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    What 2012 food allergy What 2012 food allergy Presentation Transcript

    • WHAT YOU SHOULD HAVE READ BUT….2012  food allergyAttilio BonerUniversity ofVerona, Italy
    • •Epidemiology•Prevalence•Time trends
    • Personal and parental nativity as risk factors for food sensitization Keet JACI 2012;129:169 OR for sensitization Nativity classified as to any food 2.5 – US-born or foreign-born, and 2.0 – the age of immigration was estimated. 1.5 – 2.05 p<0.001 1.0 – Food sensitization defined specific IgE 0.5 - level ≥0.35 kU/L to milk, egg, or peanut. 0.0 Compared with those born outside the United States (US), US-born children and adolescents.
    • Personal and parental nativity as risk factors for food sensitization Keet JACI 2012;129:169 OR for sensitization Nativity classified as to any food among the US-born or 3.0 – foreign-born group foreign-born, and 2.68 2.5 – the age of immigration was estimated. 2.0 – p<0.02 1.5 – Food sensitization 1.0 – defined specific IgE level ≥0.35 kU/L 0.5 - to milk, egg, or peanut. 0.0 Children arrived before 2 years of age.
    • Personal and parental nativity as risk factors for food sensitization Keet JACI 2012;129:169 OR for sensitization Nativity classified as to any food within the US-born or US-born group 2.5 – foreign-born, and the age of immigration 2.0 – was estimated. 1.5 – Food sensitization 1.0 – 1.53 defined specific IgE p<0.02 level ≥0.35 kU/L 0.5 - to milk, egg, or peanut. 0.0 Compared with children of immigrants.
    • Personal and parental nativity as risk factors for food sensitization Keet JACI 2012;129:169 Although OR for sensitization Nativity classified as to any food within the foreign-born children US-born or US-born group and adolescents 2.5 – foreign-born, and risk are at lower the age of sensitization of food immigration 2.0 – was estimated. compared with those 1.5 – born in the US, Food sensitization among those born 1.0 – 1.53 definedUS, the IgE in the specific children p<0.02 level ≥0.35 kU/L are of immigrants 0.5 - milk, egg, or peanut to at the highest risk.. 0.0 Compared with children of immigrants.
    • Season of birth and childhood food allergy in Australia Mullins Pediat Allergy Immunol 2011;22:583 Among food allergic children 60 – p<0.001 50 – 57% Season of birth in 40 – 835 children aged 30 – 43% 0–4 yr assessed 1995–2009 20 – 10 – 0 Autumn-winter Spring-summer BORN
    • Season of birth and childhood food allergy in Australia Mullins Pediat Allergy Immunol 2011;22:583 Among children prescribed EpiPens 60 – p<0.001 50 – 54% Season of birth in 835 children aged 40 – 46% 30 – 0–4 yr assessed 1995–2009 20 – 10 – 0 Autumn-winter Spring-summer BORN
    • Season of birth and childhood food allergy in Australia Mullins Pediat Allergy Immunol 2011;22:583 Among children prescribed hypoallergenic formula 60 – p<0.001 50 – 54% Season of birth in 835 children aged 40 – 46% 30 – 0–4 yr assessed 1995–2009 20 – 10 – 0 Autumn-winter Spring-summer BORN
    • Season of birth and childhood food allergy in Australia Mullins Pediat Allergy Immunol 2011;22:583 Season of birth in 835 children aged 0–4 yr assessed 1995–2009 The relationship between average monthly ultraviolet radiation exposure and food and peanut allergy rates per month.
    • Season of birth and childhood food allergy in Australia Mullins Pediat Allergy Immunol 2011;22:583 Suggest that ultraviolet light Season of birth in D exposure/vitamin 835 children aged status may be one 0–4 yr assessed of many potential 1995–2009 factors contributing to childhood food allergy pathogenesis. The relationship between average monthly ultraviolet radiation exposure and food and peanut allergy rates per month.
