Atopic dermatitis is an eczematous skin eruption. It most often occurs during childhood, but may affect adolescents and adults. The incidence in children < 5 years of age is estimated at ~3%. Individuals with atopic dermatitis often have a past history of respiratory allergy or food allergy.
Immunologic abnormalities are always present. A genetically determined susceptibility to allergic reactions seems to be present.
Linear or stellate scars in the tarsal conjunctiva fornix foreshortening and symblepharon, similar to that in ocular cicatricial pemphigoid, can occur.
Numerous small defects in the corneal epithelium may develop and appear as spots after the cornea is stained with fluorescein and, if the disease is severe, scarring and vascularization may ensue.
Abnormal and paradoxical skin responses are observed in patients with atopic dermatitis. A response known as "white dermographism" occurs after stroking the skin with a blunt instrument. Thus, while the formation of erythema and wheal characteristic of the triple response of Lewis normally develops, in individuals with atopic dermatitis the erythema is often replaced by a white line surrounded by an area of blanching. After the injection of acetylcholine or methylcholine into the skin of normal individuals, vasodilatation and erythema develop, but in patients with atopic dermatitis a white, spreading reaction appears 5-30 minutes after the injection and persists for up to one hour. This delayed-blanch phenomenon of atopy, which was originally thought to be due to paradoxical vasoconstriction, is now believed to represent vasodilation, with the erythema being obscured by edema resulting from an excessive transudation into the skin. Patients with atopic dermatitis have decreased levels of circulating plasma norepinephrine, but higher concentrations than normal in affected areas of skin.
Serum IgE concentrations are generally elevated in individuals with atopic dermatitis, and upon remission of the clinical manifestations of the disease, the level may decline markedly. Usually, the serum IgA, IgM, and IgD are normal. IgG levels may be normal or elevated by IgG4 is often high. Despite an elevated serum IgE, most persons with atopic dermatitis have normal numbers of peripheral blood lymphocytes bearing IgE and other immunoglobulins, but an increase in the number of lymphocytes with complement receptors may be found.
Recent evidence suggests a deficiency of cellular immunity in patients with atopic dermatitis. Delayed hypersensitivity skin responses to ubiquitous antigens, including Candida and streptokinase-streptodornase, may be poor. This form of delayed cutaneous anergy is most marked in children with severe dermatitis, who may also fail to become sensitized by the topical application of dinitrochlorbenzene. Furthermore, the mean percentage of T cells in the peripheral blood of patients with eczema is often lower than in normal controls. The response of T lymphocytes to low concentrations of the mitogen phytohemagglutinin may also be significantly depressed. Other abnormalities in atopic patients include an eosinophilia of the peripheral blood and an increase in the absolute number of B lymphocytes. Perhaps because of a defective cellular immunity, atopic patients have an increased susceptibility to viral and fungal infections.
Since T lymphocytes are important regulators of the synthesis of IgE and other antibodies, a disorder of T regulator cells could be responsible for the failure to terminate IgE-mediated responses of certain antigens. IgE then binds to skin mast cells, initiating a release of histamine and other chemical mediators during antigenic stimulation. The overly reactive skin of atopic patients may respond excessively to the effects of histamine and other chemical mediators.
Tissue sections of skin with atopic dermatitis contain intraepithelial vesicles, dilated dermal blood vessels, and a perivascular infiltration by lymphocytes, eosinophils and mast cells. Hyperkeratosis and acantholysis occur in chronic skin lesions.
The histopathologic and immunopathologic characteristics of conjunctiva affected by AKC are typical of chronic type I and type IV immunologically-mediated inflammatory reactions. The number of lymphocytes, plasma cells and macrophages in the conjunctival substantia propria is vast, and fibroblast proliferation and new collagen formation are obvious. Mast cells are present in the epithelium, and are more abundant (as are eosinophils) in the substantia propria than normal; a large proportion of them are degranulating. Helper (CD4) T lymphocytes far outnumber suppressor (CD8) T-cells, and the T cells are activated, with a large proportion of them expressing the interleukin 2 receptor. Cytokine liberation from the inflammatory cells induces pronounced upregulation of class II glycoprotein expression on the surface of fibroblasts and epithelial cells.