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Atopic dermatitis is a common condition of great health significance. Consensus-driven guidelines of care or specific practice parameters may be useful, as are treatment algorithms based upon disease severity. Development of consensus guidelines on diagnosis and treatment of atopic dermatitis are discussed, and disease-severity-based guidelines of care proposed.
Atopic dermatitis is a chronic, relapsing, inflammatory skin disease that is characterized by pruritic, eczematoid skin lesions. The disease results from interactions between susceptibility genes, the host environment, skin barrier defects, susceptibility to infection and immunological factors. An increased prevalence of atopic dermatitis has generated increased interest and research into each of these areas, and new treatment strategies are being developed based upon an increased understanding of these issues.
Atopic dermatitis is a chronic inflammatory skin disease characterized by inflammatory cell infiltration in the skin. In order to assess the roles of inflammatory cells in this disease, we analysed the activation status and surface markers of various leucocytes in the IL-4 transgenic mouse model of atopic dermatitis, by flow cytometry, immuofluorescence microscopy, and T cell proliferation assays. The studies were performed with a nontransgenic mouse control and transgenic mice at three disease stages: before disease onset, early skin disease, and late skin disease, so that we can delineate the immunological sequence of events. As the skin disease evolves, the skin draining lymph node cells from IL-4-Tg mice show a spontaneous proliferation and a progressively enhanced proliferative response to stimulants including anti-CD3, Con A, PHA, and Staphylococcus enterotoxins A and B. As the disease evolves, the percent of lymphoid organ T cells expressing activation molecules (CD44 and CD69) and costimulatory molecules (ICOS and PD-1) are progressively increased; the percent and total number of T cells are reduced in an incremental manner in the secondary lymphoid organs while the number of T cells infiltrating the skin increases in an incremental fashion; the total number of dendritic antigen presenting cells, macrophages, and NK cells gradually increases in the lymphoid organs. Collectively, our results suggest that there is a continued and progressive migration of activated inflammatory cells from the secondary lymphoid organs into the skin where they participate in immune responses resulting in the pathology associated with inflammation.
Atopic dermatitis often occurs in patients who have high IgE levels and positive immediate skin tests to several common allergens. However, there is considerable doubt about the role played by allergens in this disease. Patch testing for 48 h at superficially abraded skin sites revealed that allergens could induce eczematous lesions in atopic dermatitis patients but only in those who also gave a positive immediate skin reaction to the same allergen. Lesions induced by the purified house dust mite antigen, antigen P1 contained mononuclear cells, basophils, eosinophils, and neutrophils. These patients also had raised specific serum IgE against antigen P1, and their leucocytes released histamine upon exposure to the same antigen. Thus an acute eczematous lesion can be induced by the application of inhalant allergens to the skin.
Atopic dermatitis is a chronic inflammatory skin disease associated with elevated serum IgE levels and sensitization to a variety of inhalant, food and microbial allergens. Controlled challenges have provided substantial evidence that allergens can trigger acute IgE-mediated mast-cell dependent exacerbations of eczema in these patients. However, the sustained chronic skin inflammation that characterizes atopic dermatitis is likely to result from a local expansion of allergen-specific T helper type 2 cells that produce interleukin-4 and interleukin-5 and the concomitant infiltration of eosinophils. An important role for IgE in allergen presentation to T helper type 2 cells by Langerhans cells has been proposed. These observations may have important implications for the development of new approaches for the treatment of this increasingly common allergic disorder.
Atopic dermatitis is a common chronic inflammatory skin disease often preceding the development of asthma and allergic disorders, such as food allergy or allergic rhinoconjunctivitis. Pathophysiology involves a complex series of interactions between resident and infiltrating cells orchestrated by proinflammatory cytokines and chemokines. A deficiency of antimicrobial peptides might contribute to the propensity for colonization or infection by microbial organisms seen in atopic dermatitis. New treatment approaches include use of topical steroids as maintenance therapy and use of topical calcineurin inhibitors for early intervention with topical steroids used as rescue therapy.
Atopic dermatitis is a chronically relapsing inflammatory skin disease with altered immune and pharmacologic responses. Elevated serum IgE probably reflects defective immune regulation. Various other cellular immune defects rise and fall exacerbations and remissions of skin inflammation. Increased responsiveness to cholinergic and alpha adrenergic agents may relate to abnormalities of cyclic nucleotide regulation. Recent observations of abnormal cyclic adenosine monophosphate (cAMP)-phosphodiesterase activity in atopic dermatitis may provide new insights into the pathogenesis and treatment of the disease.
Atopic dermatitis is a chronic inflammatory skin disease that causes significant morbidity in affected individuals. It is characterized by dysregulated immune responses that consist of an increased systemic Th2 response and a combination of Th2 and Th1 responses in the skin lesions. In this article, we review factors that contribute to these abnormal responses, including key effector cells of the immune system, chemokines, defective skin barrier, genetic predisposition, and environmental triggers. Understanding these pathomechanisms may improve our current therapies for atopic dermatitis.