    • Race, ancestry and development of food-allergensensitization in early childhood Kumar Pediatrics 2011;128:e821 % children with food sensitization sIgE of ≥0.35 kUA/L 40 –  1104 children (mean age: 2.7 yrs).  IgE levels 30 – 20 – 35.5% of ≥0.35 kilo-units of allergen (kUA/L) for any of 8 common 10 – food allergens. 0
    • Race, ancestry and development of food-allergensensitization in early childhood Kumar Pediatrics 2011;128:e821 OR for food sensitization 3 –  1104 children (mean age: 2.7 yrs).  IgE levels of ≥0.35 kilo-units 2 – 2.34 of allergen (kUA/L) 1 – for any of 8 common food allergens. 0 Black race
    • Race, ancestry and development of food-allergensensitization in early childhood Kumar Pediatrics 2011;128:e821 OR for food sensitization African ancestry 3 –  1104 children were associated (mean age: 2.7 yrs).  IgE levels a high with number (≥3) of ≥0.35 kilo-units 2 – 2.34 of allergen (kUA/L) of food for any of 8 common 1 – sensitizations. food allergens. 0 Black race
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 % children with 649 children enrolled at birth; 50 – Vitamin D deficiency as cord blood 25(OH)D < 11 ng/ml; 40 – 44% Food sensitization: 30 – 37% sIgE ≥ 0.35 kUA/l to any of 8 common food allergens; 20 – Single-nucleotide polymorphisms (SNPs) in 11 10 – genes known to be involved in regulating IgE and 25(OH)D 0 concentrations. Vitamin D deficiency Food sensitization
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; 2 – Food sensitization: sIgE ≥ 0.35 kUA/l to any 1.79 of 8 common food allergens; 1 – Single-nucleotide polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Similar but weaker Vitamin D deficiency as cord deficiency interactions were blood 25(OH)D < 11 ng/ml; observed for SNPs 2 – in MS4 A2 Food sensitization: sIgE ≥ 0.35 kUA/l to any (rs512555), FCERIG 1.79 of 8 (rs2070901), and common food allergens; 1 – CYP24A1 Single-nucleotide (rs2762934). polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D all four SNPs When deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; were simultaneously 2 – Food sensitization:strong considered, a gene-VSS interaction sIgE ≥ 0.35 kUA/l to any 1.79 of 8 commonevident was food allergens; 1 – (pinteraction =9x10-6) Single-nucleotide polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • The incidence and risk factors of immediate type foodallergy during the first year of life in Korean infants:a birth cohort study. Kim Pediat Allergy Immunol 2011;22:715 % infants with food allergy Pregnant women 6 – ≥34 weeks of gestation were enrolled. 5 – 1177 infants. 4 – 5.3% 3 – through telephone 2 – interviews at 4, 8, 1 – and 12 months of age. 0
    • The incidence and risk factors of immediate type foodallergy during the first year of life in Korean infants:a birth cohort study. Kim Pediat Allergy Immunol 2011;22:715 OR for food allergy 4.0 – Pregnant women ≥34 weeks of gestation were enrolled. 3.0 – 3.48 3.2 p=0.005 1177 infants. 2.0 – p=0.012 through telephone 1.0 – interviews at 4, 8, and 12 months of age. 0.0 History of Born in autumn maternal AD vs spring
    • Anisakis hypersensitivity in Italy: prevalence and clinicalfeatures: a multicenter study Asero, Allergy 2011;66:1563 % Subjects 0,6 – 10 570 subjects. Consecutive subjects seen 0.4 – 4.5 % at 34 Italian allergy centers from October to (474/10570) 0.2 – December 2010. Skin prick test (SPT) with 0.0 – Anisakis simplex extract. Anisakis simplex (+) SPTs
    • Anisakis hypersensitivity in Italy: prevalence and clinical features: a multicenter study Asero, Allergy 2011;66:1563 % Subjects,6 – • 34 (52%) patients were.4 – 4.5 % monosensitized to Anisakis. (474/10570).2 – • And 66 of these (14% of those sensitized) had a history of As allergy..0 – Anisakis simplex (+) SPTs
    • Anisakis hypersensitivity in Italy: prevalence and clinical features: a multicenter study Asero, Allergy 2011;66:1563 % Subjects,6 – Marinated • 34anchovies were (52%) patients were.4 – 4.5 % the most monosensitized to Anisakis. (474/10570) frequent cause • And 66 of these.2 – of allergic (14% of those sensitized) reactions had a history of As allergy..0 – Anisakis simplex (+) SPTs
    • • Food allergy natural history
    • Ovomucoid (Gal d 1) specific IgE detected by microarray system predict tolerability to boiled hen’s egg and an increased risk to progress to multiple environmental allergen sensitization. Alessandri, Clin Exp Allergy 2012;42:441 % subjects 68 children with a suspected 60 – egg allergy. 50 – 51.4% Double- 40 – blind, placebo- controlled 30 – food challenge 28% 20 – with boiled & raw eggs. 20.5% 10 – sIgE to egg allergens available on the 00 immunosolid phase Reactive to both Reactive to Tolerated both raw&boiled egg raw egg only raw&boiled egg allergen chip (ISAC) 103 microarray.
    • Ovomucoid (Gal d 1) specific IgE detected by microarray system predict tolerability to boiled hen’s egg and an increased risk to progress to multiple environmental allergen sensitization. Alessandri, Clin Exp Allergy 2012;42:441 % Gal d 1 negative subjects 68 children 100 – with a suspected egg allergy. 94% 90 – 80 – Double-blind, 70 – placebo-controlled 60 – food challenge 50 – with boiled & raw eggs. 40 – sIgE to egg allergens 30 – available on the 20 – immunosolid phase 10 – allergen chip (ISAC) 0 103 microarray. tolerated boiled egg
    • Ovomucoid (Gal d 1) specific IgE detected by microarray system predict tolerability to boiled hen’s egg and an increased risk to progress to multiple environmental allergen sensitization. Alessandri, Clin Exp Allergy 2012;42:441 % Gal d 1 negative subjects 68 children 100 – with a suspected egg allergy. 94% 90 – Double- d 1 negative Gal 80 – 70 – blind, children placebo- have 60 – controlled frequency a high 50 – food challenge with boiledtolerance of & raw eggs. 40 – to boiled egg. 30 – sIgE to egg allergens 20 – available on the 10 – immunosolid phase 0 allergen chip (ISAC) tolerated boiled egg 103 microarray.
