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Atopic Manifestations (atopic + manifestation)
Selected AbstractsImmunoCAPTM Phadiatop® Infant , a new blood test for detecting IgE sensitisation in children at 2 years of ageALLERGY, Issue 3 2006N. Ballardini Background:, Correct diagnosis of immunoglobulin E (IgE)-mediated disease is the prerequisite for secondary allergy prevention during early childhood. Objective:, To evaluate the diagnostic efficacy of a new blood test, Phadiatop® Infant, in detecting IgE sensitisation to food and inhalant allergens among children at 2 years of age. Methods:, Children (n = 239) were followed prospectively from birth to 2 years of age for the presence of IgE sensitisation and the development of atopic manifestations. Immunoglobulin E sensitisation was evaluated by skin prick test (SPT) and analysis of allergen-specific IgE antibodies in plasma to food and inhalant allergens. The children were classified into three groups: IgE-sensitised, non-IgE sensitised and inconclusive, depending on SPT and allergen-specific IgE results. Results:, Twenty-six (11%) of the children were classified as IgE-sensitised, 182 (76%) as non-IgE sensitised and 31 (13%) as inconclusive. Phadiatop Infant was positive in 50 (21%) of the children. Ten children (4%) with identified IgE antibodies against the selected food and inhalant allergens showed negative Phadiatop Infant. Three children showed positive Phadiatop Infant but were negative in the other tests performed. These results correspond to positive and negative predictive values for Phadiatop Infant of 89 and 99%, respectively. Children with clinical symptoms of atopic diseases had significantly increased levels for Phadiatop Infant (P < 0.01). Conclusion:, Phadiatop Infant appears to be a reliable alternative to SPT and the measurement of allergen-specific IgE antibodies in plasma for detecting clinically important IgE sensitisation among children at 2 years of age. [source] Adherence to recommendations for primary prevention of atopic disease in neonatology clinical practicePEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2010Annalisa Passariello Passariello A, Terrin G, Baldassarre ME, Bisceglia M, Ruotolo S, Berni Canani R. Adherence to recommendations for primary prevention of atopic disease in neonatology clinical practice. Pediatr Allergy Immunol 2010: 21: 889,891. © 2010 John Wiley & Sons A/S The prevalence and severity of atopic manifestations in children are increasing in western countries in the last decades. Specific nutritional intervention may prevent or delay the onset of atopic diseases in infants at high risk of developing allergy. These nutritional interventions should be applied early in the perinatal period to have a chance of success. Thus, we assessed adherence to the dietary management recommendations of the Committee on Nutrition and Section on Allergy and Immunology of the American Academy of Pediatrics (AAP) for the prevention of atopic diseases in neonatal age through an audit study. Questionnaire was administered to the chiefs of 30 maternity units (MU) with more than 1500 live births/yr to report the policy applied in their MU. Twenty-two MU returned the questionnaire. Identification of high-risk newborns was routinely performed only in 7/22 MU (31.8%). High-risk newborns were identified by the presence of at least two or one first-degree relative (parent or sibling) with documented allergic disease by 18.2% and 45.5% of MU, respectively. Specific maternal dietary restrictions during lactation were adopted in 7/22 MU (31.8%). Extensively or partially hydrolyzed formula was prescribed for bottle-fed high-risk infants in 22.7% of MU. Only 2/22 MU have a policy in complete agreement with the nutritional intervention proposed by the AAP. Our study suggest a poor adherence to dietary recommendations for primary prevention of atopic disease in neonatology clinical practice. Further efforts should be planned to improve the knowledge and the application of these preventive strategies. [source] Ichthyosis vulgaris: novel FLG mutations in the German population and high presence of CD1a+ cells in the epidermis of the atopic subgroupBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2009V. Oji Summary Background, Ichthyosis vulgaris (IV) is a genetic disorder with a prevalence of 1 : 250,1000 caused by filaggrin (FLG) mutations, which also predispose to atopic diseases. Objectives, To study the genotype/phenotype relationship in IV and to analyse whether the suggested skin barrier defect is associated with differences of epidermal dendritic cells. Patients/methods, We evaluated a cohort of 26 German patients with IV, established an IV severity score and analysed epidermal ultrastructure, histology, filaggrin and CD1a antigens. Mutations were screened by restriction enzyme analysis. Particular sequencing techniques allowed the complete FLG analysis to reveal novel mutations. Results, The combined null allele frequency of R501X and 2282del4 was 67·3%. Patients also showed the mutations S3247X and R2447X as well as five novel FLG mutations: 424del17 and 621del4 (profilaggrin S100 domain), 