Atopic dermatitis (AD) is a slow-onset, relapsing, pruritic, inflammatory skin disease that seriously affects the quality of life of patients and their family members. The disease is associated with genetics, allergies, and is often associated with skin barrier dysfunction. The disease usually begins in infancy, and some data show that about 50% of all patients develop the disease before the age of 1 year, and the disease is chronic, and some patients can extend the disease into adulthood. Currently, the incidence of AD can be as high as 10%-20% in developed countries, and the 1998 epidemiological survey in China showed that the overall prevalence of school-age adolescents (6-20 years old) was 0.70%, and the prevalence of urban preschoolers (1-7 years old) was 2.78% in 2002. In general, the incidence of AD decreases with age, and the disease may gradually decrease.
I. Etiology and pathogenesis
The etiology of atopic dermatitis is not yet fully understood. Genetic, environmental and biological factors are closely related to this disease. Children of parents with a history of inherited allergies have a significantly higher prevalence, but genetics is not the only determining factor. Environmental factors, especially the degree of industrialization, changes in standard of living and lifestyle, are important risk factors for the development of AD. Among the allergic factors diet such as milk, eggs and seafood also have an influence, especially in infants and children who are more ill. Dust mites, house dust mites, and pollen may be important airborne allergens. Non-allergic factors such as irritation such as disruption of the skin barrier or detergents, scratching, microbial colonization (e.g., Staphylococcus aureus and Serratia marcescens), and psychological factors (e.g., stress, anxiety, depression) also play an important role in the pathogenesis.
The exact pathogenesis of AD is not known. It is generally believed to be the result of a genetic background and/or environmental factors that cause skin barrier dysfunction or direct dysregulation of the body’s immune response, leading to a mutagenic or non-mutagenic inflammatory response. Skin barrier dysfunction creates conditions for local sensitization of allergens or microbial colonization, which is an important basis for triggering or aggravating skin inflammation.
The development of atopic dermatitis involves both immune and non-immune aspects. Immune-mediated inflammation involves several components, including the presentation of allergens by Langerhans cells and skin dendritic cells, dysregulation of Th1/Th2 balance and regulatory T-cell dysfunction, involvement and amplification of the inflammatory response process by eosinophils and specific IgE, and the production of cytokines and inflammatory mediators by keratin-forming cells involved in the inflammatory response. In recent years it has been noted that non-immune factors such as neuro-endocrine factors or abnormal physiological and pharmacological mediator responses are also involved in the formation of skin inflammation. The above inflammatory processes are an important basis for the therapeutics of atopic dermatitis.
II. Clinical manifestations
The clinical manifestations of atopic dermatitis are varied, and the most basic features are slow-onset, recurrent-onset, pruritic rash with certain age-stage characteristics. According to the rash occurrence, development and distribution characteristics, atopic dermatitis can be divided into three stages: infantile, childhood and adult. Infantile stage (1 month to 2 years old): it is characterized as infantile eczema, and the lesions are mainly exudative and dry, mostly on both cheeks, forehead and scalp. Childhood (2-12 years): Mostly evolving from infancy or not, the lesions are eczematous and itchy, mostly occurring in the elbow fossa, N fossa and lower leg extensions. Adolescent adult (> 12 years of age): lesions are similar to those of childhood and are mostly limited dry dermatitis lesions, mainly in the elbow fossa, rouge fossa, and anterior aspect of the neck, but also on the face and back of the hands.
AD can be accompanied by a range of characteristic skin changes, including dry skin, auricular fissures, ichthyosis, palmaris, periorbital keratosis, a tendency to skin infections (especially Staphylococcus aureus and simple scar virus infections), nonspecific hand and foot dermatitis, papular eczema, labyrinthitis, recurrent conjunctivitis, Dennie-Morgan periorbital dark halo, pale face, white pityriasis, anterior cervical folds, white furunculosis, anterior cervical folds, white scratching/delayed whitening, etc. These signs are helpful in aiding the diagnosis of AD.
