Marnie Robinson

The Royal Children's Hospital, Melbourne, Victoria, Australia

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Publications (7)28.88 Total impact

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    ABSTRACT: BACKGROUND: Epidemiological evidence has shown that pediatric food allergy is more prevalent in regions further from the equator, suggesting that vitamin D insufficiency may play a role in this disease. OBJECTIVE: To investigate the role of vitamin D status in infantile food allergy. METHODS: A population sample of 5276 one-year-old infants underwent skin prick testing to peanut, egg, sesame, and cow's milk or shrimp. All those with a detectable wheal and a random sample of participants with negative skin prick test results attended a hospital-based food challenge clinic. Blood samples were available for 577 infants (344 with challenge-proven food allergy, 74 sensitized but tolerant to food challenge, 159 negative on skin prick test and food challenge). Serum 25-hydroxyvitamin D levels were measured by using liquid chromatography tandem mass spectrometry. Associations between serum 25-hydroxyvitamin D and food allergy were examined by using multiple logistic regression, adjusting for potential risk and confounding factors. RESULTS: Infants of Australian-born parents, but not of parents born overseas, with vitamin D insufficiency (≤50 nmol/L) were more likely to be peanut (adjusted odds ratio [aOR], 11.51; 95% CI, 2.01-65.79; P = .006) and/or egg (aOR, 3.79; 95% CI, 1.19-12.08; P = .025) allergic than were those with adequate vitamin D levels independent of eczema status. Among those with Australian-born parents, infants with vitamin D insufficiency were more likely to have multiple food allergies (≥2) rather than a single food allergy (aOR, 10.48; 95% CI, 1.60-68.61 vs aOR, 1.82; 95% CI, 0.38-8.77, respectively). CONCLUSIONS: These results provide the first direct evidence that vitamin D sufficiency may be an important protective factor for food allergy in the first year of life.
    The Journal of allergy and clinical immunology 02/2013; · 12.05 Impact Factor
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    ABSTRACT: Measurement of whole peanut-specific IgE (sIgE) is often used to confirm sensitization but does not reliably predict allergy. Ara h 2 is the dominant peanut allergen detected in 90% to 100% of patients with peanut allergy and could help improve diagnosis. We sought to determine whether Ara h 2 testing might improve the accuracy of diagnosing peanut allergy and therefore circumvent the need for an oral food challenge (OFC). Infants from the population-based HealthNuts study underwent skin prick tests to determine peanut sensitization and subsequently underwent a peanut OFC to confirm allergy status. In a stratified random sample of 200 infants (100 with peanut allergy and 100 with peanut tolerance), whole peanut sIgE and Ara h 2 sIgE levels were quantified by using fluorescence enzyme immunoassay. By using the previously published 95% positive predictive value of 15 kU(A)/L for whole peanut sIgE, a corresponding specificity of 98% (95% CI, 93% to 100%) was found in this study cohort. At the equivalent specificity of 98%, the sensitivity of Ara h 2 sIgE is 60% (95% CI, 50% to 70%), correctly identifying 60% of subjects with true peanut allergy compared with only 26% correctly identified by using whole peanut sIgE. We report that when using a combined approach of plasma sIgE testing for whole peanut followed by Ara h 2 for the diagnosis of peanut allergy, the number of OFCs required is reduced by almost two thirds. Ara h 2 plasma sIgE test levels provide higher diagnostic accuracy than whole peanut plasma sIgE levels and could be considered a new diagnostic tool to distinguish peanut allergy from peanut tolerance, which might reduce the need for an OFC.
    The Journal of allergy and clinical immunology 02/2012; 129(4):1056-63. · 12.05 Impact Factor
  • EAACI; 01/2010
  • EAACI; 01/2010
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    Marnie Robinson, Joanne Smart
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    ABSTRACT: Allergic diseases (asthma, atopic dermatitis, allergic rhinitis and food allergy) are the commonest chronic diseases of childhood. General practitioners commonly encounter children with allergic diseases and need to be aware of when referral to a paediatric allergist should be considered. An understanding of what diagnostic tests the allergist may use in confirming the diagnosis is also necessary. This article discusses the criteria for referral to a specialist paediatric allergist and also details the tests that may be used by the allergist as part of the diagnostic work up. Management of allergic diseases requires accurate diagnosis and avoidance of offending allergens where possible. The diagnosis of an IgE mediated allergy requires both a history of symptoms on exposure to the allergen and detection of allergen specific IgE. The most commonly employed diagnostic methods in clinical allergy assessment are skin prick testing, RAST and clinical oral food challenge procedures. The use of alternative or unorthodox tests may provide misleading results and delay correct diagnosis and therefore should not be used.
    Australian family physician 05/2008; 37(4):210-3. · 0.71 Impact Factor
  • Mimi L K Tang, Marnie Robinson
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    ABSTRACT: The prevalence of allergic disease has increased considerably in recent decades and Australia has one of the highest rates of allergic disease in the world. As there is currently no cure for allergic diseases, prevention offers a logical approach to addressing the rising burden of disease. The factors responsible for this escalation in prevalence remain unclear, and strategies for allergy prevention remain limited. This article discusses current recommendations for allergy prevention and highlights new insights into allergic disease. History of allergic disease in a first degree relative is currently the only useful indicator for increased risk of developing allergic disease in a child. Prevention strategies should be directed to these high risk individuals. Currently, maternal dietary restriction during pregnancy or lactation and aeroallergen avoidance are not recommended. Breastfeeding is recommended, and where not possible or insufficient, a partially hydrolysed formula should be used in high risk infants. Introduction of solids should be delayed to 4-6 months of age. There is no evidence that delaying solids beyond this age is of benefit. There is currently insufficient evidence to recommend the addition of probiotics for allergy prevention.
    Australian family physician 05/2008; 37(4):204-8. · 0.71 Impact Factor
  • Sam Mehr, Marnie Robinson, Mimi Tang
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    ABSTRACT: Parents and children who have been prescribed an Epipen are often unable to demonstrate its correct administration. One contributory factor may be that doctors are unfamiliar with the EpiPen and are unable to demonstrate the correct administration of the pen to the family. The aim of this study was to determine the rate of correct EpiPen demonstration by junior and Senior Medical Staff at a major tertiary paediatric Hospital. Junior and Senior medical staff were scored on their ability to correctly use the EpiPen trainer. A 6 step scoring system was used. One-hundred doctors were recruited (Residents n = 31, Senior Residents n = 39, Fellow/Consultants n = 30). Junior and Senior Medical staff had similar scores for EpiPen demonstration, the number that needed to read the EpiPen instructions prior to use and the frequancy of accidental self-injection into the thumb. Only two doctors (2%) demonstrated all 6 administration steps correctly. The most frequent errors made were not holding the pen in place for >5 seconds (57%), failure to apply pressure to activate (21%), and self-injection into the thumb (16%). Ninety five doctors needed to read the instructions, and of these, only 39 (41%) then proceeded to correctly demonstrate the remaining 5 steps. Forty-five doctors had previously dispensed an EpiPen, but only three demonstrated its use to parents/children with a trainer. The majority of doctors do not know how to use an Epipen and are unable to provide appropriate education to parents/children. In 37% of cases, the demonstration would not have delivered adrenaline to a patient.
    Pediatric Allergy and Immunology 09/2007; 18(5):448-52. · 3.38 Impact Factor