. The disease can be divided into three phases, namely, the onset phase, the stationary phase and the recovery phase. During the period of development, new hair loss spots appear, and the original hair loss spots are enlarged, but the number and size of hair loss spots are different. Most of them are the size of the nail cover to the coin, and the adjacent hair loss spots can be quickly merged. The detached hair shaft is atrophied at the proximal end, dull and dark at the end. The hair around the hair loss spot is loose, easy to pull out, and the root is made into an exclamation mark (!), that is, the hair pull test is positive. This is a feature of the disease in its infancy. The scalp in the hair loss area is normal, no inflammatory redness, no scales, no scars. The hair at the edge of the telogen effusion zone is no longer loose and no new hair loss spots appear. Most patients enter the recovery period after a quiescent period of 3 to 4 months. During the recovery period, new hair grows. It is initially a soft, light-colored fluff, similar to a mane. It gradually turns thick and black and then returns to normal.
The incidence of alopecia areata is roughly equal for men and women, but is more common among children and young people. Alopecia areata can also be found in eyebrows, eyelashes, manes, pubic hair and beards, and may be the only affected part. Most alopecia areata patients have only 1 or a few hair loss areas, and the course of disease is several months. However, there are a few patients who can recur or fall off at the long side. In severe cases, hair loss continues, and the hair loss areas merge with each other, gradually becoming a large piece of hair loss, and the course of disease can last for several years. If the hair is completely detached, it is called alopecia totalis (Fig. 3). If hair, eyebrows, eyelashes, beards, manes, pubic hair, and mane are all shed, it is called alopecia universatis. The sneak strip alopecia along the periphery of the scalp is called ophiasis.
After long-term investigation and study in Japan, Iktda divides alopecia areata into 4 types according to age, clinical manifestation and prognosis, which is helpful for guiding treatment and prognosis. Type I: Genetically allergic, accounting for 10%. In general, childhood onset, with a course of more than 10 years, a single alopecia areata often lasts more than 1 year, with a genetic allergic disease, and 75% of all alopecia. Type II: autoimmune type, accounting for 5%. It usually occurs after the age of 40, and the course of disease is prolonged, and only 10% of all cases are bald. Often accompanied by autoimmune diseases such as pernicious anemia, vitiligo, Hashimoto thyroiditis. Type III: prehypertensive type, accounting for 4%. Mainly seen in young people, one of their parents or parents is hypertensive, progressing rapidly, 39% of all baldness. Type IV: vulgaris, accounting for 83%. Those who do not belong to type I to III are more common in adults aged 20 to 40 years. The total duration of disease is less than 3 years. Individual alopecia areata can grow hair within 6 months and 6% occur in total baldness.
According to the clinical manifestations, the characteristics of skin lesions and histopathological features can be diagnosed.
Chinese medicine believes that it is a blood, and it is the owner of the kidney. The hair is sparse or dry, and it is mostly the evidence of insufficient blood. The disease is mostly due to liver and kidney deficiency, lack of yin blood, phlegm is not solid, wind evil is taking advantage of the virtual, wind and blood dry, lost and raised. In addition, the emotions are not bad, and the loss of blood and blood is also related to the occurrence of this disease. Liver and kidney yin deficiency, heart and kidney are not the common type.
The disease can be associated with the following diseases:
1. A lesions such as punctate pits, mediastinum and irregular thickening and obvious nail dystrophy, the change of total baldness and general baldness is particularly significant.
2. Genetic allergic diseases.
3. Autoimmune diseases.
4. Eye diseases such as dilated pupil dilation, eyeball invagination, vascular and pigmentary malformations, crystal opacity and cataract.
5. The incidence of alopecia areata in Down syndrome is 6%.
Diagnosis
Differential diagnosis
Symptoms of permanent baldness that are confusing:
1. Pseudo-alopecia areata: Symptoms are similar to alopecia areata, but the skin of the affected part is atrophy, the hair can not be regenerated, the surface has an island-like normal hair bundle, and the edge has a narrow and narrow red halo band, and the hair is not loose, which is more common in women aged 30-50 years.
