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Notes: Tracheal intubating conditions were assessed in 112 children after induction of anaesthesia with propofol and remifentanil 1.0, 2.0 or 3.0 µg.kg−1. Subjects in a control group were given propofol and mivacurium 0.2 mg.kg−1. Haemodynamic and respiratory parameters were recorded. Plasma catecholamine levels were measured in a subgroup of 40 children. Intubating conditions were acceptable in 14/28 (50%), 18/26 (69%) and 22/27 (82%) in those subjects given remifentanil 1.0, 2.0 or 3.0 µg.kg−1, respectively, and in 27/28 (96%) of the control group. Intubating conditions in subjects given remifentanil 3.0 µg.kg−1 were better than in those given remifentanil 1.0 µg.kg−1 (p 〈 0.05). There were no significant differences in intubating conditions between those given remifentanil 3.0 µg.kg−1 and the control group. Systolic blood pressure and heart rate increased in response to tracheal intubation in subjects given remifentanil 1.0 µg.kg−1 and in the control group (p 〈 0.05). Time to resumption of spontaneous respiration was prolonged in subjects given remifentanil 3.0 µg.kg−1 (p 〈 0.001). In conclusion, remifentanil 2 µg.kg−1 provides acceptable intubating conditions and haemodynamic stability without prolonging the return of spontaneous respiration.

Notes: αs1-Casein (CAS1_BOVIN), the major allergen of cow's milk (CM), is widely used as hydrolysates in infant diet formulae and additive to other processed food items. To date, most of the reported B-cell epitope mapping were performed on polyethylene pins or cellulose-derivative membrane. We sought to locate the motifs critical for human-specific IgE and rabbit polyclonal IgG binding using extensively purified CAS1_BOVIN, synthetic peptides and derivatives. Thirteen overlapping peptides covering the whole CAS1_BOVIN encompassing 17 : 20 amino acid (AA) were synthesized by f-moc AA solid-phase polyamide peptide synthesis. In addition, six cyanogen bromide (CNBr) cleavage fragments were prepared. Limited hydrolysis, oxidized and reduced/alkylated derivatives were also produced. The preparations were purified by ion exchange, gel filtration chromatography, reversed phase and high-performance liquid chromatography. The homogeneity was visualized by sodium dodecyl sulfate (SDS) and poly acryl amide gel electrophoresis (PAGE) followed by IgE and IgG immunoblotting. IgE binding was measured by Biotin Streptavidin (Bio/strep) fluoro enzyme immuno assay (FEIA) or ELISA-inhibition. Eighteen CM allergy (CMA) sera from 45 clinically examined children (Melbourne) and five adults (Bergen) were selected. Individual sera and pools were used for mapping IgE-binding epitopes. Rabbit IgG sera and pools were used for locating the antigenic sites of the molecule. Results indicated that all the individual CMA sera and pools recognized the intact molecule and three of the CNBr fragments as major antibody-binding allergens. The N- and C-terminal peptides (CAS 16-35; CAS 136-155) showed high IgE-binding affinity. CAS 1-18 and CAS 181-199 showed high IgG bindings. Considering the diversity of the antibody specificities, a reasonable agreement between IgE and IgG epitopes were found at the N- and C-terminals of CAS1_BOVIN. Mapping IgE B-cell epitopes by direct Bio/strep FEIA allowed the development of a sensitive modified technique for detecting unlabelled, casein immune dominant peptides in food products.

Notes: Atopic dermatitis is common in infancy. The role of food allergy in atopic dermatitis of infancy is unclear. We examined the relationship between atopic dermatitis and immunoglobulin E (IgE)-mediated food allergy in infancy. A birth cohort of 620 infants with a family history of eczema, asthma, hayfever or immediate food allergy in a parent or sibling: 487 children had complete data including skin prick tests (SPTs) to evaluate IgE-mediated food allergy to cow milk, egg and peanut. Participants were grouped as no atopic dermatitis (Gp 0) or in quartiles of increasing severity of atopic dermatitis (Gps 1–4) quantified by days of topical steroid use as reported monthly. Adverse reactions to foods were recorded. The cumulative prevalence of atopic dermatitis was 28.9% to 12 months (10.3% of the cohort of moderate severity). As atopic dermatitis severity increased so did the prevalence of IgE-mediated food allergy (Gp 0, 40/346 vs. Gp 1, 6/36 vs. Gp 2, 8/35 vs. Gp 3, 12/35 vs. Gp 4, 24/35; χ2 = 76; p 〈 10−6), and the frequency of reported adverse food allergy reactions (Gp 0, 43/346 vs. Gp 1, 4/36 vs. Gp 2, 8/35, vs. Gp 3, 5/35, vs. Gp 4, 13/35; χ2 = 17; p = 0.002). The relative risk of an infant with atopic dermatitis having IgE-mediated food allergy is 5.9 for the most severely affected group. Atopic dermatitis is common in infancy. There is a strong association between IgE-mediated food allergy and atopic dermatitis in this age group.

