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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↗
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↗
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↗
PubMed2026

P1D6 inhibits FnBP-induced extracellular proteome remodeling: proteomic evidence for a novel intervention strategy in atopic dermatitis.

Atopic dermatitis (AD) is an inflammatory skin disorder characterized by skin barrier impairment, chronic inflammation, and intense pruritus. Staphylococcus aureus (S. aureus) critically contributes to its pathogenesis; however, the mechanistic role of its virulence factor fibronectin-binding protein (FnBP) in keratinocytes remains poorly understood. This study used bibliometric analysis and quantitative proteomics to examine the relationship. We first performed a bibliometric analysis, revealing a sustained increase in publications on S. aureus and AD, peaking at 99 articles in 2023, with hotspots focused on skin barrier function, immune inflammation, and pediatrics. Quantitative proteomics was employed to investigate how FnBP reshapes the extracellular proteome and whether the anti-α5 integrin antibody P1D6 exerts interventional effects. HaCaT cells were stimulated with recombinant FnBP alone or in combination with P1D6, followed by data-independent acquisition (DIA)-based proteomic analysis of secretome changes. Proteomic analysis identified FnBP-induced differentially expressed proteins enriched in immune- and barrier-related pathways, including cell adhesion, cell junctions, and VEGFA-VEGFR2 signaling. P1D6 intervention significantly inhibited the secretome profile and identified 241 core responsive proteins, of which approximately 52% returned to baseline levels after intervention (P > 0.05). These proteins were primarily enriched in pathways governing protein homeostasis, folding, proteasomal degradation, and interleukin-7 signaling. Notably, P1D6 modulated the downregulation of ATP5F1B and P4HB, key effectors within the interleukin-7 pathway. This study demonstrates that FnBP remodels the keratinocyte secretome by disrupting protein homeostasis, consequently inducing barrier injury and chronic inflammation related to AD, which can be effectively blocked by P1D6. Combined with bibliometric trends and proteomic evidence, this study focuses on FnBP, an underexplored virulence factor, and provides novel insights into AD pathogenesis and therapeutic interventions.

Humans↗
PubMed1992

The relationship between allergy, clinical symptoms and bronchial responsiveness in atopic dermatitis.

Atopic Dermatitis (AD) and asthma are closely associated with respect to epidemiology, hereditary factors and occurrence in the same individuals. Bronchial Hyperresponsiveness (BH), the hallmark of asthma, can also be a physiopathological feature of AD, even in the absence of clinical asthma. We studied 78 subjects with AD. A follow-up study was performed in 27 of these. Data on respiratory and dermatologic symptoms were collected by means of a standardized questionnaire. Skin reactivity was evaluated by prick testing, and in 57 subjects BH was assessed with a methacholine test (Mch). Twenty-one subjects had asthma and 36 showed a positive skin reaction. A PC20 FEV1 was measurable in 38 subjects. Males were found more likely to be Mch responders than females (p < 0.05). Mch responders also showed an earlier age at onset of AD than nonresponders (2.1 yrs vs. 6.2, p = 0.03). Determinants of the degree of BH were evaluated by a stepwise multiple regression analysis, taking the log of the slope of the concentration response curve as dependent variable. In the final model we found that the degree of BH was directly related to wheezing (p = 0.0017) and coughing (p = 0.04) and inversely related to lung function (p = 0.0082) and age (p = 0.0008). Neither skin reactivity nor grading of AD were statistically significant. The longitudinal study demonstrated that the courses of AD and BH seem to run parallel only in skin-negative subjects, whereas an increase in BH was observed in skin-positive subjects.

Adolescent↗
PubMed1992

Lesional elastase activity in psoriasis, contact dermatitis, and atopic dermatitis.

Human leukocyte elastase (HLE) is a broad spectrum serine protease derived from neutrophils and macrophages. We developed an assay to determine HLE activity on the skin surface in patients with inflammatory skin diseases. HLE activity was absent in the skin of healthy controls. A massive increase of HLE activity was found in lesional skin of psoriasis (31 times), allergic contact dermatitis (55 times), and atopic dermatitis (35 times), but not in uninvolved skin of diseased patients. Therefore, this assay appears to represent a useful biochemical marker of epidermal inflammation. The presence of proteolytically active HLE in diseased epidermis, which is known to contain specific inhibitors of this enzyme, suggests a pathophysiologic role of this enzymatic activity in psoriasis, contact dermatitis, and atopic dermatitis.

Adult↗
PubMed1992

Dry skin in atopic dermatitis.

