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At least 19 recordsLinked to original sources
PubMed1992

Secular change in the occurrence of atopic dermatitis.

Atopic dermatitis is a common disease, and population-based studies indicate that the frequency of atopic dermatitis has increased substantially during recent decades. It has been generally accepted that disease onset occurs before 7 years of age in 80-90% of the cases, and consequently the epidemiology of atopic dermatitis has been studied mostly in children on admission of first grade school. Before 1960 about 2-3% of children suffered from atopic dermatitis. In the 1960s, some 4-8% was recorded in several studies, and for those born after 1970 most researchers found that 9-12% developed atopic dermatitis during childhood. The diagnostic criteria of Hanifin and Rajka are cumbersome for population studies not designed specifically for children. In order to compare epidemiologic data from varying times and locations, a framework for questionnaire studies in atopic dermatitis is proposed.

Child↗
PubMed1992

Factors influencing the localization of atopic dermatitis.

Atopic dermatitis is clinically characterized by the involvement of preferential sites. Some of these localizations, such as the face in the first year of life and later on the flexural aspect of the limbs, are constant and thus characteristic of atopic dermatitis. They are probably determined by factors that are identical for all subjects, whereas the less constant localizations are probably influenced by individual factors. The author discusses from a clinical point of view the factors that can influence localization and the lack of involvement of certain sites in atopic dermatitis. An unusual localization of atopic dermatitis, such as around congenital nevi, is also discussed.

Age Factors↗
PubMed1991

Skin levels of vasoactive intestinal polypeptide in atopic dermatitis.

Atopic dermatitis (AD) can be exacerbated by various factors, including emotional stress, scratching and sweating. The aim of the present study was to evaluate the hypothesis that the inflammatory reaction in AD is also neurogenic. For this purpose, the levels of vasoactive intestinal polypeptide were measured radioimmunologically in whole-tissue homogenates of lesional skin of 13 patients with atopic dermatitis. Radioimmunoassay was performed using an antiserum, AH78, recognizing the carboxy-terminal fragment vasoactive intestinal polypeptide (22-28). Vasoactive intestinal polypeptide immunoreactivity was detected in relatively low amounts in control skin (0.428 +/- 0.08 pmol/g tissue), whereas a marked increase in the peptide was observed in lesional skin of patients with atopic dermatitis (5.62 +/- 1.25 pmol/g tissue). These results seem to suggest that vasoactive intestinal polypeptide could have a pathogenetic relevance in skin lesions of atopic dermatitis.

Adolescent↗
PubMed1989

Recent investigations on the relationship between fungal skin diseases and atopic dermatitis.

Atopic dermatitis may be associated with chronic dermatophyte infections and Pityrosporum related disorders. Recent epidemiologic studies in school children and young recruits have confirmed that atopic individuals have an increased susceptibility to Trichophyton rubrum infections of the feet and an increased risk for persistent infections. In contrast, an investigation on skin reactivity in dermatophyte infected atopic patients indicated that a group of these patients is fully able to eliminate the fungi concomitant with the development of a delayed type skin reactivity. Facial erythema and scaling, often including neck and shoulders, is present in many young adults with atopic dermatitis. Preliminary data from a Danish-Swedish investigation have shown that atopic dermatitis patients with head-neck-shoulder dermatitis compared to a group without this disorder and normal individuals more often demonstrate positive prick test, RAST and specific histamine release using extract of Pityrosporum ovale. These findings indicate that the presence of Pityrosporum ovale in the skin may cause an allergic reaction leading to dermatitis.

Arthrodermataceae↗
PubMed1991

[Pathogenesis of atopic dermatitis].

Atopic dermatitis shows a familial disposition and is characterised clinically by extreme pruritus, typical eczematoid pathology and distribution on the integument, a chronic relapsing course, and a personal or familial history of atopic diseases (allergic bronchial asthma, rhinitis and allergic conjunctivitis, atopic dermatitis), as well as numerous other stigmata and microsymptoms. Although numerous exogenous factors help trigger the disease, more recent findings point to an immunological basis. In recent years, numerous cellular malfunctions of immune cells have been reported, with disturbances in T-lymphocyte predominating. The latest investigations now suggest that the reported changes in the immune response are due to an imbalance in the cytokine network. Thus, it has been observed that disturbances of cytokine production depend upon the severity of the disease, and show an AD-characteristic pattern. The pathogenesis of atopic dermatitis however, is not yet fully understood.

Dermatitis, Atopic↗
PubMed1987

[Pathogenesis of atopic dermatitis].