Notes: Background While the ingestion of small amounts of an offending food can elicit adverse reactions in individuals with IgE-mediated food allergies, little information is known regarding these threshold doses for specific allergenic foods. While low-dose challenge trials have been conducted on an appreciable number of allergic individuals, a variety of different clinical protocols were used making the estimation of the threshold dose very difficult.Objective A roundtable conference was convened to develop a consensus clinical protocol for low-dose challenge trials for the estimation of threshold doses for specific allergenic foods.Methods In May 2002, 20 clinical allergists and other interested parties were invited to participate in a roundtable conference to develop consensus of the key elements of a clinical protocol for low-dose challenge trials.Results A consensus protocol was developed. Patients with convincing histories of food allergies and supporting diagnostic evidence including past challenge trials or high CAP–RAST scores can be enrolled in low-dose challenge trials. Care must be taken with younger patients to assure that they have not outgrown their food allergy. An approach was developed for the medication status of patients entering such trials. Challenge materials must be standardized, for example, partially defatted peanut flour composed of equal amounts of the three major varieties of peanuts (Florunner, Virginia, Spanish). Challenge materials must be appropriately blinded with sensory evaluation used to confirm the adequacy of blinding. A double-blind, placebo-controlled design should be used for low-dose challenge trials. Low-dose challenge trials would begin at doses of 10 μg of the allergenic food and would continue with doses of 100 μg and 1 mg followed by specific higher doses up to 100 mg depending upon the expert judgement of the physician; even higher doses might be applied to assure that the patient is indeed reactive to the particular food. A 30-min time interval would be used between doses, and reactive doses would be expressed as both discrete and cumulative doses. The goal of each challenge would be to develop objective symptoms; trials should not be discontinued on the basis of subjective symptoms only. Statistically, a minimum of 29 patients would be enrolled in low-dose challenge trials for each allergenic food because 0 reactors out of 29 patients at a particular dose allow the conclusion that there is 95% certainty that 90% of allergic individuals will not react to that dose.Conclusion A consensus protocol was developed. Using this protocol, it will be possible to estimate threshold doses for allergenic foods, the lowest amount that elicits mild, objective symptoms in highly sensitive individuals.

Notes: Background Australia has one of the highest prevalence rates internationally of allergic conditions, such as asthma and eczema. Atopy is one hallmark for the development of allergic disease and predisposes to allergic inflammation in the target organs. ω-3 (n-3) fatty acids (FAs) are thought to act as precursors to the formation of less active inflammatory mediators, with the potential to reduce inflammation.Objective To investigate whether increased n-3 FA levels in maternal breast milk are associated with a lower risk of developing atopy in infancy.Methods Subjects were part of the prospective Melbourne atopy cohort study, which involved 620 children born into families where at least one first-degree relative had an atopic disease. Some 224 women (mean age 31.4±4.2 (SD) years, with 73.2% (n=164) having self-reported atopy) provided either a colostrum (n=194) or 3-month expressed breast milk (EBM) sample (n=118). Maternal colostrum and 3-month EBM samples were analysed for FA content by gas chromatography. Skin prick tests (SPTs) to six common allergens were performed on infants at 6, 12 and 24 months of age and on mothers who agreed at study entry.Results For infants sensitized to foods at 6 months (n=29), the total n-3 FA level in the colostrum was significantly higher (P=0.004) as were levels of individual long-chain n-3 FAs, docosoapentaenoic acid (DPA, C22:5, P=0.001) and docosahexaenoic acid (DHA, C22:6, P=0.002) than in non-sensitized infants. Infants with aero-allergen sensitization at 24 months (n=30) had higher levels of the n-3 FA, DPA (P=0.002) and DHA (P=0.007), and similarly higher total n-3 FA (P=0.009) in maternal colostrum than those infants who were not sensitized.Conclusion Higher n-3 FA levels in the colostrum do not appear to confer protection against, but may be a risk factor for, the eventual development of atopy in high-risk breastfed infants.