    • Ovomucoid (Gal d 1) specific IgE detected by microarray system predict tolerability to boiled hen’s egg and an increased risk to progress to multiple environmental allergen sensitization. Alessandri, Clin Exp Allergy 2012;42:441 % Gal d 1 positive subjects 68 children 100 – with a suspected egg allergy. 95% 90 – 80 – Double- 70 – blind, placebo- 60 – controlled 50 – food challenge with boiled & raw eggs. 40 – 30 – sIgE to egg allergens 20 – available on the 10 – immunosolid phase 0 allergen chip (ISAC) reacting to raw eggs 103 microarray.
    • Ovomucoid (Gal d 1) specific IgE detected by microarray system predict tolerability to boiled hen’s egg and an increased risk to progress to multiple environmental allergen sensitization. Alessandri, Clin Exp Allergy 2012;42:441 % Gal d 1 positive subjects 68 children 100 – with a suspected egg allergy. 95% 90 – 80 – Double-blind,1 positive Gal d 70 – placebo-controlled children have food challenge 60 – witha high frequency boiled & raw eggs. 50 – of hen’s egg allergy. sIgE to egg allergens 40 – 30 – available on the 20 – immunosolid phase 10 – allergen chip (ISAC) 0 103 microarray. reacting to raw eggs
    • Presence of functional, autoreactive human milk-specific IgE in infants with cow’s milk allergy. Järvinen, Clin Exp Allergy 2012;42:238Background Occasionally, exclusively breastfed infantswith cow’s milk allergy (CMA) remain symptomaticdespite strict maternal milk avoidance.Objective To determine whether or not persistenceof symptoms could be due to sensitization againstendogenous human milk proteins with a high degreeof similarity to bovine allergens.
    • Presence of functional, autoreactive human milk-specific IgE in infants with cow’s milk allergy. Järvinen, Clin Exp Allergy 2012;42:238 1. 9 of the 15 breastfed 10 peptides representing known bovine milk IgE-binding epitopes infants became [α-lactalbumin (ALA), β- and k-casein] asymptomatic and the corresponding, highly during strict maternal homologous human milk peptides avoidance of milk labelled with sera from 15 breastfed & other major food infants with CMA. allergens. Functional capacity of specific IgE antibodies assessed by measuring 2. 6 infants remained β-hexosaminidase release from rat basophilic leukaemia cells passively symptomatic until sensitized and stimulated with weaned. human and bovine ALA.
    • Presence of functional, autoreactive human milk-specific IgE in infants with cow’s milk allergy. Järvinen, Clin Exp Allergy 2012;42:238 % of allergic infants with serum IgE recognizing at least 1 human milk peptide 10 peptides representing known 100 – bovine milk IgE-binding epitopes 90 – [α-lactalbumin (ALA), β- and k-casein] and the corresponding, highly 80 – homologous human milk peptides 70 – labelled with sera from 15 breastfed 60 – 60% infants with CMA. 50 – Functional capacity of specific IgE 40 – antibodies assessed by measuring 30 – 9/15 β-hexosaminidase release from rat 20 – basophilic leukaemia cells passively 10 – sensitized and stimulated with human and bovine ALA. 0
    • Presence of functional, autoreactive human milk-specific IgE in infants with cow’s milk allergy. Järvinen, Clin Exp Allergy 2012;42:238 % of allergic infants with serum IgE recognizing at least 1 human milk peptide 10 peptides representing known There was a trend 100 – bovine milk IgE-binding epitopes towards specific IgE [α-lactalbumin (ALA), β- and k-casein] 90 – being detected and the corresponding, highly 80 – homologous human milk peptides to more human milk peptides 70 – labelled with sera from 15 breastfed in those infants who 60 – 60% infants with CMA. respond did not 50 – to the maternal Functional capacity of specific IgE 40 – antibodies assessed by measuring milk elimination diet 30 – 9/15 β-hexosaminidase release from rat than in those who did 20 – basophilic leukaemia cells passively (p=0.099). sensitized and stimulated with 10 – human and bovine ALA. 0
    • Allergens types
    • Seafood allergy in children: a descriptive study Turner Ann Allergy Asthma Immunol 2011;106:494 % children with co-existent atopic disease 100 – 90 – 167 children with 80 – 70 – 94% history of 60 – definite clinical 50 – reaction to 40 – seafood and/or 30 – positive food 20 – challenge. 10 – 0
    • Seafood allergy in children: a descriptive study Turner Ann Allergy Asthma Immunol 2011;106:494 Common seafood triggers in children with seafood allergy Prawn/shrimp was the most common seafood implicated. One-fifth presented with a history of anaphylaxis to seafood.
    • Seafood allergy in children: a descriptive study Turner Ann Allergy Asthma Immunol 2011;106:494Size of skin prick test (SPT) wheal in relation to outcome of oral food challenges performed to seafood (all challenges), crustacean only, and canned fish.
    • Seafood allergy in children: a descriptive study Turner Ann Allergy Asthma Immunol 2011;106:494Size of skin prick test (SPT) wheal in relation to outcome of oral food challenges Over 50% of crustacean-allergic children performed to seafood (all challenges), crustacean only, and canned fish. could tolerate non-crustacean fish.
