Etiology
Atopic dermatitis mainly affects children living in large cities or developed countries, the prevalence of this disease has increased over the past 30 years; up to 20% of children and 1-3% of adults from developed countries are susceptible to the disease. In most people, the disease develops up to 5 years, in many – up to 1 year. According to the yet unconfirmed hygienic hypothesis, a decrease in contact with infectious agents in childhood (for example, with stricter hygiene in the home) may increase the incidence of atopy and autoimmune disorders directed at their own proteins, many patients or their relatives with atopic dematioma also have asthma or allergic rhinitis.
Pathophysiology
All of the following factors contribute to the development of atopic dermatitis (AD):
Genetic factors
Dysfunction of the epidermal barrier
Immunological mechanisms
Environmental triggers
Genes encoding epidermal and immunological proteins are involved in blood pressure. The main predisposing factor for AtD is the presence in many patients of a mutation in the gene encoding the filagrin protein, which is part of the corneocyte envelope formed by the keratinocyte during cell differentiation.
Defects in the epidermal barrier of the skin affected by blood pressure also include a decrease in the level of ceramides and antimicrobial peptides and an increase in transepidermal water loss, which increase the penetration of environmental irritants, allergens, microorganisms, causing inflammation and sensitization.
In acute blood pressure lesions, Th2 cytokines (interleukin [IL]-4, IL-5, IL-13) predominate, whereas in chronic lesions, Th1 cytokines (gamma interferon, IL-12) are present. Numerous other cytokines, including thymus stromal lipoprotein, CCL17 and CCL22, play a role in the inflammatory response in blood pressure. New treatments targeting specific cytokines help identify specific immune pathways in AD.
The most common provoking environmental factors include:
Food products (e.g. milk, eggs, soy, wheat, peanuts, fish)
Airborne allergens (e.g. house dust mites, mold, dandruff)
Staphylococcus aureus, colonizing the skin as a result of a deficiency of endogenous antimicrobial peptides
External products (e.g. cosmetic products, perfumes, exfoliating soap)
Increased sweating
Coarse fabrics
Clinical manifestations
Atopic dermatitis usually develops in infancy, usually before the age of 3 months.
During the acute phase, the lesions are red, edematous, with scaly spots or plaques, may be moist. Sometimes vesicles are present.
During the chronic phase, the clinical picture is represented by dry and lichenized rashes that occur as a result of combing and friction of the skin.
The location of the damage depends on the age. In infants, lesions usually appear on the face, scalp, neck, and extensor surfaces of the extremities. In older children and adults, lesions appear on flexor surfaces, such as the neck, elbow and popliteal pits.
Intense itching is a key feature. Itching often precedes lesions, it increases when exposed to allergens, dry air, sweating, local irritation, contact with woolen clothing and after emotional stress.
Complications
Secondary bacterial infection (superinfection) often develops, especially staphylococcal and streptococcal (for example, phlegmon and regional lymphadenitis). Exfoliative dermatitis may develop.
Herpetic eczema (another name is Kaposi’s herpetiform eczema) is a diffuse infection with herpes simplex virus (HSV) that develops in patients with atopic dermatitis. The clinical picture is represented by grouped vesicles in the area of existing or recently regressed AtD rashes, although outwardly healthy skin may also be affected. After a few days, the body temperature may rise and lymphadenopathy may join. Sometimes the infection can become systemic, and in this case it can be life-threatening. Sometimes the eyes are affected with the formation of painful rashes on the cornea.
Fungal and non-herpetic viral infection can also be attached (for example, vulgar warts, contagious mollusc).
Patients with long-term AtD may develop cataracts in the second or third decade of life.
Frequent use of products for external use is associated with the patient’s contact with a variety of potential allergens, and contact dermatitis caused by these substances can aggravate and complicate AtD, can also provoke dry skin, which is common for these patients.
Diagnostics
Clinical evaluation
Sometimes an analysis is carried out for sensitivity to allergens using a skin scarification test, a test with a radioallergosorbent or a skin test
The diagnosis of atopic dermatitis is made clinically. {blank} Diagnostic clinical signs of atopic dermatitis* modified, clinically relevant, diagnostic criteria proposed by the American Academy of Dermatology in 2003 (for the modified clinically relevant diagnostic criteria proposed by the American Academy of Dermatology in 2003.)
Atopic dermatitis is often difficult to distinguish from other dermatoses (e.g., seborrheic dermatitis, contact dermatitis, coin-shaped dermatitis, psoriasis), but the history of atopic diseases in relatives and the characteristic localization of rashes can help. In differential diagnosis, the determination of the characteristic localization can help
Psoriasis is usually located on the extensor surfaces than on the flexor surfaces, can be accompanied by damage to the nail plates and is characterized by the formation of thicker and whiter (mica) scales.
Seborrheic dermatitis most often affects the skin of the face (for example, nasolabial folds, eyebrows, bridge of the nose, scalp).
Nummular dermatitis is not located on the flexor surfaces and is rarely accompanied by lichenification.
Since patients may develop other skin diseases, not all subsequent dermatological disorders should be attributed to atopic dermatitis (AtD).
