Treatment principles of atopic dermatitis

Atopic dermatitis (AD) is today the most common, chronic inflammatory skin disease among children in developed countries. Its cumulative prevalence varies from 20% in northern Europe and the USA to approximately 5% in Mediterranean countries. As a chronic disease it puts a special demand on treatment. There is no curative therapy, but competent guidance on treatment principles can control the disease in most, if not all children. This article summarizes the evidence-based knowledge that relates to the treatment of atopic eczema. It also gives advice and opinions on prophylactic measures as these are the focus of interest from most parents. LEARNING OBJECTIVE: This article should enable you to give advice and guidance to parents of children with AD, including what is necessary for diagnosis, what is of value and importance considering allergies and allergological investigations, allergen exposure, prophylactic measures, diets and indoor environment. Finally, you should be able to explain the diversity of treatment principles for parents.     

Mutational analysis of immunoglobulin E-binding epitopes of β-casein and β-lactoglobulin showed a heterogeneous pattern of critical amino acids between individual patients and pooled sera

BACKGROUND: For immunotherapeutic approaches, 'critical' amino acids (AAs) within allergenic epitopes are replaced with alternate AAs to eliminate IgE antibody binding. OBJECTIVE: To determine the critical AAs for IgE binding in beta-casein and beta-lactoglobulin (BLG). METHODS: Peptides of 10-14 AAs in length were synthesized on a derivatized cellulose membrane with single AA substitutions (alanine or glycine) at each position. Membranes were incubated with a pool of sera from 15 cow's milk-allergic patients and individual sera from six of the 15 patients. In cases where no decrease in binding occurred with a single AA substitution, peptides with two AA substitutions were generated and labelled. RESULTS: Using pooled patient sera, single AA substitutions led to complete elimination of binding to six of 11 peptides for beta-casein and to all six peptides for BLG. Substituting two AAs led to an elimination of binding to four of the remaining five beta-casein epitopes. However, in three of the 11 modified beta-casein peptides and five of the six BLG peptides, no decrease in IgE binding occurred in at least one individual patient. For these patients, critical AAs other than those defined by the patient serum pool were identified, indicating a heterogeneous pattern of IgE recognition. CONCLUSION: These results indicate that AAs critical for IgE binding are more heterogeneous than initially defined by pooled milk-allergic patient sera. For future immunotherapeutic interventions with mutated peptides, critical AAs should also be identified with individual patient sera to account for heterogeneity of IgE binding between patients.     

Latex allergy risk assessment in children and adolescents with type I diabetes mellitus

An increased frequency of allergic reactions to latex has been reported in specific populations with chronic latex exposure. However, relevance of latex allergy to children and adolescents with type I diabetes mellitus (DM1) has not been studied yet. The aim of the studty is to assess latex allergy risk in children and adolescents with DM1. Thirty-nine children with DM1 and 35 controls were enrolled. In a case-control study, we applied to all subjects a standard questionnaire, and specific Immunoglobulin E (IgE) concentrations for latex, common aeroallergens, and food-allergens were measured in serum samples. Latex exposure rates by means of medical procedures, operations, and latex glove usage were not different between DM1 and controls. Symptoms due to latex exposure were not determined in both groups. Three (7.7%) subjects in DM1 tested positive for latex-specific antibodies (LSIE), whereas no subject in controls. Diabetics that tested positive for latex-specific antibodies had the disease for three, 5 and 8 years. Nine (23.1%) of diabetics, and two (5.7%) of controls were atopic (p = 0.04). In our investigation, we found that children and adolescents with DM1 are not a risk group for latex allergy, and LSIE in children with DM1 was not accompanied by symptoms of latex allergy, or, presumably, increased risk of latex anaphylaxis.     