Based on the presence or absence of combined systemic allergic diseases in AD, it can be divided into simple type, which presents with skin involvement only, and mixed type, which combines other atopic diseases such as allergic asthma and allergic rhinitis. The former lacks allergic evidence, while the latter has positive allergen-specific IgE, increased IgE levels in blood or peripheral blood eosinophils. The endogenous type of AD is easily missed clinically and should be taken seriously.
Diagnostic criteria
At present, there are various diagnostic criteria at home and abroad, including Hanifin and Rajka criteria, Willlam criteria and Conkefer criteria, etc. Among them, William criteria are concise and easy to use, and their specificity and sensitivity are similar to Hanifin and Rajka AD criteria and Conkefer criteria, and they are especially suitable for outpatient work, so they are recommended. The williams criteria for diagnosis are: pruritus must be present, plus 3 or more of the following 5 items.
(i) History of flexural dermatitis eczema, including elbow fossa, N fossa, anterior ankle, and neck (including cheek in children under 10 years of age).
(ii) Personal history of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative of a child younger than 4 years of age).
(iii) History of generalized dry skin in recent years.
④ flexural visible eczema (or eczema on the cheeks/forehead and extensor surfaces of the extremities in children under 4 years of age)
⑤ Onset before 2 years of age (for patients over 4 years of age).
IV. Treatment
Because atopic dermatitis has a long course and is prone to recurrence, its treatment principles are mainly aimed at restoring the normal barrier function of the skin, finding and removing the triggering and (or gongkou heavy factors, and reducing or relieving symptoms. When administering the necessary medication, it is important to provide health education to patients and/or family members so that they have a clear understanding of the disease, treatment methods and processes, and pay attention to various precautions in life, such as avoiding or reducing exposure to triggering factors as much as possible; understanding the importance of emollients and other adjuvant treatments and how to use them; avoiding or reducing the need to seek so-called “special effects “treatment”; understand the effects and adverse effects of relevant drugs, understand the benefits and risks of various treatments, and cooperate with doctors to obtain the best possible results.
(I) Basic treatment
1. Avoid triggering and aggravating factors: Try to avoid all possible stimuli. Should try to wear cotton products clothes, to loose appropriate, diligent change of clothing and bed sheets and other household items, to avoid forceful scratching and friction; avoid excessive washing skin, especially scalding and excessive use of soap; pay attention to maintain a suitable environmental temperature to reduce the stimulation of sweat; pay attention to maintain a clean living environment to reduce such as house dust, dragon, animal hair, pollen, fungi and other allergens; pay attention to observe the reaction to the food eaten, avoid Eating allergenic food.
2. Restore and maintain skin barrier function: Correcting dry skin, protecting skin barrier function and stopping itching are the key measures to treat AD. In the acute stage, bathing with warm water once or twice a day can increase the humidity and at the same time help to reduce exudation and remove the demented skin and residual drugs; in the diffuse stage, bathing can be done once a day.
Whether in the acute stage or in the remission stage, the application of emollients and/or moisturizers is extremely necessary and should be applied topically (mostly for systemic use) at least one or two times a day, especially immediately after bathing, in order to maintain the hydrated state of the skin and protect the barrier function and reduce the symptoms of cancer itch.
(II) Drug treatment
1.Topical treatment.
(1) Glucocorticoids: Intermittent topical glucocorticoids, together with emollients and moisturizers, are the first-line treatment for AD. According to the patient’s age, lesion location and the degree of disease clearance, different types and strengths of glucocorticoid preparations should be selected to control inflammation and reduce symptoms quickly and effectively. Generally, preparations of sufficient strength should be used for initial treatment to achieve significant control of inflammation within a few days. However, relatively weak glucocorticosteroids should be used on the face, neck and folds, and strong fluoride preparations should be avoided. Long-term use may cause certain skin adverse reactions (such as skin atrophy, capillary dilation, swelling lines, hirsutism, glucocorticoid acne, bacterial infection, purpura, etc.), and long-term large-scale application may sometimes cause systemic adverse reactions (medical adrenocortical insufficiency, Cushing’s syndrome, psychoneurological symptoms, glaucoma, cataracts, and menstrual cycle disorders, etc.). ). Therefore, for chronic thick lesions, a more potent glucocorticoid preparation should be used topically, and after a short period of control, a weaker preparation or a non-glucocorticoid drug should be used.