Atopic dermatitis (AD) is a common, chronically recurring skin disorder. Dry skin is a common finding in patients with AD, apart from the dermatitis. Although there are obvious clinical signs of an impaired barrier function of the skin, few investigators have studied this aspect of AD. The stratum corneum, where the barrier is located, has been studied with different techniques in patients with AD, and the results are now presented. The water-binding capacity of dry atopic skin was found to be reduced when measured with an in vitro microbalance technique. TEWL (transepidermal water loss) measured with and Evaporimeter Ep1, was increased in dry skin and in clinically normal skin of atopics on predilection areas. Water content was decreased in dry atopic skin, when measured with the Corneometer CM 420. In a quantitative electron microscopic study, the lamellar bodies were found to have an increased relative volume in dry atopic skin. When using chromatographic analysis, preliminary data suggested reduced amounts of extractable stratum corneum lipids in patients with AD. In a clinical study, 80% of the patients with AD regarded their skin as being dry. Fifty percent were found to have areas of dry skin, on clinical examination. By scanning electron microscopy (SEM), the surface pattern of dry atopic skin was found to be coarse and irregular. When using profilometry, quantitative differences in roughness parameters were found in dry atopic vis-à-vis to normal skin.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Water↗
PubMed1992

Serum eosinophil cationic protein (ECP) is a sensitive measure for disease activity in atopic dermatitis.

Atopic dermatitis (AD) is characterized by alterations in cellular and humoral immunity including elevated serum levels of IgE, IL-2 receptor (IL-2R) and eosinophil cationic protein (ECP). In order to evaluate the relevance of these serum parameters as indicators of disease activity, the concentrations of IgE, IL-2R and ECP were measured in serum samples of patients with an acute exacerbation of AD (n = 19) on admission to hospital and every 6 days up to discharge, and compared with those from normal non-atopic controls (n = 15). The severity of the disease in the AD patients was examined using an established clinical scoring system. On admission, AD patients showed significantly elevated serum levels of IgE, IL-2R and ECP compared with normal controls (P less than or equal to 0.0001). Clinical improvement was associated with a decrease of both the clinical score (P less than or equal to 0.001) and serum ECP levels (P less than or equal to 0.005). No significant changes in serum IgE and serum IL-2R were observed. In addition, there was a significant correlation between serum ECP and the clinical score (R = 0.67, P less than or equal to 0.001). These data indicate that serum ECP may be a helpful tool for monitoring disease activity in AD.

Acute Disease↗
PubMed1992

Relationship between increased cyclic AMP-phosphodiesterase activity and abnormal adenylyl cyclase regulation in leukocytes from patients with atopic dermatitis.

Atopic dermatitis (AD) is characterized by a variety of abnormal physiologic and pharmacologic responses in the skin. Leukocyte abnormalities of the cyclic nucleotide system include increased cAMP phosphodiesterase (PDE) and adenylyl cyclase activities. We have evaluated the possibility that a defect of the inhibitory GTP-binding protein (Gi) might cause inadequate modulation of adenylyl cyclase activity in AD leukocytes. We carried out a series of studies assessing adenylyl cyclase and Gi subunits in monocyte membranes. Using both pertussis toxin ribosylation and direct monoclonal antibody labeling of Gi proteins, we have shown evidence for a decrease or possible absence of one of the Gi proteins in atopic monocyte membranes. A genetic defect or toxin-mediated abnormality in leukocyte membrane Gi could account for these findings. Increased cAMP degradation by PDE may be a compensatory mechanism for increased cAMP synthesis that is regulated by GTP-binding proteins. But this increased PDE activity also rendered AD leukocytes hypo-responsive to immunofunction regulatory signals mediated by cAMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Allergic contact dermatitis in atopic dermatitis.

Of 73 adult patients attending a clinic specially provided to treat patients with atopic dermatitis, 31 (42%) showed one or more positive patch reaction on contact testing. There was a striking female preponderance in the patch test positive group (26F:5M) in contrast to those with negative test results (9F:17M). The commonest allergens identified were fragrances in 13 patients, nickel (7), rubber (5), lanolin (4) and formaldehyde (3). In 21 patients, topical preparations, cosmetic or medically prescribed, could be implicated. Contact sensitivity seems to be relatively common in adult patients who have a continuing problem with their atopic dermatitis. Recognizing this sensitization may be important in their management.

Adolescent↗
PubMed1992

[Clinical diagnosis of atopic dermatitis].