Atopic dermatitis (AD) is a familial inflammatory skin disorder, which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing course, and the personal or family case history of atopy (asthma, allergic rhinitis, atopic dermatitis); moreover, we find a variety of additional features, which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, we have not clearly understood its pathogenesis so far. This article reviews the reported deviations of the immune system and the alterations of the mediators of inflammation as well as the abnormalities of cyclic nucleotide regulation. These findings are correlated to the clinical symptoms. The following topics have been dealt with in detail: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation, and particularly, observations on the cAMP-phosphodiesterase. These extremely complex findings, which are based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system, may provide a better understanding of the pathogenesis of atopic dermatitis.

Cyclic AMP↗
PubMed1985

[Pathogenesis of atopic dermatitis].

Atopic dermatitis (AD) is a familial inflammatory skin disorder which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing time course and the personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis). However, there exists a variety of additional features which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, the pathogenesis is not clearly understood at present. This review summarizes the reported deviations of the immune system as well as the alterations of the mediators of inflammation and the abnormalities of cyclic nucleotide regulation. These findings will be correlated with clinical symptoms. In particular the following topics were taken into consideration: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation and especially the observations on the cyclic adenosine monophosphate (cAMP)-phosphodiesterase. These extremely complex findings based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system may provide a better understanding of the pathogenesis of atopic dermatitis.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Phosphodiesterase and immune dysfunction in atopic dermatitis.

Atopic dermatitis and the other atopic conditions occur as a result of direct or indirect influences from cells of hematopoietic origin. Cellular immune abnormalities have been described, but appear to be secondary to cutaneous inflammation in atopic dermatitis. Pharmacophysiologic abnormalities are numerous and may relate to defective cyclic nucleotide metabolism in circulating and infiltrating leukocytes. A consistent leukocyte abnormality is elevated cyclic AMP-phosphodiesterase. This enzyme abnormality results in reduced intracellular cyclic AMP, creating a net permissive effect upon cell function. Phosphodiesterase inhibitors have been demonstrated to reduce abnormal histamine release and IgE production by cultured leukocytes. Studies of phosphodiesterase and associated defects in atopic leukocytes may lead to delineation of basic pathogenetic mechanisms as well as providing the potential for therapeutic targeting.

Dermatitis, Atopic↗
PubMed1992

[Etiologies of atopic dermatitis].

Atopic dermatitis is no longer a constitutional illness that cannot be influenced. The discovery of IgE fixed to the cells of Langerhans changes the physiopathological concept of this illness. There must be a minutely careful search for all the possible etiologies before advising therapy or long-term treatment. Attention must be given to the role of foods, discovery of causal pneumoallergens and a systematic search for a contact allergen must be made. This systematic and scrupulous search also gives confidence to a patient who is discouraged by the development of the condition.

Allergens↗
PubMedDate not supplied

Recognizing and managing clinical problems in atopic dermatitis.

Atopic dermatitis is a pruritic, inflammatory cutaneous disorder found most frequently among patients with a personal or family history of atopic disease. A primary defect is found in bone marrow cells. The most consistent abnormality relates to the overproduction of IgE. Pharmacophysiologic abnormalities include abnormal vascular responses, abnormal sweating responses, and a reduced threshold for itch. In addition, seven of 12 patients with pure atopic dermatitis with no respiratory disease have an abnormal methacholine inhalation test. There is an abnormal response of leukocyte cyclic AMP to a variety of adenylate cyclase stimulants. Characteristic histological findings are interepidermal edema, called spongiosis, which is consistent with a composite of late-phase and delayed hypersensitivity. The brittle stratum corneum can be treated with hydration, a commonly neglected aspect of management. An overlooked complication is herpes simplex infection of the eye. Overall management includes stress control, treating allergenic trigger factors, topical steroids, systemic antibiotics, antihistamines, ultraviolet light, and hospitalization in severe cases.

Adrenal Cortex Hormones↗
PubMed1990

Current considerations and management of atopic dermatitis.

Atopic dermatitis is a common, chronic, and relapsing disease. This continuing education article outlines the key therapy points to be considered for all patients with atopic dermatitis, although each patient requires individualized therapy.

Adolescent↗
PubMed1989

Immunology of atopic dermatitis.

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.

Adult↗
PubMed1976

[Cytokinetics of epidermal and dermal cells in allergic contact dermatitis and atopic dermatitis (author's transl)].