Atopic dermatitis is a chronic inflammatory skin disease which often persists until adulthood. In severe cases, eczematous lesions and pruritus are resistant to therapy and result in depression, impairment of professional activities and social withdrawal. The goal of inpatient rehabilitation measures is to keep the patient involved and active in professional and social activities. Rehabilitative measures include diagnostics and medical therapy according to current guidelines, instruction in basic medical information, psychological intervention (relaxation techniques, improvement of self-confidence), dietetic measures, exercise, and social advice. Patients with atopic dermatitis often have work-related problems which should be identified as early as possible during rehabilitation.
Atopic dermatitis (AD) is a common inflammatory disease involving the skin and often other organs and systems, mainly respiratory. A definitive general consensus on the AD pathogenesis has not yet been established, however several lines of evidence suggest that T-cells play a crucial role in priming AD early-stage lesions. Main topics involved in the disease pathogenesis have been reviewed, which considered the concept of local and systemic haemopoietic events as important contributors to allergic inflammation, a concept now achieving great acceptance. The recently recognised atopic nature of the skin inflammation in AD has raised increasing interest for treatment with allergen-specific immunotherapy. However, we only found eight studies using specific immunotherapy (SIT) in AD, two double-blind, placebo-controlled (DBPC) and six observational. One controlled and five observational reported favourable outcomes. The one unique study providing negative results was flawed by the ineffective oral route of extract administration. Despite being encouraging, the reported results do not allow definitive conclusions based on meta-analytic techniques because the amount and quality of information in the literature is not sufficient. The highly promising sub-lingual immunotherapy (SLIT) is discussed with its potential capability of controlling not only the skin lesion severity but also its capability of preventing the development of atopic dermatitis into asthma.
Atopic dermatitis is a highly pruritic inflammatory disorder of the skin characterized by onset in infancy or childhood and a chronically relapsing course. Mainstay treatments are emollients and topical corticosteroids, but the latter are limited by side-effects from longterm use. Pimecrolimus is an ascomycin macrolactam derivative and a calcineurin inhibitor that targets T-cell activation but does not inhibit antigen-presenting cells in the skin. In multiple clinical trials comprising more than 19,000 patients, pimecrolimus cream has been shown to be very effective in suppressing atopic dermatitis and to have an excellent safety profile. This has also been shown in long-term studies (>2 years) and by postmarketing experience.
Atopic dermatitis is under the influence of series of environmental factors. The contact with unsuited cleaning agents and rough textiles can exacerbate pruritus and inflammation. Preventive and adjuvant measures can thus help the care procedures of the disease. Appropriate hygiene measures and the use of emollients are particularly helpful. Clothing measures are also in place. Undergarments and pyjamas made of knitted natural silk are available. Other measures, sometimes corresponding to anecdotal claims--antihistamines, thermal cures, unconventional medicine, probiotics, chinese herbals, essential fatty acids--have not proven their preventive efficacy in atopic dermatitis.
Atopic dermatitis is a disorder that affects up to 4.3% of the pediatric population. Its etiology is unknown, but is probably multifactorial. Evidence has been presented to implicate a role for "allergy" in the pathogenesis of AD. Disregarding the myriad of clinical reports, there is sufficient data in the literature to suggest an etiologic role for inhalants (pollen, mold, and dust mite) and foods in some patients with AD. Definitive studies have demonstrated that both inhalant and food antigens can be absorbed rapidly and transported to the skin, where sensitized mast cells can be activated. Controlled challenges have demonstrated skin reactions following exposure to inhalant and food antigens in sensitive subjects. Activiation of mast cells and/or basophils has been shown following oral food challenges in sensitized children with AD. Although sufficient evidence is now available to implicate "allergy" as an etiologic factor in atopic dermatitis, the link between mast cell activation and the development of eczematous skin changes remains to be clearly defined.
Atopic dermatitis (AD) is a common inflammatory skin disease characterized by several clinical, immunological and biochemical alterations. Comparing the patients with the 'extrinsic' and 'intrinsic' types of AD, we investigated the role of immunological mechanisms in the pathogenesis of AD. To confirm it, we calculated serum markers of T lymphocyte activation: soluble interleukin-2 receptor (sIL-2R), interleukin-4 (IL-4), interleukin-10 (IL-10) and interferon-gamma (IFN-gamma). The soluble CD14 (sCD14) and tumor necrosis factor-alpha (TNF-alpha) in serum were measured as monocyte/macrophage activation markers. We examined 29 patients with the 'extrinsic' type AD (serum IgE > 10000 IU/ml: High-AD), 23 patients with the 'intrinsic' type AD (serum IgE < 37 IU/ml: Low-AD) and 11 healthy controls. Serum sIL-2R levels were increased in High-AD and Low-AD compared with the controls. They were also significantly increased in High-AD compared with Low-AD. Serum sCD14 levels were increased in High-AD compared with Low-AD and the controls. Severity index of AD were correlated with serum sIL-2R levels but not with sCD14 levels in sera. In conclusion, IgE may not relate with the pathogenesis of atopic dermatitis. Serum sIL-2R levels may be increased according to inflammatory skin lesions and it may be exaggerated with the immunological activation in the patients with the 'extrinsic' type AD.
