Atopic dermatitis (AD) is a common chronic, recurrent, inflammatory skin disease that can develop in all ages, most commonly in children, and is characterized by dry skin, intense pruritus, and often a family history of “atopic”, the pathogenesis of which is not yet fully understood. About 10% to 20% of children and 1% to 3% of adults worldwide suffer from AD, and the incidence of AD has been increasing significantly in recent years. The significant itching often causes insomnia, which affects the quality of life of patients and their families, and even affects the self-confidence of patients. The development of atopic dermatitis may be genetically related, with about 70% of cases having a family history of atopic conditions (e.g., asthma, allergic rhinitis, atopic dermatitis, etc.). Other etiologic factors include abnormal immune response, abnormal vascular and vascular drug response, neuropsychiatric factors, infection, climate and living environment. Patients have certain temporal characteristics of skin lesions. The distribution of the typical rash and the manifestation of the lesions vary at different ages. Most patients have increased serum total IgE or specific IgE (food or inhalation) and increased eosinophils and their products. 1. Diagnostic criteria 1 .1 Hanifin and Rajka’s criteria can be used as the basic criteria for the diagnosis of atopic dermatitis (1980) and are described as follows: The main criteria include at least 3 items: (1) pruritus. (2) Typical rash morphology and distribution: (i) mossy lesions on flexural skin in adults. (2) Involvement of the skin on the face and extensor side of the limbs in infants. (3) Chronic or chronic recurrent dermatitis. (4)Personal or family history of atopic (including asthma, allergic rhinitis, atopic dermatitis). Secondary criteria:At least 3 items are included: (1)Dry skin disease. (2) Ichthyosis, hyperkeratosis, and peripapillary keratosis. (3) Positive IgE-mediated immediate skin test reaction (or positive RAST test). (4) Elevated serum IgE levels. (5) Early onset. (6) Susceptibility to skin infections (especially Staphylococcus aureus and herpes simplex virus infections). (7) Tendency to non-specific hand and foot dermatitis. (8) Papillary eczema. (9) Labyrinthitis. (10) Recurrent conjunctivitis. (11) Dennie-Morgan folds (transverse folds at the lower eyelid margin). (12) Cone cornea. (13) Anterior subcapsular cataract. (14) Dark halo around the eye. (15) Facial pallor and erythema. (16) White pityriasis. (17) Itchy skin when sweating. (18) Intolerance to wool and fat solvents. (19) Peri-hair bulges. (20) Food hypersensitivity. (21) Course of the disease is influenced by environmental and emotional factors. (22) White skin scratching or delayed response to choline drug whitening test. 1.2 On the basis of the above adult criteria, the diagnostic criteria for infantile patients were revised as follows: Main features: (1) Family history of ectasia. (2) Typical dermatitis of the face or extensor side of the limb. (3) manifestations of pruritus. Secondary features: (1) Dry skin disease, ichthyosis, and excessive palmar lines. (2) Peri-hair bulges. (3) Lateral cleft behind the ear chakra. (4) Chronic scaling of the scalp. 1.3 On this basis, skin workers in many countries and regions have made appropriate modifications to the diagnostic criteria for atopic dermatitis. Our Professor Kang Kefei et al. proposed the following diagnostic references based on clinical observations and the pathogenesis of atopic dermatitis:Basic features: (1) Pruritus, chronic or chronic recurrent dermatitis: inflammatory, exudative eczematous lesions distributed on the face and extensor surfaces of the limbs in infants and children; mossy lesions on the flexor and extensor surfaces of the limbs in adolescents and adults. (2) Personal or family history of genetic allergies (asthma, allergic rhinitis, atopic dermatitis). Secondary features: (1) Genetically related: (i) early onset; (ii) dry skin, ichthyosis, and palmar hypermetropia. (2) Immune-related: (i) related to type I allergic reactions: immediate skin test reaction, eosinophilia, increased serum IgE levels, angioedema, allergic conjunctivitis, food allergy; (ii) related to immunodeficiency: propensity for skin infections (especially Staphylococcus aureus and herpes simplex virus infections), damaged cell-mediated immunity. (3) Related to physiology and pharmacology: (i) white skin scratching, cholinergic delayed whitening and/or pallor; (ii) perifollicular bulges, nonspecific dermatitis tendency, periorbital dark halo. The diagnosis is established where two essential features or one of the first essential feature and three (one point of each) secondary features are present. 1.4 Because most of the diagnostic criteria involve more clinical indicators, which are cumbersome and time-consuming to apply clinically and not easy to master, Williams (1994) in the UK developed a simple minimum criterion for the diagnosis of AD: there must be a history of pruritus, plus 3 or more of the following: (1) History of flexural skin involvement, including the elbow fossa, N fossa, anterior ankle or around the neck for one week (in children under 10 years of age including the cheek). (2) Personal history of asthma or chytridiomycosis (or history of AD in children under 4 years of age in first-degree relatives). (3) History of generalized dry skin. (4) Eczema on the flexor side. (5) Onset before 2 years of age (for those older than 4 years of age). The criteria are concise and easy to use, and their specificity and sensitivity are similar to those of Hanifin and Rajka and Kangyitian (domestic). 