The cytokinetics of epidermal and dermal cells was examined in 16 patients with subacute or chronic allergic contact dermatitis and 11 with atopic dermatitis. In allergic contact dermatitis a H3-thymidine-labelling index (H3-1) of 4.55 +/- 2.4% was found in the epidermis and of 0.7 +/- 0.44% in the dermal infiltrate. In comparsion, in atopic dermatitis the values were 5.5 +/- 2.31% in the epidermis and 0.93 +/- 0.72% in the dermis. The DNA-synthesis-time (ts) was lengthened slightly with 11.4 +/- 2.4 h in allergic contact dermatitis and 11.75 +/- 3.68 h in atopic dermatitis. In comparsion with normal skin, the cell-cycle-time (tc) was slightly shortened in allergic contact dermatitis (244 +/- 110 h) and in atopic dermatitis (233 +/- 83 h). There was no significant difference between both types of dermatitis regarding cytokinetics.

Cell Division↗
PubMed1992

Recent advances in the pathogenesis of atopic dermatitis.

Atopic dermatitis (AD) is an inflammatory skin disorder affecting 5%-10% of children. Although basic mechanisms remain largely speculative, recent studies on the pathogenesis have elucidated new insights, pointing to the importance of food and inhalant allergens. The pathogenesis of AD can be more easily explained by the model of late skin reaction occurring after mast cell activation. The present report highlights some of the more recent developments in the mechanisms of AD which can be important in understanding and treating this troublesome disease.

Allergens↗
PubMed1991

Serum eosinophil cationic protein in patients with atopic dermatitis.

Atopic dermatitis (AD) is a chronic inflammatory disease of the skin, frequently associated with a family history of atopy, raised serum IgE levels and other immunological abnormalities. Both eosinophils and their basic proteins have been detected in the skin lesions of AD patients. We measured the levels of eosinophil cationic protein (ECP) in sera of 24 children with AD and found them to be increased, compared to nonatopic controls, both children and adults. High ECP values were also obtained in 3 patients with the hyper-IgE syndrome. However, no direct relationship between IgE and ECP serum levels could be established. We found no correlation between serum ECP and the number of circulating eosinophils, suggesting that part of ECP was produced by cells infiltrating the tissues. Measurement of ECP might represent a noninvasive tool to assess the activity of AD in relation to eosinophil involvement in this disease.

Adolescent↗
PubMed1991

CD4+ memory T cells in peripheral blood are not decreased in patients with atopic dermatitis.

Atopic dermatitis (AD) is a severe and chronic eczematous skin disease, to which increased IgE levels and imbalances of CD4+ T cells are related. CD4+ T cells, however, are heterogeneous and include at least two subpopulations being designated as CD4+ naive and memory T cells. They represent sequential maturational stages (naive into memory) in CD4+ T cell development differing in function and phenotype. Of these two subpopulations the CD4+ memory T cell compartment is a potent producer of gamma-interferon which suppresses IgE synthesis in B cells. Therefore, we speculated whether an inborn maturation defect of CD4+ memory T cells causes the increased IgE production in AD. In patients with AD and age- and sex-matched controls (both n = 10) we analyzed the distribution of both subpopulations in peripheral blood by two-color flow cytometry using monoclonal antibodies against the CD4, CD45RA and CD29 antigen. We provide evidence that the numerical values of CD4+ memory T cells and CD4+ naive T cells are equivalent in both groups. This supports the view that functional disturbances of lymphocytes or lymphocyte subsets are responsible for IgE excess and the pathogenesis of AD.

Adolescent↗
PubMed1991

Injection of allergen-antibody complexes is an effective treatment of atopic dermatitis.

Atopic dermatitis (AD) can be exacerbated by contact with airborne allergens, amongst which Dermatophagoides pteronyssinus (Dpt) appears to be potentially important. Specific IgE antibodies towards Dpt are often found in AD, and it can therefore be speculated that suppression of the production of anti-Dpt IgE might result in a significant clinical improvement. Complexes of antigen and specific antibodies have been shown to suppress the production of antibody in other systems; we report here the evaluation in an open trial of the capacity of such complexes to improve symptoms of AD. Ten adult patients were enrolled in this study. In addition to satisfying the criteria of AD, they all suffered from a severe disease (more than 20% of the body surface involved) that had been stable for at least the last 2 years. The patients had high titers of total IgE antibodies and specific anti-Dpt antibodies. Allergen-antibody complexes were prepared from Dpt allergens and an excess of autologous specific anti-Dpt antibodies obtained by immunoadsorption. The patients received regular injections of these complexes throughout 1 year, during which clinical parameters of disease intensity, percentage of body surface affected and intensity of pruritus were regularly monitored. A significant clinical improvement was obtained after 3-4 months of therapy and was maintained through the 9th month. After 1 year of treatment, 2 patients were completely free of disease, 4 had residual lesions which continued to improve and 4 patients had a partial recurrence of dermatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