Abstract Atopic Dermatitis Research Articles

Evaluation of efficacy and safety of desloratadine syrup in childhood atopic dermatitis

Atopic dermatitis (AD) is an inflammatory, pruritic, relapsing, chronic skin disease, that constitutes a significant burden to patients and their families. It currently affects 10% to 15% of children in many parts of the world and its prevalence is increasing. AD tipically begins in early childhood and may continue or recur as adult disease. The management of AD is difficult and reflects the lack of knowledge of the complex pathophysiological mechanisms.

Genetics of atopic dermatitis

Atopic dermatitis (AD) is a common skin disorder that is typified by itchy, inflamed skin. Although atopy is a prominent feature of AD, the cause of the disease is unknown, and approximately 10% of patients with AD are not atopic. The disease is under strong genetic control, so identification of the genes and genetic variants underlying AD might lead to new treatments and better classification of children with the disease. Preliminary genetic studies have identified that the genes or clusters of genes that affect the barrier functions of the skin are as important as genes that might modify the atopic process. These genes might influence other diseases, including psoriasis. The findings emphasize that the barrier function of the skin is not merely passive, and the polymorphic nature of genes and gene families expressed in the skin suggest a polyvalent response to a number of different stimuli, including infections.

Clinical features of atopic dermatitis

Atopic dermatitis (AD) remains a common affliction that requires clinical acumen to diagnose. Presently, there is no diagnostic laboratory test, and biopsies primarily are research tools, except when ruling out cutaneous T-cell lymphoma. Other than the clinician's ability to recognize AD, the laboratory can only confirm the clinical impression. Deviations from the criteria discussed in this article suggest the possibility of alternative diagnosis.

Promoting Health in Children with Atopic Dermatitis

Atopic dermatitis (AD), or eczema, can be a very challenging disease to manage. The etiology of the disease is not completely understood, and its incidence has risen in the past 10 years to more than 10% of the population. AD is characterized primarily by intense itching and the development of papules, scaly lesions, fissures, and crusting. The onset occurs primarily in childhood, and much of the disease management is conducted by the family. Patients and their families often experience multiple recurrences and exacerbations, repeated attempts at cures and treatments, lowered self-esteem of the child, impaired growth and development of the child, loss of sleep, discipline problems, and multiple clinic and emergency department visits for exacerbations. Management primarily consists of prevention (i.e., good daily skin care and management of environmental trigger factors such as infection, irritants, emotional stress, and allergens). These children and their families need education and the support of health care professionals. This article outlines specific techniques to help parents and children manage AD at home and minimize exacerbations.

Severe Complications of Folk Remedies for Atopic Dermatitis

Atopic dermatitis (AD) is a chronic disorder, and its course is often punctuated by remissions and relapses despite various treatments, including steroid therapy. Therefore, a tendency exists for the parents to administer to their children various folk remedies, most of which are not medically or scientifically evaluated. In this report, we present the cases of three children with AD who developed severe complications following the administration of folk remedies, the safety of which had been evaluated inadequately. The patient in case 1 had electrolyte abnormalities, in case 2, iron-deficiency anemia, and in case 3, severe hypoproteinemia and electrolyte abnormalities.

Section Reviews: Pulmonary-Allergy, Dermatological, Gastrointestinal & Arthnlis: New therapeutic approaches to atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease which affects some 10 - 15% of the population during childhood. The prevalence of the disease is increasing and there are few, if any, current therapies which are directed at the underlying cause of the disease. A better understanding of the mechanisms of AD is starting to offer potential therapeutic approaches to this disease. The understanding of the role of cytokines in AD, in particular interleukin-4, interferon-gamma and tumour necrosis factor-alpha, has indicated several potential approaches, including inhibition of cytokine processing (matrix metalloproteinase inhibitors), inhibition of cytokine release (phosphodiesterase type IV inhibitors) and modulation of cytokine levels, as well as newer approaches to immunomodulation.

Down-regulating effects of IL-4 and IL-10 on the IFN-gamma response in atopic dermatitis.

Atopic dermatitis (AD) is a chronic allergic disease associated with toxin (superantigen)-producing Staphylococcus aureus skin infections, impaired delayed hypersensitivity responses, and the expansion of IL-4-secreting Th2 cells, as well as diminished IFN-gamma synthesis. IL-12 is known to induce IFN-gamma synthesis and to augment Th1 responses. In this study, therefore, we examined the potential role of IL-12 in the immunopathogenesis of AD. We show that, after stimulation with staphylococcal toxic shock syndrome toxin-1 (TSST-1) or IL-12, PBMC from patients with AD are deficient in their ability to produce IFN-gamma. PBMC from AD patients, however, produced normal quantities of IL-12 and expressed normal levels of IL-12R. Induction of IFN-gamma by TSST-1 was decreased by neutralizing anti-IL-12 Ab in normal donors, but not in AD patients. The latter observation is consistent with a defective response to IL-12 in AD PBMC. Because AD is associated with increased production of IL-4 and IL-10, we examined the effect of IL-4 on IL-12- or TSST-1-induced IFN-gamma production in normal donors. IL-4 inhibited IL-12-induced IFN-gamma production. Furthermore, Ab neutralization of IL-4 caused increased production of IFN-gamma in AD PBMC. However, neutralization of IL-10 activity caused an even greater augmentation of IFN-gamma production. Our data suggest that despite normal levels of IL-12 production and IL-12R expression, PBMC from AD patients are unable to generate normal IL-12-induced IFN-gamma responses. This defective response may be due to the excess production of IL-4 and IL-10 in this common allergic condition.

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.

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.

Chemiluminescence response of polymorphonuclear leukocytes in atopic dermatitis.

Atopic dermatitis (AD) is characterized by many signs of immunodeficiency. Our interest was to investigate if there are also alterations of the chemiluminescence (CL) response of polymorphonuclear leukocytes (PMN) as a measure of the release of toxic oxygen radicals. Isolated PMN of 13 patients with AD with mild to moderate disease activity were stimulated with a chemotactic peptide (f-met-phe), zymosan-activated serum (ZAS), zymosan particles and phorbolmyristate acetate. In the AD group, we found a significantly decreased response after stimulation with ZAS in comparison to the controls. With the other stimuli tested no significant difference was detected. The decreased response of PMN to stimulation with ZAS from patients with AD associated with a normal reactivity to the other stimuli could be due to specific desensitization of the PMN by C5a in vivo.