    • Seafood allergy in children: a descriptive study Turner Ann Allergy Asthma Immunol 2011;106:494 Risk Factors for Anaphylaxis to Seafood aa
    • Spice allergy Chen Ann Allergy Asthma Immunol 2011;107:1911) Spice allergy seems to be rare, affecting between 4 and 13 of 10,000 adults and occurring more often in women because of cosmetic use.2) Most spice allergens are degraded by digestion; therefore, IgE sensitization is mostly through inhalation of cross-reacting pollens, particularly mugwort and birch.3) The symptoms are more likely to be respiratory when exposure is by inhalation and cutaneous if by contact.4) Studies on skin testing and specific IgE assays are limited and showed low reliability.5) The diagnosis primarily depends on a good history taking and confirmation with oral challenge.
    • Spice allergy Chen Ann Allergy Asthma Immunol 2011;107:191Manifestations of Immunologically Mediated Reactions to Spices
    • Spice allergy Chen Ann Allergy Asthma Immunol 2011;107:191 Allergens Identified in SpicesaaFrom Scholl and Jensen-Jarolim, Vieths et al, Breiteneder and Radauer, Egger et al, and Gomez-Gomez et al.
    • • Food allergy diagnosis• SPTs• sIgE
    • Is epitope recognition of shrimp allergens useful topredict clinical reactivity? Ayuso, Clin Exp Allergy 2012;42:293Background Shrimp is a frequent cause of severeallergic reactions world-wide. Due to issues such ascross reactivity, diagnosis of shrimp allergy is stillinaccurate, requiring the need for double-blind,placebo-controlled food challenges (DBPCFC).A better understanding of the relationship betweenlaboratory findings and clinical reactivity is needed.Objective To determine whether sensitization to certainshrimp allergens or recognition of particular IgE epitopesof those allergens are good biomarkers of clinical reactivityto shrimp.
    • Is epitope recognition of shrimp allergens useful topredict clinical reactivity? Ayuso, Clin Exp Allergy 2012;42:293 % of patients with a positive challenge to shrimps 100 – 37 patients with 90 – shrimp allergy. 80 – 70 – Skin prick test, 60 – sIgE, DBPCFC. 50 – IgE binding to synthetic 46% 40 – peptides 30 – (Lit v1, Lit v2, Lit v3, Lit v4). 20 – 10 – 17/37 0
    • Is epitope recognition of shrimp allergens useful topredict clinical reactivity? Ayuso, Clin Exp Allergy 2012;42:293 % of patients with a positive challenge to shrimps 37 patientsmicroarray, By with 100 – 90 – patients shrimp allergy. 80 – with positive 70 – Skin prick test, challenges showed specific IgE 60 – more intense binding determinations, DBPCFC. 50 – to shrimp peptides. 46% 40 – IgE binding to synthetic Particularly peptides (Lit v1, Lit 30 – 20 – v2, for Lit v1 & Lit v2 Lit v3, Lit v4). 10 – 17/37 epitopes. 0
    • Is epitope recognition of shrimp allergens useful topredict clinical reactivity? Ayuso, Clin Exp Allergy 2012;42:293 % of patients with a positive challenge to shrimps 100 – 37 patients with 90 – IgE antibodies shrimp allergy. 80 – Skin prick these shrimp to 70 – epitopes could be IgE test, specific used 60 – as biomarkers for determinations, DBPCFC. 50 – 46% 40 – IgE prediction of clinical binding to synthetic 30 – reactivity. peptides (Lit v1, Lit 20 – v2, Lit v3, Lit v4). 10 – 17/37 0
    • Tropomyosin IgE-positive results are a good predictor of shrimp allergy Gàmez, Allergy 2011;66:1375 Background: Shrimp is a common cause of food allergy. Our aims were to determine the value of IgE antibodies in the diagnosis of shrimp allergy and to study red shrimp (Solenocera melantho) tropomyosin both as a new allergen and as a crossreactive IgE-binding protein.
    • Tropomyosin IgE-positive results are a good predictor of shrimp allergy Gàmez, Allergy 2011;66:1375 1) Shrimp allergy was confirmed in 18 shrimp-allergic patients.45 subjects; 2) Skin prick test and IgE antibodies to shrimp were positive in all shrimp-allergicSkin prick test (SPT) patients.and specific IgE (sIgE) toshrimp, recombinant and 3) sIgE to rPen a 1 was detected innatural shrimp 98% of these patients.tropomyosins rPen a 1 andnPen m 1, recombinant 4) Of the 18 shrimp-tolerantDer p 10, and patients, 61% had positive SPT toDermatophagoides shrimp, 55% were IgE-positive topteronyssinus shrimp, and 33% showed IgE antibodies to rPen a 1.
    • Tropomyosin IgE-positive results are a good predictor of shrimp allergy Gàmez, Allergy 2011;66:1375 1) Shrimp allergy was confirmed in 18 shrimp-allergic patients.45 subjects; 2) Skin prick test and IgE antibodies to shrimp were IgE levels positive in all shrimp-allergicSkin prick test (SPT) patients.and specific IgEa 1 to rPen (sIgE) to providedshrimp, recombinant and 3) sIgE to rPen a 1 was detected innatural shrimp value additional 98% of these patients.tropomyosinsdiagnosis and to the rPen a 1 ofnPen m 1, recombinant 4) Of the 18 shrimp-tolerantDer p shrimp allergy. 10, and patients, 61% had positive SPT toDermatophagoides shrimp, 55% were IgE-positive topteronyssinus shrimp, and 33% showed IgE antibodies to rPen a 1.