2. Clinical typing According to the difference of ectopic manifestations and the results of reaction to allergens, ectopic dermatitis is typed as follows: (1) Simple type: not complicated by respiratory symptoms. (1) Exogenous: skin or serum test sensitization to polyvalent IgE from inhalants and/or food. (2) Endogenous: No specific IgE can be detected and total serum IgE levels are normal. (2) Mixed: Complicated respiratory allergy symptoms, such as asthma and allergic rhinitis. Polyvalent IgE sensitization of specific inhalants and food. 3.Clinical manifestations Most often develop 2-6 months after birth (more than half within 2 years after birth), but can also occur at any age. There are slightly more male patients than female. The main manifestations of polymorphic rash are: erythema, papules, papules, exudative nodules, mossy lesions and skin scratches, dry skin, secondary infection, and mostly pruritus. The distribution and performance of the rash varies with age. 3.1 Infancy: The rash is most commonly seen on the face, but also on other exposed or friction-prone areas, such as the extensor surfaces of the limbs. The perineum and buttocks are generally less commonly involved. The rash mostly appears as erythematous, scattered or fused edematous papules and papular scars, which may have exudation and nodules, with intense itching. Secondary infection or lymph node enlargement is common. The course of the disease is recurrent, and changes can be affected by teething, respiratory infections, emotional stimulation, climate change, etc. 3.2 Childhood: The rash is mostly distributed on the flexor side of the elbow and knee, the side of the neck, wrist and ankle. The erythema and papules in infancy are gradually replaced by lesions dominated by mossy changes. Pruritus is intense. 3.3 Adult stage: The skin lesions in the adult stage behave similarly to those in late childhood, mainly showing mossy lesions on the flexors of the limbs and hands. Itching is intense. 4. Treatment 4.1 General treatment: AD patients have increased sensitivity to the external environment. To avoid irritation, wear cotton and loose clothing as much as possible, avoid contact with animal dander, and avoid swimming in swimming pools containing chlorine. In recent years, with the increasing understanding of the correlation between the barrier function of the skin and the development of AD, restoring and protecting the barrier function of the skin has become an important measure in the treatment of AD. It is reported in the literature that the number of sebaceous glands in the skin of AD patients is reduced, the volume is reduced, the lipid content of the skin surface is decreased, the water content is reduced, the decrease of free fatty acids changes the acidic PH of the stratum corneum, the barrier function of the skin is destroyed, which makes it easy for Staphylococcus aureus to grow and increase the toxicity, thus aggravating or triggering AD. After bathing, use a mild and non-irritating moisturizing cream to moisturize the skin and restore the barrier function of the skin. The restoration of skin barrier function can also enhance the efficacy of local glucocorticoids and reduce the severity of AD lesions and recurrence rate. 4.2 Topical treatment: 4.2.1 Glucocorticoids: Since the introduction of hydrocortisone in the 1950s, glucocorticoids (hereinafter referred to as hormones) have been used in the treatment of AD for more than 40 years, and they are still the first choice of topical drugs for the treatment of AD. This can not only improve the efficacy, but also reduce the dosage and side effects of topical glucocorticoids. 4.2.2 New class of topical immunomodulators: In December 2000 and December 2001, the US FDA approved the first class of topical immunomodulators 0.1% and 0.03% of tacrolimus ointment (FK506 , Protopic) and 1% of pimecrolimus ((SDZ ASM981, Elidel), respectively, as short-term and long-term intermittent therapy for the treatment of AD in children over 2 years of age and adults. Tacrolimus is used for the treatment of moderate and severe AD, while pimecrolimus is used for the treatment of mild and moderate AD,0 .03% tacrolimus is used only for children aged 2 to 15 years and 0 .1% tacrolimus is used for children and adults aged 16 years and older. In recent years, a large number of multicenter clinical studies have been conducted in the United States, Europe and Japan on the clinical efficacy, safety, tolerability and side effects of tacrolimus and pimecrolimus in the treatment of AD. The results show that tacrolimus or pimecrolimus monotherapy for the treatment of AD in children and adults has a rapid onset of action, with symptomatic improvement within 3 days of treatment and a sustained increase in efficacy over a long period of time (1 year), reducing relapses and controlling acute attacks. No other significant side effects were found during the drug administration, and it is suitable for long-term use. The relatively large molecular size and high lipid solubility of tacrolimus and pimecrolimus limit the diffusion of both into the blood through the skin, thus providing effective treatment without hormone-like side effects such as skin atrophy. 4.3 Systemic therapy 4.3 .1 Immunosuppressants: Traditional immunosuppressants for the treatment of AD include azathioprine and cyclosporine for AD patients resistant to conventional therapy. The former limits the use of the drug because of its myelosuppressive effect, which can cause leukopenia and increased chance of infection and carcinoma, and the latter is effective for short-term application in the treatment of AD because of nephrotoxicity, which limits the long-term clinical application of the drug. Leflunomide (Elidel), a new generation immunomodulator, has a similar mechanism of action to cyclosporine and has been shown to have a good safety profile for systemic therapy, but the efficacy of oral administration for the treatment of AD is uncertain. Recently, a new immunomodulator FTY720 has been introduced, and experimental studies have demonstrated that FTY720 has a strong inhibitory effect on serum 19E production, epidermal hyperproliferation and granulocyte degranulation, and oral administration (0.1 mg/kg, once a week) can completely prevent the occurrence of simulated AD in mice. AD treatment in the near future. 