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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↗
PubMed2000

Immune regulation in atopic dermatitis.

Atopic dermatitis is a chronic inflammatory skin disease with a pathogenesis of complex immune dysregulation and interplay of genetic, environmental and psychological factors. Activation and skin-selective homing of peripheral-blood T cells, and effector functions in the skin, represent sequential immunological events in the pathogenesis of atopic dermatitis. Both CD4(+) and CD8(+) T cells bearing the cutaneous-lymphocyte-associated antigen represent activated memory/effector T cell subsets and induce IgE, mainly via IL-13, and prolong eosinophil lifespan, mainly via IL-5. Dysregulated apoptosis in skin-homing T cells and keratinocytes contributes to the elicitation and progress of atopic dermatitis. T cell survival is enhanced in the skin by cytokines and extracellular-matrix proteins. These activated T cells induce keratinocyte apoptosis, leading to eczema formation.

Animals↗
PubMed1986

Increased in vitro cell-mediated immune response to staphylococcal antigens in atopic dermatitis.

Atopic dermatitis patients have both a chronic colonization of their skin with Staphylococcus aureus and a delayed cutaneous hyporesponsiveness to intradermally injected staphylococcal antigens. It has not been established whether the cutaneous anergy merely reflects a specific lymphocyte hyporesponsiveness to staphylococcal antigens. Therefore the lymphocyte proliferative response to staphylococci was assessed in twelve patients with slight to severe atopic dermatitis and in eleven healthy subjects. Compared to the normal subjects, the patients showed significantly higher stimulation indices with S. aureus Wood 46 (p less than 0.05) and purified S. aureus cell walls (p less than 0.05). There was no significant correlation between the lymphocyte stimulation and the clinical severity of the disease. Therefore, chronic colonization of the skin of atopic dermatitis patients by S. aureus does not correlate with a defect in the cellular immune response to the bacteria but may rather stimulate such a response.

Adolescent↗
PubMed2001

Prednicarbate emollient cream 0.1% in pediatric patients with atopic dermatitis.

Atopic dermatitis, common among infants and children, is an intensely pruritic, chronic, inflammatory dermatosis that is traditionally treated with emollients for dry skin and topical corticosteroids for inflamed areas. A multicenter, 3-week, open-label study evaluated prednicarbate emollient cream 0.1%, a nonhalogenated midpotency corticosteroid, in 55 patients aged 4 months to 12 years who were diagnosed with atopic dermatitis. No suppression of the hypothalamic-pituitary-adrenal (HPA) axis was evidenced by serum cortisol levels obtained before and after intravenous injection of 250 mg of cosyntropin on days 1 and 22, and biochemical tests detected no other systemic effects. Adverse events were few and within the expected range. Prednicarbate resulted in improvements based on global evaluations and sign/symptom scores. In conclusion, this study found prednicarbate emollient cream 0.1% to be safe and effective for the treatment of atopic dermatitis in pediatric patients for up to 3 weeks.

Administration, Topical↗
PubMedDate not supplied

The precipitation of symptoms by common foods in children with atopic dermatitis.

Atopic dermatitis (AD) is a chronic and disabling condition that has a major impact on financial and social resources of the individual and the community. Its incidence is increasing dramatically, and no cure is available. Pharmacological treatment is only partially effective. The evidence that diet plays a role in children with atopic dermatitis is now irrefutable. Prophylactic measures can prevent or limit the development of AD, and partially restricted diets can modify the disease's course or severity. This study reports the reactions to various foods as perceived by parents of 112 children affected by AD. It demonstrates that many foods exacerbate AD and that reactions are caused by two distinct groups of food. The commonest triggers of cutaneous symptoms are tomatoes, oranges, sweets, pineapple, chocolate, and softdrinks preserved with sulfur dioxide. These foods result in symptoms in 30% to 49% of the children. The traditional IgE reaction type foods, namely egg, fish, milk, and peanut, resulted in reactions in 14% to 25% of the children, and with many non-cutaneous symptoms. The study further shows that allergen avoidance measures are not practiced in our community, and that sound advice is not often proffered. Practical advice on prophylactic dietary preventative measures and dietary management of children with atopic dermatitis is presented.

Adolescent↗
PubMedDate not supplied

Practical approaches to the treatment of atopic dermatitis.