(2) Calcium-modulated neurophosphatase inhibitors: These drugs, including tacrolimus ointment and pimecrolimus cream, have good efficacy in AD, have strong selective anti-inflammatory effects, and can be used for a relatively long time in all areas of the disease, especially the face and neck and other tender areas of the skin. Adverse reactions are mainly local burning and irritation for a short period of time after administration, no significant systemic adverse reactions have been found (transdermal absorption of both drugs is low), and no adverse reactions of glucocorticoids
(3) Topical antibiotics: Since bacteria or fungi can induce or aggravate the disease by producing super antigens or acting as allergens, the early addition of antibacterial or antifungal drugs while using glucocorticoids, especially when treating exudative lesions, can help control the disease, but long-term use should be avoided.
(4) Anti-itch agents: 5% doxepin cream or non-residual anti-inflammatory drugs can effectively reduce itchy symptoms in the short term, and can be used alternately with glucocorticoid preparations or calcium-regulated neurophosphatase inhibitors
(5) other: according to the different disease clear and lesions, can choose wet compress, zinc oxide oil (paste) agent, tar, black bean distillation oil, etc.
2.Systematic treatment.
(1) antihistamines and cell membrane stabilizers: according to the different conditions and medication objects can choose the first generation or second generation antihistamines
(2) anti-infective drugs: for patients with serious disease (especially those with exudate) or confirmed secondary bacterial or fungal infection, anti-infective drugs can be given for a short period of time (7-10 d), but do not abuse.
(3) Glucocorticoids: In principle, these drugs should not be used or used sparingly, especially in children. However, patients with severe disease can be given small to medium doses for a short period of time, and use the morning dose method. After the condition improves, the dosage should be gradually reduced and discontinued in time to avoid adverse reactions brought about by long-term use or the rebound of the disease due to too rapid discontinuation of the drug.
(4) Allergen-specific desensitization therapy: For some mixed AD and exogenous AD that do not heal, allergen-specific desensitization therapy has selective therapeutic value.
(5) Immunosuppressants: For patients with severe disease that cannot be easily controlled by conventional therapy. Cyclophilin, azathioprine and mortezapine can be used as appropriate. But children should be used with caution, and the use of systemic adverse reactions should be noted.
(6) Anti-leukotriene therapy: Anti-leukotriene agents such as zallust and montelukast have been reported to be effective in the treatment of AD, especially in patients with allergic asthma.
(7) Other: trinostat, glycopyrrolate and multivitamins can be chosen for the treatment of AD, and interferon-γ, which has adjuvant therapeutic effect, may be effective for the treatment of AD, but often requires long-term maintenance medication.
(3) Traditional Chinese medicine: According to clinical symptoms and signs, evidence-based treatment is administered.
(iii) Physical therapy
Ultraviolet light is an effective treatment for AD, and narrow-spectrum medium-wave ultraviolet light (NB-UVB) and UVAI are more effective. Emollients should be used after phototherapy. The carcinogenicity of this therapy after long-term repeated use needs further evaluation, and it is generally believed that patients under 12 years of age should avoid using UV therapy.
V. Prognosis
AD in young children is more serious, but the disease decreases with age, and 40% of AD starting in infancy can heal spontaneously after 5 years of age. Most authors report that 40%-50% of those with mild disease are cured by the age of 15. Some people have followed up 2000 cases of AD for 15 years and about 90% were cured. In general, those with a family history, asthma or cushings, late age of onset and severe dermatitis have a longer duration of disease.
In conclusion, in the process of AD treatment, the patient’s history, duration, severity and extent of involvement should be evaluated first, and the corresponding “comprehensive treatment” should be given according to the different conditions. Since this disease is chronic and requires long-term treatment, the cooperation between the doctor and the patient is very important to obtain good results.
Patients with eczema or atopic dermatitis should be seen in the allergy department to identify allergic factors and their possible atopic immunotherapy.