[Overview]

Atopic dermatitis, also known as atopic dermatitis or atopic dermatitis, has a genetic history and high blood IgE. It is often accompanied by asthma and allergic rhinitis, which is a chronic recurring, itchy, inflammatory skin disease. "Infantile eczema" and "cubital and popliteal eczema" in Chinese medicine may be manifestations of different stages of this disease.

[Etiology]

The mechanism of disease is relatively complex and is related to genetics, immunity, and abnormal responses to physiological and pharmacological mediators. Environmental factors also play a very important role in the occurrence of this disease. About 70% of patients have a history of genetic allergies such as atopic dermatitis, asthma or allergic rhinitis in their families.

If both parents have a history of genetic allergies, their children have a higher chance of developing genetic allergies than if only one parent has a history of genetic allergies. Recently, it was found that the gene on chromosome 11ql3 is related to the onset of allergic asthma. Immunological abnormalities are manifested by increased blood IgE. Recent studies have pointed out that skin Langerhans cells have high-affinity IgE Fc receptors (Fc e RI). "Inhaled" antigens enter the skin of atopic dermatitis, causing activation of Langerhans cells, releasing IL-1β and activating the atopic-specific T helper cell subtype TH-2 to produce IL-4 and IL-5 and other cytokines, stimulate B cells to produce IgE, and IL-5 is an important cytokine for the differentiation and proliferation of human eosinophils. In patients with atopic dermatitis, an eczematous skin reaction caused by patch testing to an environmental allergen (mongolian snakegourd root) behaves similarly to a cutaneous late-phase reaction. There is eosinophil infiltration in the skin lesions, so it is believed that IgE-mediated "contact allergy" plays an important role in the development of atopic dermatitis. In terms of physiological pharmacology, the patient's leukocytes and epidermal cells are slow to respond to β-adrenergic agonists, the level of cAMP produced and the function of inhibiting epidermal cell mitosis are reduced, and the affinity of β-adrenergic receptors and β-agonists is reduced, a Increased adrenergic receptor ratio, etc. In addition, it was found that the activity of cAMB phosphodiesterase (PDE) in mononuclear cells increased, resulting in a decrease in cAMP levels.

[Clinical manifestations]

The symptoms of this disease are diverse, and the inflammation can range from acute to chronic, with repeated attacks, severe cutaneous pruitus, and a long course. As we age, the characteristics of the rash change. It can usually be divided into three stages: infancy, childhood, and young adulthood. Some patients develop symptoms in each stage sequentially, but others only have one or two stages.

The disease generally develops early in infancy, with about 60% of the disease occurring within 1 to 6 months after birth, and some occurring as early as one week after birth. About 90% develop the disease within 5 years of age, and less than 5% develop the disease over the age of 35.

(1) The clinical manifestations in infancy are the same as those of infantile eczema. The lesions are mainly on the forehead, cheeks, auricle, scalp and lower cheeks, and can also occur on the limbs and trunk. It starts as acute erythema, and gradually, pinhead-sized papules, papules and blisters appear on the basis of the erythema, which may be densely packed into sheets with unclear boundaries. The rash was polymorphic and cutaneous pruitus was evident. Severe scratching may result in scratches, serous fluid oozing out, and a bright red eroded surface with a large amount of exudate. After the exudate dries, scabs form, and the scalp may show yellow seborrheic scabs. The condition may be severe or mild, and factors such as certain foods or environment may aggravate the condition. It usually recovers gradually within 2 years of age.

(2) In childhood, the disease usually starts to occur at about 4 years old after remission for 1 to 2 years in infancy, and a few cases continue to occur since infancy. Skin lesions often involve the extensor or flexural sides of the limbs, and are often limited to the (lunar) fossa and cubital fossa. The flushing of the skin lesions is usually lighter than in infancy, the papule is dark red, the oozing is lighter, and there may be scratching. Over time, the rash becomes thickened and becomes lichen-like. A few may show itchy rash-like lesions, with normal skin color or dark brown, rough surface, and are spread on the extended sides of the limbs. Nearby lymph nodes may become swollen.

(3) Young adulthood refers to atopic dermatitis in adolescents and adults after the age of 12, which can develop from childhood or occur directly. The skin lesions are often lichenoid or acute or blood-acute eczema-like lesions, which are more likely to occur in the cubital fossa, (lunar fossa) fossa, limbs and trunk. In addition to the above symptoms, patients often suffer from dry skin all over the body or changes like grade I ichthyosis. The texture of the palms is thick and the complexion is often pale. The grade I pigmentation around the eyes is light brown. White scratches appear on the skin after being stimulated by blunt objects. Cold and heat stimulation, mood swings, sweating and contact with woolen fabrics can easily aggravate cutaneous pruitus. About 60 to 70% of cases may be accompanied by a history of bronchial asthma or allergic rhinitis.

[Diagnosis]

Diagnosis can be made based on the characteristics of the disease.

(1) Skin rashes in infants and children are more common on the face and extended sides of limbs or on elbows and fossae, showing polymorphous lesions such as erythema, papule and exudation;

(2) Youth and adults The damage is often a lichenoid rash on the flexor or extension sides of the limbs, which is a chronic and recurring process;

(3) Personal or family history of genetic allergies (asthma, allergic rhinitis, atopic dermatitis);

(4) Severe cutaneous pruitus;

(5) Laboratory tests may show increased eosinophils and increased serum IgE.

[Treatment measures]

Special attention should be paid to the prevention and treatment of infants and young children.

1. Instruct parents to not only pay attention to drug treatment, but also pay attention to food reactions, reasonably avoid allergic foods and protect the skin, do not wash excessively, avoid excessive irritation and excessive scratching.
2. When there are active eczema lesions, contact with herpes simplex patients should be avoided to avoid secondary infection and the occurrence of eczema herpetiformis (eczema herpetiformis).
3. Avoid woolen clothing and its environmental triggers from direct contact with the skin.

For internal and external treatments, see eczema medication. Recently, interferon, thymosin and cyclosporin A have been used as treatments. Those who are allergic to specific allergens such as dust mites can try desensitization therapy.