    • Patients suffering from non-IgE-mediated cow’s milk protein intolerance cannot be diagnosed based on IgG subclass or IgA responses to milk allergens Hochwallner H, Allergy 2011;66:1201Background: Cow’s milk is one of the most common causes of foodallergy. In two-thirds of patients, adverse symptoms following milkingestion are caused by IgE-mediated allergic reactions, whereasfor one-third, the mechanisms are unknown.Aim of this study was to investigate whether patients sufferingfrom non-IgE-mediated cow’s milk protein intolerance can bedistinguished from persons without cow’s milk protein intolerancebased on serological measurement of IgG and IgA specific forpurified cow’s milk antigens.
    • Patients suffering from non-IgE-mediated cow’s milk protein intolerance cannot be diagnosed based on IgG subclass or IgA responses to milk allergens Hochwallner H, Allergy 2011;66:1201 IgG1–4 subclass and IgA antibody to recombinant αS1-casein, Cow’s milk protein αS2-casein, β-casein, κ-casein, intolerant patients α-lactalbumin, and β-lactoglobulin. cannot be distinguished from Patients with IgE-mediated cow’s persons without milk allergy (CMA, n = 25), cow’s milk protein patients with non-IgE-mediated intolerance (CMPI, n = 19), intolerance on the patients with gastrointestinal basis of symptoms not associated with IgG subclass or cow’s milk ingestion (GI, n = 15) IgA reactivity to and control persons (C, n = 26) cow’s milk allergens.
    • • Food allergy diagnosis• challenges
    • The eliciting dose of peanut in double-blind, placebocontrolled food challenges decreases with increasing age and specific IgE level in children and young adults Zee, JACI 2011;128:1031Background:Several risk factors for severe anaphylactic reactions to foodin daily life are known.However, to date, it is not possible to predict the severityof allergic reactions to food in the individual patient with accuracy.Some studies show that a history of severe reactions is associatedwith a lower eliciting dose in double-blind, placebo-controlled foodchallenges (DBPCFCs). Therefore, in this study, the eliciting dosewas used as a measure of clinical sensitivity.
    • The eliciting dose of peanut in double-blind, placebocontrolled food challenges decreases with increasing age and specific IgE level in children and young adults Zee, JACI 2011;128:1031 The cumulative doses of peanut in the 3 age groups. Children who had clinical reactions to peanut during DBPCFCs (2001-2009). 126 positive DBPCFCs.
    • The eliciting dose of peanut in double-blind, placebocontrolled food challenges decreases with increasing age and specific IgE level in children and young adults Zee, JACI 2011;128:1031 Kaplan-Meier survival curves Kaplan-Meier survival curves for for 3 age groups. children in tertiles of specific IgE.
    • The eliciting dose of peanut in double-blind, placebocontrolled food challenges decreases with increasing age and specific IgE level in children and young adults Age older than JACI 2011;128:1031 Zee, 10 years and a specific IgE Kaplan-Meier survival curves lowest tertile (≥5.6 kU/L) for level above the Kaplan-Meier survival curves were associated with for 3 age groups. children in tertiles of specific IgE. reactions to lower doses.
    • The eliciting dose of peanut in double-blind, placebocontrolled food challenges decreases with increasing age and specific IgE level in children and young adults Zee, JACI 2011;128:1031 This finding may explain why adolescents experience Kaplan-Meier survival curves severe allergic reactions in daily life to curves for Kaplan-Meier survival peanut for 3 age groups. children in tertiles of specific IgE. more often than do younger children.
    • Outcomes of office-based, open food challenges in themanagement of food allergy. Lieberman, JACI 2011;128:1120 Open oral food challenges (OFCs) performed at % of (+) challenge outpatient practice. 25 – Patients were typically 20 – not referred if the likelihood of a positive reaction 15 – 18.8% was thought to be >50%. 10 – sIgE levels and/or SPT. 05 – A total of 701 open OFCs in 521 different patients. 0
    • Outcomes of office-based, open food challenges in themanagement of food allergy. Lieberman, JACI 2011;128:1120 Open oral food challenges All but 1 reaction (OFCs) performed the was managed in at % of (+) challenge outpatient practice. office setting; 25 – Patients weretransferred1 patient was typically 20 – not referred if the to the emergency likelihood of a department positive reaction and 15 – 18.8% for monitoring was thought to be >50%. intravenous fluids due 10 – to persistent vomiting sIgE levels and/or SPT. 05 – following a challenge A totalto peanut. OFCs of 701 open in 521 different patients. 0
    • Outcomes of office-based, open food challenges in the management of food allergy. Lieberman, JACI 2011;128:1120• Patients who passed the OFC without adverse symptoms had significantly smaller SPT wheal size (median=3.00 mm vs 4.00 mm, p=0.0001) and significantly lower sIgE levels to the challenged foods (median=0.63 kUA/L vs 1.06 kUA/L, p=0.027) as compared with the group that had a reaction during the OFC.• Patients who had an identifiable history of anaphylaxis to the challenged food were more likely to have a reaction during the OFC (38.5%) than those who did not have a history of anaphylaxis (18.6%).• Patients who had never actually ingested the challenged food but were avoiding it because of evidence of sensitization were less likely to have a reaction during the OFC (14.0%) as compared with those patients who had previously ingested the challenged food and had a reaction (23.8%), p=0.0013.