胸腺免疫抑制组分的抗变态反应作用

整体实验表明，胸腺免疫抑制组分肌内注射１ｗｋ对大鼠被动皮肤过敏反应（８、２０、５０和１２５ｍｇ·ｋｇ－１）兔Ａｒｔｈｕｓ反应（４和１２ｍｇ·ｋｇ－１）均有明显的抑制作用。体外实验表明，该药能抑制致敏豚鼠离体回肠平滑肌的过敏性收缩，ＩＣ５０为４４６．７ｍｇ·Ｌ－１。上述结果表明，胸腺免疫抑制组分有抗Ⅰ和Ⅲ型变态反应的作用。     

Reduction of nickel-induced contact hypersensitivity reactions by topical tea tree oil in humans

Objective and Design: Whilst the anti-microbial properties of tea tree oil (TTO) are established, the anti-inflammatory effects of TTO in human skin remain largely anecdotal and require evaluation. This study examined the effect of topically applied TTO on nickel-induced contact hypersensitivity reactions in human dorsal skin.Treatment: TTO (100%), a 5% TTO lotion, a placebo lotion (no TTO), or 100% macadamia oil were applied at days 3 and 5 after nickel exposure.Methods: The flare area and erythema index were measured on days 3, 5 and 7. The regulatory effects of TTO were also investigated on the proliferative response to nickel or polyclonal mitogens by peripheral blood mononuclear cells from nickel-sensitive and control subjects.Results: TTO (100%) significantly reduced the flare area and erythema index when compared to the nickel-only sites. With respect to the erythema index, the anti-inflammatory effects were predominantly, but not exclusively, seen in a subgroup of nickel-sensitive subjects with a prolonged development phase of nickel-induced contact hypersensitivity response. The 5% TTO lotion, the placebo lotion and the 100% macadamia oil were all without significant effect. TTO significantly inhibited proliferation to nickel but not to non-specific polyclonal mitogens by peripheral blood mononuclear cells from nickel-sensitive subjects.Conclusions: Topical application of 100% TTO may have therapeutic benefit in nickel-induced contact hypersensitivity in human skin. The mode of action of TTO requires further investigation, but may be an effect on the antigen presenting cells or the antigen presenting process in nickel-induced contact hypersensitivity, as well as vascular changes associated with this response.Received 14 February 2004; returned for revision 30 June 2004; accepted by J. S. Skotnicki 13 September 2004     

Low-level exposure to house dust mites stimulates T-cell responses during early childhood independent of atopy

Background The imtnune responses which underlie the expression of allergic symptotns in childhood are believed lo be initiated in infancy and early childhood. The kinetics of this response have hardly been researched. Objective To analyse, in an environment with low house dust mite (HDM) exposure levels, the relationship between house dust mite (HDM)-specific T-cell reactivity as expressed by in vitro proliferation of blood mononuclear cells. Methods The study comprised a prospective analysis of patterns of allergen-specific T-cell reactivity in a cohort of 19 children, from whom blood samples were obtained in the spring during their second and third years of life. Blood mononuclear cell cultures were established in 200 μL AIM-V serum free medium. Crude house dust mite (HDM) and purified Der p 1 and Der p 2 extracts were used at optimal concentrations, i.e. 100μg/mL for HDM and 30μg/mL for the purified allergens. Tetanus toxoid (0.5 μglrnL) and ovalbumin (10 μg/mL) served as positive controls. A clinical diagnosis of allergy was verified with skin-prick tests. Dust samples were collected from a mattress and/or carpet or sofa in homes, day care centres and day care homes. Major mite allergen levels (Der p 1/Der f 1) in dust were analysed by an enzyme linked immunosorbent assay (ELISA). Results Specific T-cell responses were seen in the majority of the children against house dust mite (crude HDM extract. Der p 1 and Der p 2). The levels of the house dust mite allergens Der p 1 and Der f I were low, i.e. < 0.68 μg/g fine dust in the homes of the children and the day care centres that they were attending. This indicates that doses of mite antigen well below the suggested sensitization threshold level of 2 μg/g dust can induce mite-specific T-cell responses in young children. None of them showed clinical reactivity to house dust mites as indicated by negative skin-prick tests. Conclusions The findings suggest that active immunological recognition of environmental allergens and the ensuing initiation of allergen-specific T-cell responses, is a normal part of the ‘education’ of the immune system in early childhood and can occur even at very low exposure levels. Priming per se does not imply clinically significant sensitivity, however.