Atopic eczema is a pruriginous dermatosis that most often starts before one year, but which may show for the first time after 50 years. The diagnosis is essentially clinical, with signs of banal eczema (especially acute in young infants, more chronic later) but of which the topography develops characteristically as a function of age and in the context of atopy. The development of is chronic, dotted with inflamed eruptions and may be complicated by an alteration of general state with bacterial (very frequent) or viral superinfections. The appearance of asthma is frequent when the dermatosis is extended. It usually disappears before adult age. Differential diagnosis is needed especially when there is an atypical form or association with another pruriginous dermatosis. Questioning must cover the environment, food habits and search for signs that may show the responsibility of an allergen.

Adolescent↗
PubMed1992

Topical corticosteroids and Staphylococcus aureus in atopic dermatitis.

BACKGROUND: Atopic dermatitis is commonly colonized with Staphylococcus aureus in high densities. OBJECTIVE: Our purpose was to study the effect of topical corticosteroids on the colonization of S. aureus in atopic dermatitis. METHODS: Sixty-six patients were treated with moderately potent, or very potent corticosteroids. Quantification of S. aureus and evaluation of the severity of the eczema was performed before, after 1 week, and after 2 weeks of treatment. RESULTS: Fifty-three patients carried S. aureus in the most pronounced lesion before treatment. The colonization was significantly correlated with the severity of the eczema. The density of S. aureus was reduced by topical corticosteroids. The reduction increased with the potency of the corticosteroid and was most pronounced during the first week. S. aureus was eliminated after a successful 2-week treatment with a very potent corticosteroid. Propylene glycol 25% added to a moderately potent corticosteroid did not significantly increase the reduction of S. aureus. CONCLUSION: Topical corticosteroids of sufficient potency reduce the density of S. aureus in atopic dermatitis.

Administration, Cutaneous↗
PubMed1978

Immunofluorescence of the skin in allergic diseases: an investigation of patients with contact dermatitis, allergic vasculitis and atopic dermatitis.

Skin biopsies for immunofluorescent studies were taken from patients with contact dermatitis (positive patch tests), atopic dermatitis and allergic vasculitis for comparison with normal-appearing skin from the same patients, and from healthy controls. A variety of deposits of immunoglobulins, complement components and fibrinogen were demonstrated in 6 out of 20 patients with contact dermatitis, 7 out of 10 with atopic dermatitis, 8 out of 10 with allergic vasculitis, and in 4 out of 20 control individuals. No diagnostic pattern of deposits was found. Elevated serum IgE and eosinophilic counts were found in patients with atopic dermatitis, and high serum IgA and fibrinogen levels were found in the allergic vasculitis group.

Adolescent↗
PubMed2026

Single-cell transcriptome revealed the aberrant keratinocytes activation in antigen presentation in atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD), a common chronic inflammatory skin disease, has been extensively studied using single-cell genomics. However, keratinocytes, as key effector cells in AD, have underlying mechanisms remain incompletely understood and require further investigation. METHODS: We integrated single-cell transcriptomic data from skin tissues of healthy controls, chronic active AD patients, spontaneously healed AD (SHAD) patients, and an ovalbumin-induced AD mouse model. The study particularly emphasized the gene expression and cellular dynamics of keratinocytes across the different groups, as well as their interactions with immune cells. RESULTS: Compared to healthy controls, we observed significant changes in the keratinocyte transcriptome, cellular state, and keratinocyte-immune cell ligand-receptor interactions in AD skin, particularly the marked activation of genes involved in antigen processing and presentation. Interestingly, such gene activation was not observed in keratinocytes from the ovalbumin-induced AD mouse model, despite its phenotype closely resembling human AD. Furthermore, in SHAD, we identified a recovery of both the ligand-receptor interaction patterns and antigen processing and presentation genes, accompanied by a notable shift in the transcriptome. This involved a significant downregulation of genes related to cytoplasmic transcription and oxidative phosphorylation. Notably, this pattern was not observed in the self-healing mouse model following the removal of ovalbumin stimulation. CONCLUSION: Our results suggest that the persistent activation of antigen processing and presentation pathways in keratinocytes may be a key driver of chronic inflammation in AD. Therefore, redirecting anti-allergic therapeutic strategies from solely targeting immune cells to targeting of keratinocyte-mediated antigen presentation may offer a more effective approach. Furthermore, we raise concerns about the use of ovalbumin-induced mouse models to recapitulate human chronic AD, as the underlying mechanisms may differ significantly.

Dermatitis, Atopic↗