    • Outcomes of office-based, open food challenges in the management of food allergy. Lieberman, JACI 2011;128:1120 % of reactions100 –080 – 87.9%060 – 56.8%040 –020 – 9% 5% 1.5% 00 Involving Antihistamine epinephrine prednisolone albuterol the skin alone TREATED WITH
    • Outcomes of office-based, open food challenges in the management of food allergy. Lieberman, JACI 2011;128:1120• Given the median specific IgE levels and the skin test results, the majority of these patients were at relatively ‘‘low risk’’ for reaction.• It is this exact population for which the risk-to-benefit ratio is optimal for performing an OFC.• A previous report of open OFC by Perry et al (JACI2004;114:1164) in a higher-risk population (ie, individuals with higher median specific IgE levels) demonstrated an OFC reaction rate of 43% which is higher than may be desirable for a busy office practice.
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285The diagnosis of food allergy is based mainly on oral food challenge (OFC).Anaphylaxis represents the most serious outcome of OFC.Anaphylaxis has been proposed to be highly likely when exposure to known allergens elicits a 30% or greater decrease in systolic blood pressure (SBP) or a low SBP for age either isolated or accompanied by gastrointestinal, skin, or respiratory symptoms.
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 80 children % Patients with: (18 months to 16 years). 40 – Not antihistamines for 7 days and corticosteroids, 30 – 32% theophylline, leukotriene (26/80) modifiers, or 20 – chromoglycates for 24 h. 10 – 13.75% Increasing doses of food 1.25% (egg, milk, wheat, soy). 0 Skin Gastro Bronchospasm, Brachial blood pressures symptoms intestinal wheezing, were measured. reactions and coughing
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 80 children % Patients with: (18 months to 16 years). 40 – 3 of the 26 children Not antihistamines for with positive OFC results had 7 days and corticosteroids, 30 – 32% symptoms consistent theophylline, leukotriene (26/80) with anaphylaxis modifiers, or 20 – chromoglycates for 24 h. 10 – 13.75% Increasing doses of food 1.25% (egg, milk, wheat, soy). 0 Skin Gastro Bronchospasm, Brachial blood pressures symptoms intestinal wheezing, were measured. reactions and coughing
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 Percentage of systolic blood pressure decrease in children with positive or negative oral food challenge results SBP Positive oral Negative oral food challenge food challenge (n=26) (n=54)
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 Percentage of systolic blood pressure decrease in children with positive or negative oral food challenge results SBP children who had anaphylaxis Positive oral Negative oral food challenge food challenge (n=26) (n=54)
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 Percentage of systolic blood pressure decrease in children Among reactive children, a SBP decrease with positive or negative oral food challenge results greater than 30% was measured in 1 child when anaphylactic symptoms occurred. SBP children who had anaphylaxis Positive oral Negative oral food challenge food challenge (n=26) (n=54)
    • Blood pressure monitoring in children undergoing food challenge: association with anaphylaxis Caffarelli, Ann Allergy Asthma Immunol 2012;108:285 Percentage of systolic blood pressure decrease in children with positive or negative oral not associated Decreased SBP was food challenge results with the outcomes of OFCs. SBP children who had anaphylaxis Positive oral Negative oral food challenge food challenge (n=26) (n=54)
    • Thermographic imaging during nasal peanut challenge may be useful in the diagnosis of peanut allergy. Clark, Allergy 2012;67:574Background: Double-blinded challenges are widely used for diagnosingfood allergy but are time-consuming and cause severe reactions.Outcome relies on subjective interpretation of symptoms, which leadsto variations in outcome between observers.Facial thermography combined with nasal peanut challenge wasevaluated as a novel objective indicator of clinical allergy.
    • Thermographic imaging during nasal peanut challenge may be useful in the diagnosis of peanut allergy. Clark, Allergy 2012;67:574 Change in mean nasal temperature from baseline (Δt) over time (min) for placebo and active peanut nasal challenge arms. 16 children with positive peanut challenge. Nasal challenge with 10 μg peanut protein or placebo. Mean skin temperatures recorded from the mouth & nose using infrared thermography over 18 min.
    • Thermographic imaging during nasal peanut challenge may be useful in the diagnosis of peanut allergy. Clark, Allergy 2012;67:574 Change in mean nasal temperature from baseline (Δt) over time (min) for placebo and active peanut The area under curve nasal challenge arms. of nasal skin temperature 16 children with elevated was significantly positive peanut peanut vs placebo after challenge. (18.2 vs 4.8°Cmin). Nasal maximum increase μg The challenge with 10 peanut protein or placebo. in temperature was also significantly greater Mean aftertemperatures skin peanut: recorded from +0.9°C. mean difference the mouth & nose using infrared thermography over 18 min.