Atopic dermatitis (AD) has cellular immunohistochemical features similar to those of allergic contact dermatitis (ACD). There is plenty of evidence for T-cell activation in this disease such us the presence of T-lymphocytes which carry CD30, CD3, CD4, CD45RO markers. The aim of this study was to show the presence of lymphocyte-surface antigens including CD30, CD3, CD4, CD45RO in patients with acute AD and to compare the presence of the same molecules in patients with acute ACD (nickel-induced) because of the possible morphologic difference of these two entities. The presence of the stated molecules is immunohistochemically evaluated in biopsies of lesional skin in dermis and epidermis. Biopsies were obtained from twelve patients suffering from acute AD and from thirteen patients with ACD. The results show statistically significant higher average of presence and also much higher range of presence of CD30+, CD3+, CD4+, CD45RO+ lympohocytes in dermis and epidermis of patients with AD compared to the average and range in patients with ACD. Statistically much higher average of CD30, CD3, CD4, CD45RO is noticed in those occasions more in dermis than in epidermis in both groups of patients. High number of CD30+ lymphocytes in patients with acute AD does not however correlate with the severity of the disease evaluated according to clinical score for the evaluation of the severity of the disease, so called the SCORAD-index (Severity Scoring of Atopic Dermatitis). Our results showed an association betwen CD30 expression and acute AD but not with acute ACD which could evaluate CD3 as the useful marker in differentiating these two diseases.
Atopic dermatitis is an increasingly common and debilitating childhood disorder that is often accompanied by asthma and allergic rhinitis. Although the pathology of these disorders is distinct, the majority of cases are atopic, typified by elevated serum IgE. A new locus at chromosome 13q14 centred on the genes SETDB2 and PHF11 and associated with increased total serum IgE has recently been identified. Although the precise functions of SETDB2 and PHF11 are not known, both proteins are expressed in cells of the immune system and include conserved domains that suggest a role in chromatin remodelling or transcriptional regulation, respectively. In a family-based association study across the SETDB2 and PHF11 genes, we have identified two single-nucleotide polymorphisms in the PHF11 gene significantly associated with childhood atopic dermatitis in an Australian cohort. These results provide further evidence that this locus is a novel and important regulator of human atopic disease.
Atopic dermatitis (AD) is an inherited cutaneous inflammatory condition which may affect 10% of infants. Persons with this diathesis are more susceptible to irritants and to superficial infections. Little is known about diaper rash and diapering materials in AD. In this study we set firm criteria to identify a large group of infants with AD for comparison with a nonatopic, normal control group in terms of severity of diaper dermatitis; relationship of diaper dermatitis to diaper materials; and influence of modifying factors (bacterial and candidal colonization/infection, diarrhea, antibiotics, other illnesses, food allergy or intolerance). Babies with eczema were recruited and, from a group of 2,443 respondents, 87 satisfied carefully defined criteria for atopic dermatitis. A similarly sized (90) control group matched for age, sex, and weight was selected for absence of features of atopy or familial atopic history. Infants were assigned into balanced subgroups wearing cloth diapers, conventional cellulose diapers, or diapers containing cellulose and absorbent gelling material (AGM). Assessment of grading for atopic parameters showed statistically significant differences between the AD and normal groups at every visit. Mean diaper rash grades, as assessed by the same physicians at each visit, were significantly higher in the AD group wearing cloth diapers compared with those in AGM subgroups at five of eight visits. There was significant correlation between AD severity and diaper rash scores overall and in the AD cloth group, but not in other subgroups. Quantitative total bacterial plate counts were significantly lower in AGM than cloth diaper areas on three of eight sampling periods in the AD group.(ABSTRACT TRUNCATED AT 250 WORDS)
Atopic dermatitis is a chronic eczematous skin disease which characteristically starts early in life and later tends to disappear. Genetic predisposition seems important for the development of the disease. The immune system is involved through a lymphocyte-mediated inflammation in the skin creating the eczema, and an increased incidence of type I and possibly type IV allergies induced by environmental allergens. Recent findings of a changed concentration of some interleukins in atopic patients support the evidence for an increased T-lymphocyte activation and may explain the increased amount of polyclonal IgE in many of the patients. Hypothetically, atopic dermatitis can be considered to be due to an inborn error of the maturation of epithelial tissue. Maturation of epithelial tissue is essential for both the appearance of normal skin and for correct maturation of the cell-mediated immune system. The immune deviation is later more or less corrected through maturation which explains why the disease in most patients disappears in childhood. However, it still leaves a certain increased capacity for inflammation of the atopic persons.