2. Head lice: the head white pheasant is gray-white scaly patch, the hair is broken from the scalp 2 ~ 4mm, the peripheral white fungus sheath, fungal test positive, more common in children. Black spots, scalp damage is similar to whitehead, but the damage is small and the number is often accompanied by varying degrees of inflammatory response. The disease often reveals that the scalp is broken, non-alopecia, and the fungus is positive. Astragalus vulgaris is atrophic scar, which is sparsely scattered on the remaining hair, and there are typical symptoms of jaundice.
3. Pulling hairpin: The patient has mental abnormalities, and often unconsciously removes hair frequently, which can be identified according to his medical history and clinical manifestations.
4. Leprosy alopecia: Hair loss begins at the hairline and gradually spreads upwards. In severe cases, only the flaky or linear hair remains along the vascular path. His hair was completely detached, and other hair loss and paresthesia were found in addition to hair loss.
5. Alopecia folliculitis: the first occurrence of hair follicle purulent inflammation, the atrophic scar after the recovery, easy to repeat.
6. syphilitic hair loss: a history of syphilis or a history of unclean sexual intercourse. Hair loss is worm-like, irregularly distributed, and hair loss in the hair loss area is not complete. More common in the occipital side, syphilis serological test positive.
There are scars on the affected area, hair follicle damage, and permanent alopecia. The corresponding clinical manifestations of various causes can also be seen. Other skin manifestations and histopathology, laboratory changes, etc. of visible lupus erythematosus caused by lupus erythematosus. Multiple alopecia areata occur suddenly, with round or oval hair loss on the scalp. Because there is no self-consciousness, it is often found inadvertently and by others. It is also noticed that a large amount of hair is lost when combing the hair, and the flaky hair loss area is found. The disease can be divided into three phases, namely, the onset phase, the stationary phase and the recovery phase. During the period of development, new hair loss spots appear, and the original hair loss spots are enlarged, but the number and size of hair loss spots are different. Most of them are the size of the nail cover to the coin, and the adjacent hair loss spots can be quickly merged. The detached hair shaft is atrophied at the proximal end, dull and dark at the end. The hair around the hair loss spot is loose, easy to pull out, and the root is made into an exclamation mark (!), that is, the hair pull test is positive. This is a feature of the disease in its infancy. The scalp in the hair loss area is normal, no inflammatory redness, no scales, no scars. The hair at the edge of the telogen effusion zone is no longer loose and no new hair loss spots appear. Most patients enter the recovery period after a quiescent period of 3 to 4 months. During the recovery period, new hair grows. It is initially a soft, light-colored fluff, similar to a mane. It gradually turns thick and black and then returns to normal.
The incidence of alopecia areata is roughly equal for men and women, but is more common among children and young people. Alopecia areata can also be found in eyebrows, eyelashes, manes, pubic hair and beards, and may be the only affected part. Most alopecia areata patients have only 1 or a few hair loss areas, and the course of disease is several months. However, there are a few patients who can recur or fall off at the long side. In severe cases, hair loss continues, and the hair loss areas merge with each other, gradually becoming a large piece of hair loss, and the course of disease can last for several years. If the hair is completely shed, it is called alopecia totalis. If hair, eyebrows, eyelashes, beards, manes, pubic hair, and mane are all shed, it is called alopecia universatis. The sneak strip alopecia along the periphery of the scalp is called ophiasis.
After long-term investigation and study in Japan, Iktda divides alopecia areata into 4 types according to age, clinical manifestation and prognosis, which is helpful for guiding treatment and prognosis. Type I: Genetically allergic, accounting for 10%. In general, childhood onset, with a course of more than 10 years, a single alopecia areata often lasts more than 1 year, with a genetic allergic disease, and 75% of all alopecia. Type II: autoimmune type, accounting for 5%. It usually occurs after the age of 40, and the course of disease is prolonged, and only 10% of all cases are bald. Often accompanied by autoimmune diseases such as pernicious anemia, vitiligo, Hashimoto thyroiditis. Type III: prehypertensive type, accounting for 4%. Mainly seen in young people, one of their parents or parents is hypertensive, progressing rapidly, 39% of all baldness. Type IV: vulgaris, accounting for 83%. Those who do not belong to type I to III are more common in adults aged 20 to 40 years. The total duration of disease is less than 3 years. Individual alopecia areata can grow hair within 6 months and 6% occur in total baldness.
According to the clinical manifestations, the characteristics of skin lesions and histopathological features can be diagnosed.