    • Thermographic imaging during nasal peanut challenge may be useful in the diagnosis of peanut allergy. Clark, Allergy 2012;67:574 Change in mean nasal temperature from baseline Thermography (Δt) over time (min) for placebo and active peanut can detect inflammation nasal challenge arms. caused by nasal challenges 16 children with positive whilst employing 1000-fold peanutpeanut than an oral less challenge. challenge. Nasal challenge with 10 μg This novel technique could peanut protein or placebo. be developed to provide a rapid, safe Mean skin temperatures recorded from clinical and objective allergy test. the mouth & nose using infrared thermography over 18 min.
    • Effect of roasting on the allergenicity of major peanut allergens Ara h 1 and Ara h 2/6: the necessity of degranulation assays. Vissers CEA 2011;41:1631 Background Peanuts are often consumed after roasting, a process that alters the three-dimensional structure of allergens and leads to Maillard modification. Such changes are likely to affect their allergenicity. Objective We aimed to establish the effect of thermal treatment mimicking the roasting process on the allergenicity of Ara h 1 and a mix of 2S albumins from peanut (Ara h 2/6).
    • Effect of roasting on the allergenicity of major peanut allergens Ara h 1 and Ara h 2/6: the necessity of degranulation assays. Vissers CEA 2011;41:1631 Conclusions and Clinical Relevance Extensive heating: 1) reduced the degranulation capacity of Ara h 2/6 but 2) significantly increased the degranulation capacity of Ara h 1. This observation can have important ramifications for component-resolved approaches for diagnosis.
    • Small-bowel capsule endoscopy in patients with gastrointestinal food allergy. Hagel, Allergy 2012;67:286Background: Food allergy may presentwith a plethora of gastrointestinaland extraintestinal symptoms such asabdominal pain, diarrhea, cardiocirculatory symptoms,cutaneous reactions, or rhinitis.Macropathological lesions like lymphofollicular hyperplasiaand erosive or ulcerative lesions have seldom beendescribed in gastroscopy and colonoscopy previously.
    • Small-bowel capsule endoscopy in patients with gastrointestinal food allergy. Hagel, Allergy 2012;67:286 % of patients with 100 – 90 – 15 patients presenting with 80 – unspecific abdominal symptoms 70 – in which food allergy was 60 – detected. 50 – 40 – Indications for small-bowel 30 – capsule endoscopy: - weight loss; 20 – 28.6% 10 – - anemia. 4/15 0 Erosive lesions such as aphtoid lesions, erosions and petechiae.
    • Small-bowel capsule endoscopy in patients with gastrointestinal food allergy. Hagel, Allergy 2012;67:286 % of patients with 100 – 90 – 15 patients presenting with 80 – unspecific abdominal symptoms Anemia improved 70 – in which food allergy was 60 – within 1 yr detected. 50 – after adequate 40 – Indications for small-bowel antiallergic 30 – capsule endoscopy: treatment. - weight loss; 20 – 28.6% 10 – - anemia. 4/15 0 Erosive lesions such as aphtoid lesions, erosions and petechiae.
    • Small-bowel capsule endoscopy in patients with gastrointestinal food allergy. Hagel, Allergy 2012;67:286 % of patients with 100 – 90 – 15 patients presenting with 80 – unspecific abdominal symptoms 70 – in which food allergy was 60 – detected. 50 – 40 – 57.1% Indications for small-bowel 8/15 30 – capsule endoscopy: 20 – - weight loss; 10 – - anemia. 0 Nonerosive lesions such as erythema, swelling, lymphoid hyperplasia.
    • Small-bowel capsule endoscopy in patients with gastrointestinal food allergy. Hagel, Allergy 2012;67:286 % of patients with 100 – 90 – Lymphoid 15 patients presenting with 80 – hyperplasia unspecific abdominal symptoms 70 – was the most in which food allergy was 60 – detected. prominent finding in 50 – 57.1% 7 patients (50%), Indications for small-bowel 40 – 30 – 8/15 albeit capsule endoscopy: 20 – - weight loss; disease infectious 10 – - anemia. had been 0 excluded. Nonerosive lesions such as erythema, swelling, lymphoid hyperplasia.
    • • Food allergy pathogenesis
    • Cutaneous lymphocyte antigen and α4β7 T-lymphocyte responses are associated with peanut allergy and tolerance in children. Chan, Allergy 2012;67:336Background: It is unclear whether the initial route of allergenexposure in early life could influence the subsequent developmentof allergy, with cutaneous sensitization leading to peanut allergy,and tolerance induced by oral exposure.The skin- and gastrointestinal (GI)-homing markers, cutaneouslymphocyte antigen (CLA) (skin) and α4β7 integrin(gastrointestinal), are used to determine whether the state ofpeanut allergy correlates with peanut-specific CLA responses, withtolerance associated with predominant α4β7 responses.
    • Cutaneous lymphocyte antigen and α4β7 T-lymphocyte responses are associated with peanut allergy and tolerance in children. Chan, Allergy 2012;67:336 Stimulation indices to increasing peanut antigen concentration in the CLA+ & α4β7+ subsets of peanut allergic&non-allergic participants. Proliferation of CLA+ and α4β7+ memory T-cells isolated and cultured with peanut extract. p=0.008 Stimulation indices compared in peanut allergic & non-allergic (NA) groups.
