Atopic dermatitis, also known as atopic eczema or allergic dermatitis, is a chronic, relapsing, pruritic, and inflammatory skin disease with a genetic predisposition, elevated serum IgE levels, and frequent association with asthma and allergic rhinitis. In traditional Chinese medicine, conditions such as "infantile eczema" and "cubital and popliteal eczema" may represent different stages of this disease.

bubble_chart Etiology

The pathogenesis of this disease is relatively complex, involving genetic factors, immune dysfunction, and abnormal responses to physiological and pharmacological mediators. Environmental factors also play a significant role in its occurrence. Approximately 70% of patients have a family history of atopic dermatitis, asthma, or allergic rhinitis.

If both parents have a history of atopy, their children have a higher likelihood of developing atopic diseases compared to those with only one parent having such a history. Recent studies have identified a gene on chromosome 11q13 associated with the development of allergic asthma in this disease. In terms of immune abnormalities, elevated serum IgE levels are observed. Recent research indicates that Langerhans cells in the skin possess high-affinity IgE Fc receptors (FcεRI). "Inhaled" antigens entering the skin of atopic dermatitis patients activate Langerhans cells, which release IL-1β, thereby activating the atopic-specific T-helper cell subset TH-2. This leads to the production of cytokines such as IL-4 and IL-5, which stimulate B cells to produce IgE. Additionally, IL-5 is a crucial cytokine for the differentiation and proliferation of human eosinophils. In patients with atopic dermatitis, eczema-like skin reactions induced by environmental allergens (e.g., house dust mites, Mongolian snakegourd root) resemble cutaneous late-phase reactions. Eosinophil infiltration is observed in skin lesions, suggesting that IgE-mediated "contact hypersensitivity" plays an important role in the pathogenesis of atopic dermatitis. From a physiological and pharmacological perspective, leukocytes and epidermal cells in these patients exhibit reduced responsiveness to β-adrenergic agonists. This results in decreased cAMP levels and diminished inhibitory effects on epidermal cell nuclear division, along with reduced affinity of β-adrenergic receptors for β-agonists and an increased ratio of α-adrenergic receptors. Furthermore, elevated activity of cAMP phosphodiesterase (PDE) in mononuclear cells has been observed, leading to a decline in cAMP levels.

The symptoms of this disease are diverse, with inflammation ranging from acute to chronic, recurring episodes, severe cutaneous pruritus, and a prolonged course. The characteristics of the rash also change with age. It can generally be divided into three stages: infancy, childhood, and adolescence/adulthood. Some patients progress sequentially through all stages, while others may only experience one or two.

The onset in infancy is usually early, with approximately 60% of cases occurring within 1–6 months after birth, and some as early as one week after birth. About 90% of cases manifest before the age of 5, while less than 5% occur after the age of 35.

(1) Clinical manifestations in infancy are identical to infantile eczema. The lesions primarily affect the forehead, cheeks, auricle, scalp, and chin, but may also occur on the limbs and trunk. Initially, there is acute erythema, which gradually develops into needle-sized papules, papulovesicles, and blisters that may densely cluster, with indistinct borders. The rash is polymorphous, with marked cutaneous pruritus. Severe scratching may lead to excoriation, oozing of serous fluid, and the appearance of bright red erosive surfaces with copious exudate. After the exudate dries, crusts form, and the scalp may develop yellow seborrheic crusts. The condition fluctuates in severity, and factors such as certain foods or environmental triggers may exacerbate it. Generally, it resolves gradually by the age of 2.

(2) Childhood onset typically occurs 1–2 years after infancy subsides, starting around age 4, though a minority of cases persist from infancy. Lesions often involve the extensor or flexor surfaces of the limbs, particularly the popliteal and antecubital fossae. Erythema is usually milder than in infancy, with dark red papules and less exudation, though excoriation may occur. Over time, the rash thickens and becomes lichenified. A minority may present with prurigo-like lesions, with normal or dark brown skin, rough surfaces, scattered over the extensor surfaces of the limbs. Nearby lymph nodes may become enlarged.

(3) Adolescence/adulthood refers to atopic dermatitis in individuals aged 12 and older, which may develop from childhood or arise directly. Lesions are often lichenified or present as acute or subacute eczematous eruptions, commonly affecting the antecubital and popliteal fossae, limbs, and trunk. In addition to the above symptoms, patients often exhibit generalized dry skin or grade I ichthyosiform changes, prominent palmar creases, a generally pale complexion, and grade I periorbital hyperpigmentation, appearing as a light brown halo. The skin may show white dermographism upon blunt stimulation. Pruritus is easily exacerbated by temperature changes, emotional stress, sweating, or contact with wool. Approximately 60–70% of patients have a history of bronchial asthma or allergic rhinitis.

The diagnosis can be made based on the characteristics of the disease.

(1) In infants and children, the rash is commonly seen on the face and extensor surfaces of the limbs or in the elbow and popliteal fossa, presenting as polymorphic lesions such as erythema, papules, and exudation;

(2) In adolescents and adults, the lesions often manifest as lichenified rashes on the flexural or extensor surfaces of the limbs, following a chronic recurrent course;

(3) A personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis);

(4) Severe cutaneous pruritus;

(5) Laboratory tests may reveal elevated eosinophils and increased serum IgE levels.

bubble_chart Treatment Measures

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

1. Parents should be guided to not only focus on drug treatment but also observe food reactions, reasonably avoid allergenic foods, and protect the skin. Avoid excessive washing or scalding, and minimize irritation from Gleditsia Spine as well as excessive scratching.
2. When active eczema lesions are present, contact with individuals infected with herpes simplex should be avoided to prevent secondary infections leading to eczema herpetiformis.
3. Avoid direct skin contact with woolen clothing and environmental triggers.