Atopic dermatitis (AD) is a chronic skin disease associated with genetic predisposition and characterized by distinctive “atopic” features seen in oneself or in one’s family. “Atopic” means: 1) a familial predisposition to asthma, allergic rhinitis, and eczema; 2) allergy to allergic proteins; 3) high serum IgE; and 4) the highest number of blood eosinophils. Typical atopic dermatitis has the above four characteristics in addition to the specific clinical manifestations of eczema. What are the clinical manifestations of atopic dermatitis? Atopic dermatitis has many forms of clinical manifestations, which can be divided into three stages: infancy, childhood and adolescent-adult according to the characteristics of rash occurrence, development and distribution. Atopic dermatitis develops in infancy when the patient is less than 2 years old and is mainly manifested as infantile eczema, with lesions occurring mainly on the cheeks, forehead, scalp and neck. The lesions are mainly of the exudative and dry type, with the former being more common in clinical practice. Many children develop the rash a few months after birth and typically present with itchy skin accompanied by erythematous patches with dense blisters and pinpoint papules. It is also sometimes called infantile eczema or tinea cruris when it develops in infancy. The childhood phase refers to children between the ages of 2 and 10 years and mostly evolves from the infantile phase, when the scalp layer may be a little better than the original. The lesions are mainly of the eczema and itchy rash type, with typical sites of onset in the anterior elbow fossa, N-fossa, flexural wrist, eyelids, face and neck. The most subjective symptom of this period is intense itching, so that a large number of scratches on the lesions are followed by infection, resulting in a vicious cycle of “itching – scratching – itching”. The lesions in adolescence and adulthood are similar to those in childhood, and are mostly limited dry dermatitis lesions, erythema or papules, which fuse to become mossy skin with grayish white scales. The lesions mainly occur in the elbow fossa, N fossa and anterior and lateral parts of the neck, with the flexion side being the most important. It can be accompanied by other allergic diseases, such as asthma, allergic rhinitis, etc. The pathogenesis of atopic dermatitis: The cause of atopic dermatitis is very complex and has not been completely clarified. Studies have shown that the onset of AD is caused by environmental factors acting on genetically susceptible individuals, resulting in immune dysregulation. The etiology is mainly related to genetic susceptibility, food allergy, airborne allergens, skin lesion infection and skin barrier dysfunction. In atopic dermatitis associated with genetic factors, usually if both parents have allergic diseases, such as atopic dermatitis and allergic rhinitis, the probability of the child getting an allergic skin disease is 50-75%. If one parent has the disease, the child’s chance of getting the disease is 25-50%. If both parents do not have it, the child’s chance of getting it is 7-25%. Environmental factors have also contributed to the yearly increase in atopic dermatitis patients in recent years. There are also a number of allergens that can act as atopic triggers, including airborne allergens, food allergens, and microorganisms. Diet can also have an impact on the onset of atopic dermatitis, especially in children who eat certain seafood, milk, eggs, etc. This can also aggravate the condition. The incidence of atopic dermatitis may be higher in autumn and winter when the season is drier, and in spring when there is more pollen of all kinds, pollen can aggravate allergies. In addition, insect mite allergy is also an important factor in the development of atopic dermatitis. There are also some atopic dermatitis that are not caused by allergic factors. For example, burning, excessive friction or the use of some alkaline lotions and other stimuli can also have a triggering effect on the disease. In addition, some mental factors such as anxiety and stress can also have an impact on the development of the disease.