4.3.2 Glucocorticoids: Systemic hormone therapy for AD should only be used in patients with severe AD who have failed conventional therapy and is in principle contraindicated in pediatric AD patients. 4.3.3 Antihistamines: Antihistamine therapies include conventional H1 receptor antagonists, newer non-drowsy H1 receptor antagonists, and combinations of the two. In recent years, third-generation antihistamines have come into clinical use. First-generation antihistamines act on central and terminal H1 receptors and have drowsy and anticholinergic effects; second-generation antihistamines do not cross the blood-brain barrier and have a less inhibitory effect on the central system; third-generation antihistamines, in addition to antagonizing histamine, have the effects of inhibiting eosinophil wandering and degranulation and inhibiting the release of inflammatory mediators. Preliminary studies have shown that histamine is an important factor causing pruritus in AD patients. Recent studies have shown that traditional antihistamines for AD are not effective through antagonism of peripheral H1 receptors, but through drowsiness of the central nervous system, so antihistamines with drowsiness effects should be selected for the treatment of pruritus in AD, and this class of drugs is still a conventional adjuvant therapy for the treatment of AD, and their exact The exact mechanism and efficacy remain to be elucidated. 4.3.4 Other anti-inflammatory agents: leukotriene antagonists can significantly reduce inflammation in AD patients, however, long-term application requires monitoring of liver function, and the efficacy and safety of these drugs still need to be elucidated in a large number of clinical trials. In recent years, clinical studies have demonstrated that:, Y interferon is safe and effective in the treatment of AD, but the efficacy still needs to be proven in clinical trials with larger samples. monoclonal antibodies to the Fc segment of the IgE receptor and certain antagonists of interleukins and chemokines are currently under experimental research for the treatment of AD. 4.3 .5 Chinese herbal medicine: Some clinical studies at home and abroad have shown that certain Chinese herbal medicines are effective in the treatment of AD, however, there is a lack of clinical research data and reports on hepatic and renal toxicity, and their efficacy and safety need further clinical observation. 4.3 .6 Antibiotics AD patients’ skin barrier function is destroyed, the pH of the stratum corneum is reduced, easy to secondary infection of microorganisms such as Staphylococcus aureus, Staphylococcus aureus can make AD recurrence or aggravation by releasing super antigen, oral or topical antibiotics to prevent or inhibit secondary infection, has important clinical significance for the treatment of AD. However, antibiotics have the following shortcomings in the treatment of AD: while killing Staphylococcus aureus, they will also destroy the normal flora on the skin surface, such as Staphylococcus epidermidis, weakening its inhibitory effect on pathogenic microorganisms; they will also enable the growth of drug-resistant pathogenic bacteria to promote the relapse or aggravation of AD; in addition, topical antibiotics are irritating to the skin of AD patients. Recently, a study showed that the application of cream containing xylitol for the treatment of AD can inhibit the formation of biofilm of Staphylococcus aureus without affecting Staphylococcus epidermidis, which can improve the clinical symptoms of AD patients and is promising to be used for the treatment of AD instead of antibiotics. 4.4 Phototherapy It is well known that PUVA can reduce spasmodic itching and lesion occurrence in patients; UVB alone or in combination with tar preparations has better efficacy in treating AD resistant to conventional methods; in recent years, UVA and narrow-wave UVB have been reported to be effective in treating AD, and the mechanism of UVB treatment of AD is to act by regulating keratinocytes, dendritic cells and T lymphocytes, and phototherapy because of its carcinogenic Because of its carcinogenic potential, care should be taken to use it in combination with oral or topical immunomodulators, however, hormones have been used in combination with phototherapy for decades and no clinically significant signs of increased infections or skin cancer development have been seen. 4.5 Psychotherapy Many controlled clinical studies have shown that psychological relief such as relaxation, stress reduction and prevention of scratching can reduce clinical symptoms and recurrence in AD patients, and can be used as adjuvant therapy for AD. 4.6 Other therapies Studies have reported that intravenous administration of high-dose immunoglobulin therapy is effective in adults with severe AD resistant to conventional therapy, but further clinical randomized controlled studies are needed to support this. Hoppu, a Finnish scholar, reported that ingestion of a vitamin C-rich diet by mothers with AD resulted in a significant increase in the vitamin C content of breast milk and reduced the risk of AD in the infant. Recent studies have found that inactivated hypervirulent streptococcal preparations have stronger immunomodulatory effects than BCG ribonucleic acid and can downregulate T12 cells while increasing the composition of T11 cells23 and are effective in treating AD, however, the efficacy needs further clinical observation. As the understanding of the etiology and pathogenesis of AD continues to improve, it is believed that more effective therapies will emerge for the treatment of AD.