Textbook of Atopic Dermatitis
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Primary infections with herpes simplex virus E herpeticum are often severe in atopic E patients and require hospitalization. Besides reducing the epidermal immunity, Th2 cells also further decrease the epidermal barrier function by inhibition of genes belonging to the EDC e. While acute E lesions are infiltrated by a vast majority of Th2 cells, more chronic lesions are characterized by a broader immune response of mostly Th1, Th2, and Th22 cells. In line with that observation, the clinical hallmarks of acute versus chronic E are strikingly different, but the reduced epidermal barrier function with dryness of the skin and the skin colonization with extracellular microorganisms are constantly observed throughout all stages of E.
The dry skin with reduced epidermal barrier function causes a non-specific hypersensitivity of the skin towards all kinds of irritant factors. This involves substances with irritative potential e. There is no doubt that psychology greatly influences E, and most patients report stress results in aggravation of the disease. The field of psychoneuroimmunology is rapidly evolving and initial theories report a functional and morphological interaction of mast cells, neuropeptides, and nerve fibers.
Textbook Atopic Dermatitis
While initial studies reported an association with attention deficit hyperactivity disorder in children, the current concept assumes concentration problems in children might occur secondary as a consequence of the permanent and agonizing itch and sleep loss. Itching and social stigma are also the two main explanations why E patients suffer from a severely reduced quality of life.
In the early lesions Th2 cells predominate, later in the more chronic phase Th1 cells prevail. More than in other allergic diseases, E is characterized by increased serum IgE levels. T cells play a major role in regulation of IgE production. While Th2 reactions are crucial for triggering reactions, in chronic skin lesions Th1 reaction patterns can be observed.
However, the hypothesis of a lower prevalence of T cell-mediated contact allergy in E has been questioned. Greater prevalence rates of contact allergy are found in E patients than in a normal population. Rather, these patients show a different contact allergen spectrum compared to individuals lacking the atopic constitution metal allergy more frequent; lanolin, fragrance, etc. Clinically, the white dermatographism and some psychosomatic interactions may partially be explained by this imbalance, which also gives rise to enhanced releasability of vasoactive mediators, e.
An exacerbation of atopic E by foods in food allergic patients has been repeatedly reported, with the vast majority of cases seen in children.
Learning module: Atopic dermatitis
This should be considered in the management of E when there is a history of food allergy, or when conventional treatment measures are ineffective. Whereas the IgE-mediated reactions are the most common ones, a non-immunological hypersensitivity reaction to food additives can also worsen AE in some cases. An appropriate diagnosis of the suspected food allergy should be made.
Some patients with atopic E suffer exacerbations of their skin lesions after contact with certain aeroallergens, e. In certain patients, E skin lesions can be induced by epicutaneous patch testing with aeroallergens, e. The term "atopy patch test" APT has been proposed for this test procedure. The clinical appearance of E inflamed lesions emerging on dry, scaling skin is suggestive of an impairment of skin barrier function.
An enhanced transepidermal water loss TEWL and reduced skin surface water content are physical parameters that directly reflect this impaired barrier function. The barrier function is maintained by the stratum corneum which forms a continuous sheet of alternating squamae, which are protein-enriched corneocytes embedded in an intercellular matrix, consisting mainly of non-polar lipids which have developed as lamellar sheets.
Even uninvolved skin of E patients is characterized by distinct differences in skin surface lipid composition, especially in the ceramide fraction. Profound changes in cutaneous flora occur in some patients with E and the pathogenic importance of microbial organisms is recognized. Among these, Malassezia furfur and Staphylococcus aureus seem to play a major role. Aureus is responsible for a known, very often quite dramatic complication of E, named "impetiginised E," requiring systemic antibacterial treatment, and in addition S.
The inflammatory reaction may be caused by enterotoxin production, possibly with superantigen effects. It is speculated that staphyloccocal superantigens, when released within the epidermis, cause a marked immune stimulation. The ability of staphylococcal enterotoxin B to elicit dermatitis after application to intact normal or intact atopic skin has been shown. It is likely that reduced innate immune responses, eg, reduced formation of antimicrobial peptides like defensins, give rise to increased microbial colonization.
Severity of pruritus in E has been described as directly related to severity of depressive symptoms. Increased itch and sweating in lichenified skin areas, following emotional stimuli, can be recorded by psychophysiological methods.
Vasculitis, Purpura and Other Vascular Diseases. Collagen Diseases. Physiochemical Injury and Photosensitive Diseases. Blistering and Pustular Diseases.
Textbook of atopic dermatitis - Semantic Scholar
Disorders of Abnormal Keratinization. Disorders of Skin Color. Metabolic Disorders. Disorders of the Dermis and Subcutaneous Fat. Disorders of the Skin Appendages.
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