Atopic dermatitis is a chronic pruritic cutaneous disease that occurs in 0.5% to 1% of the general population and affects almost 10% of all children. Since this is a disease that is associated with both a very high level of total IgE and a high incidence of allergic respiratory disease, it behooves the practicing allergist to become familiar with the diagnosis and treatment of atopic dermatitis. This following discussion will focus on the identification of major and minor clinical features of the disease and review the spectrum of immune dysregulation that is frequently seen with these patients. The primary focus of this review will be directed at the identification of treatment options available to allergists within the published practice guidelines of the American Academy of Dermatology and practice guidelines that are currently being developed by the American Academy of Allergy & Immunology. Atopic dermatitis is an "itch which rashes and not a rash which itches" and therefore, any patient treatment program should address the multiplicity of potential trigger factors that provoke this itching. These factors include heat, humidity, and perspiration, in addition to the ingestion of certain food allergens and the topical exposure to both dust mite antigen and animal dander. Recent studies suggest that the pathogenesis of allergic disease entails a complex inflammatory process in which the TH2 lymphocyte might play a major role in shifting the immune response in favor of disease. Accordingly, recent immunomodulating treatments, such as interferon gamma and cyclosporine, might offer therapeutic options to the physician beyond the standard topical forms of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2006

Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis.

Atopic disease, including atopic dermatitis (eczema), allergy and asthma, has increased in frequency in recent decades and now affects approximately 20% of the population in the developed world. Twin and family studies have shown that predisposition to atopic disease is highly heritable. Although most genetic studies have focused on immunological mechanisms, a primary epithelial barrier defect has been anticipated. Filaggrin is a key protein that facilitates terminal differentiation of the epidermis and formation of the skin barrier. Here we show that two independent loss-of-function genetic variants (R510X and 2282del4) in the gene encoding filaggrin (FLG) are very strong predisposing factors for atopic dermatitis. These variants are carried by approximately 9% of people of European origin. These variants also show highly significant association with asthma occurring in the context of atopic dermatitis. This work establishes a key role for impaired skin barrier function in the development of atopic disease.

Alleles↗
PubMed2004

Genetic association between an AACC insertion in the 3'UTR of the stratum corneum chymotryptic enzyme gene and atopic dermatitis.

Atopic dermatitis is a disease with an impaired skin barrier that affects 15%-20% of children. In the normal epidermis, the stratum corneum chymotryptic enzyme (SCCE) thought to play a central role in desquamation by cleaving proteins of the stratum corneum (e.g., corneodesmosin and plakoglobin). Genetic variations within the SCCE gene could be associated with dysregulation of SCCE activity leading to an abnormal skin barrier. We screened the SCCE gene for variations and performed a case-control study on 103 atopic dermatitis patients and 261 matched controls. 16 synonymous single nucleotide polymorphisms (SNPs) have been identified and a 4 bp (AACC) insertion has been found in the 3'UTR. We performed an association study of the SCCE AACC insertion in the 3'UTR, and found a significant trend between the AACC allele with the two insertions and disease in the overall data set [odds ratio (OR)=2.31; p=0.0007]. The AACC insertion in the SCCE gene may result in a change to SCCE activity within the skin barrier. These findings suggest that SCCE could have an important role in the development of atopic dermatitis.

3' Untranslated Regions↗
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↗
PubMed2003

Atopic dermatitis.

Atopic dermatitis, the dermatologic manifestation of the atopic diathesis, has a variety of clinical presentations. This disease probably should be considered a syndrome--a group of signs and symptoms that frequently occur together in an identifiable pattern. The following update describes the spectrum of atopic dermatitis and summarizes current thinking about the etiology of the disease.

Dermatitis, Atopic↗
PubMed2003

Association of cathepsin E deficiency with development of atopic dermatitis.

Atopic dermatitis (AD) is a pruritic inflammatory skin diseases associated with a family history of atropy. Here we show that mice lacking the endolysosomal aspartic proteinase cathepsin E spontaneously develop skin lesions similar to those of humans with AD when reared under conventional conditions but not under specific pathogen-free conditions. These mice showed the increase in the ratio of CD4+/CD8+ T cells, the strong polarization of naïve T cells to T helper 2 cells, and the systemic accumulation of IL-18 and IL-1beta accompanied by a marked increase in IL-4, IL-5, and IgE. The relative rates of degradation of IL-18 and IL-1beta were significantly lower in cathepsin E-deficient mice than wild-type mice. These results strongly suggest that the development of AD in cathepsin E-deficient mice is initiated by systemic accumulation of IL-18 and IL-1beta, mainly due to their reduced turnover rates. In addition, the reduced expression of cathepsin E was also observed in erythrocytes of both humans with AD and the AD mouse model NC/Nga. Cathepsin E deficiency might thus be responsible for the induction of AD in humans and mice.

Animals↗
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↗
PubMed2002

[Cataract progression in patients with atopic dermatitis].

Atopic dermatitis is a relatively common hereditary condition. Ocular sequellae are commonly seen in this disorder, and may include involvement of both the anterior and posterior segments of the eye. The case of female patient with atopic dermatitis and ocular manifestations is presented.

Anti-Allergic Agents↗