2974delGA (repeat 2), R3766X (repeat 101) and E4265X (repeat 102). Their combined allele frequency in controls was < 0·7%. No mutation was found in one IV patient, all in all ,27% were heterozygous, and the majority (,69%) showed two null alleles. The IV severity score and ultrastructure showed a significant correlation with genotypes. Interestingly, CD1a cell counts showed a significant difference between nonatopic and atopic IV patients both with eczema and without eczema. Conclusions, We confirm that the mutations R501X and 2282del4 represent the most frequent genetic cause in German IV patients. The novel mutations are probably population and family specific. The observed differences of CD1a cells support the hypothesis that there is a barrier defect that predisposes to atopic manifestations, possibly independent of atopic eczema. [source] Chromosome 7p linkage and GPR154 gene association in Italian families with allergic asthmaCLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2007G. Malerba Summary Background Several genome scans have reported linkage of markers on chromosome 7p with asthma and related phenotypes in different populations. A fine mapping in Finnish and French-Canadian populations has associated the GPR154 gene (also known as G-protein-coupled receptor for asthma susceptibility, GPRA) with elevated IgE or asthma. Objective To confirm chromosome 7p linkage and candidate gene association in Italian families with atopic asthma. Methods In a two-phase approach, we first performed a linkage analysis of chromosome 7, and then a family-based association study on the GPR154 gene for allergic asthma phenotypes in the Italian population. Results The screening of 117 families with 19 microsatellite markers showed potential linkage for elevated IgE (P<0.002 at 22 cM from p-ter), asthma (P<0.005 at 44 cM), or atopy (P<0.005 at 54 cM). In the second phase of the present study, candidate gene GPR154, which is located in the phase one-linked region, was investigated in 211 families with seven single nucleotide polymorphisms (SNPs) that tag most haplotype variability, by the pedigree disequilibrium test. Elevated IgE levels were associated with two GPR154 gene SNPs (SNP 546333, P=0.0046; rs740 347, P=0.006), and with haplotypes in the global test (P=0.013). Haplotype analysis performed in nuclear families having at least 1 asthmatic parent showed a significant association with asthma (P=0.0173), atopy (P=0.0058), SPT (P=0.0025), and bronchial hyper reactivity (P=0.0163). Conclusion These results support a susceptibility locus for asthma and related phenotypes on chromosome 7, and are in agreement with recent reports suggesting that a common susceptibility factor for atopic manifestations in asthma is likely conferred by the locus containing the GPR154 gene. [source] Do parents with an atopic family history adopt a ,prudent' lifestyle for their infant? (KOALA Study)CLINICAL & EXPERIMENTAL ALLERGY, Issue 4 2006I. Kummeling Summary Background Atopic parents may adopt lifestyle characteristics that allegedly protect against atopic disease. If this is true, infants from atopic parents will be characterized by low-risk behaviour. Consequently, aetiologic studies on lifestyle factors and allergic disease in childhood may be biased by confounding by indication. Objective We explored whether the prevalence of ,prudent' lifestyle characteristics differs between atopic and non-atopic families. Methods Information about a family history of atopic manifestations and lifestyle characteristics was collected by repeated questionnaires in the Dutch KOALA Birth Cohort Study in 2469 infants from families with divergent lifestyle practices (conventional vs. alternative). Results In conventional lifestyle families, infants were less often exposed to environmental tobacco smoke when parents were atopic than when they were non-atopic (10.0% vs. 14.7%, P=0.001). In alternative lifestyle families, exposure to smoking was very rare in both groups (1.7% vs. 2.6%). Pets were less often present in families with than without parental atopy (38.8% vs. 51.1%, P=0.008 for conventional lifestyle families; 43.0% vs. 48.4%, P=0.014 for alternative lifestyle families). Infants with atopic siblings had less often been vaccinated according to the standard scheme than infants with non-atopic siblings in conventional lifestyle families (76.6% vs. 85.5%, P<0.001). In alternative lifestyle families, the difference was in the same direction but not statistically significant (30.1% vs. 40.5%, P=0.143). Antibiotic use, breastfeeding and consumption of organic foods were unrelated to a family history of atopic manifestations. Conclusion Some ,prudent' lifestyle characteristics differed between atopic and non-atopic families, depending on whether atopic manifestations were present in parents or older siblings. This has important consequences for the validity in epidemiological studies on the aetiology of allergy in children. Confounding by indication because of a family history of atopic manifestations can best be controlled for by considering atopy in parents and siblings as separate confounders. [source] | ||||||||||