    • Cutaneous lymphocyte antigen and α4β7 T-lymphocyte responses are associated with peanut allergy and tolerance in children. Chan, Allergy 2012;67:336 Stimulation indices to increasing peanut antigen concentration in the CLA+ & α4β7+ subsets of The predominance of peanut allergic&non-allergic participants. Proliferation+ of CLA+ the CLA response andto peanut in peanut α4β7+ memory T-cells isolated and allergic patients cultured with peanut is consistent with extract. the hypothesis that p=0.008 Stimulationsensitization allergic indices occurs through compared in peanut the skin. allergic & non-allergic (NA) groups.
    • Cutaneous lymphocyte antigen and α4β7 T-lymphocyte responses are associated with peanut allergy and tolerance in children. Chan, Allergy 2012;67:336 Stimulation indices to increasing peanut antigen concentration in the CLA+ & α4β7+ subsets of peanut allergic&non-allergic participants. The predominant α4β7 Proliferation of CLA+ + and response in peanut α4β7+ memory tolerant groups T-cells isolated and suggests that allergen cultured with peanut exposure through the extract. p=0.008 GI tract induces Stimulation indices tolerance. compared in peanut allergic & non-allergic (NA) groups.
    • T cell activation genes differentially expressed at birth in - CD4+ T cells from children who develop IgE food allergy - Martino, Allergy 2012;67:191 T-cell gene expression in longitudinal samples collected at At birth, birth and at 1 yr of age. the allergic group showed a reduced n°of genes Children with (n=30) upregulated in response to & without (n=30) IgE-mediated food allergy. anti–CD3 treatment on the microarray A low-level soluble anti-CD3 and a reduced stimulus to activate lymphoproliferative the T-cell receptor (TCR) capacity, suggesting and surveyed gene expression by DNA microarray clear differences in purified CD4+ T-cells. in T-cell signalling pathways.
    • T cell activation genes differentially expressed at birth in - CD4+ T cells from children who develop IgE food allergy - Martino, Allergy 2012;67:191 Although transient, T-cell gene expression in longitudinal samples collected at suboptimal neonatal At birth, birth andactivationage. T-cell at 1 yr of pathways the allergic group showed that signal through a reduced n°of genes Children with (n=30) the NF-kB complex upregulated in response to & without (n=30) may affect the IgE-mediated food allergy. anti–CD3 treatment developmental transition on the microarray of T-cell phenotypes A low-level soluble anti-CD3 and a reduced in the periphery stimulus to activate lymphoproliferative shortly after birth the T-cell receptor (TCR) capacity, suggesting and may increase and surveyed gene expression by DNA microarray of clear differences the risk in purified CD4+ T-cells. food allergy. in T-cell signalling pathways.
    • Svezzamento
    • Early complementary feeding and risk of foodsensitization in a birth cohort. Joseph JACI 2011;127:1203 % Infant exposure to complementary food <4 months Introduction of complementary food 40 – <4 months. IgE to 30 – 39.7% egg, milk, and 20 – peanut allergen at 2 yrs. 10 – 594 maternal-infant 00 pairs.
    • Early complementary feeding and risk of foodsensitization in a birth cohort. Joseph JACI 2011;127:1203 % children with sIgE ≥0.35 IU/mL at age 2 yrs 35 – Introduction of 30 – complementary food 30.6% 25 – <4 months. 20 – 23.9% IgE to 15 – egg, milk, and 10 – peanut allergen at 2 11.4% yrs. 05 – 00 594 maternal-infant Egg Milk Peanut pairs.
    • Early complementary feeding and risk of foodsensitization in a birth cohort. Joseph JACI 2011;127:1203 % children with sIgE ≥0.35 IU/mL at age 2 yrs 35 – Introduction of Early feeding reduced 30 – complementary food 30.6% the risk of peanut 25 – <4 months. sensitization among 20 – 23.9%children with a parental IgE to 15 – history egg, milk, and peanut allergen at0.2; (adjusted OR= 2 10 – 11.4% yrs. P = 0.007 ) 05 – 00 594 maternal-infant Egg Milk Peanut pairs.
    • Early complementary feeding and risk of foodsensitization in a birth cohort. Joseph JACI 2011;127:1203 % children with sIgE ≥0.35 IU/mL at age 2 yrs 35 – Introduction of 30 – The association food complementary between 25 – 30.6% <4 months. early feeding and sensitization was modified 20 – 23.9% IgE to egg,parental history of by milk, and 15 – asthma or allergy. peanut allergen at 2 10 – 11.4% yrs. 05 – 00 594 maternal-infant Egg Milk Peanut pairs.
    • The introduction of allergenic foods and the development of reported wheezing and eczema in childhood Tromp APAM 2011;165:933 % children wheezing 605 preschool children. 40 – Timing of introduction 30 – of cow’s milk, hen’s 31% egg, peanuts, tree 20 – nuts, soy, and gluten collected by questionnaires at 6 and 10 – 14% 12 months of age. 0 2 yrs 3-4 yrs
    • The introduction of allergenic foods and the development of reported wheezing and eczema in childhood Tromp APAM 2011;165:933 % children with eczema 605 preschool children. 40 – Timing of introduction 30 – 38% of cow’s milk, hen’s egg, peanuts, tree nuts, soy, 20 – and gluten collected by questionnaires at 6 and 10 – 20% 18% 12 months of age. 18% 0 2 3 4 age (years)
    • The introduction of allergenic foods and the development of reported wheezing and eczema in childhood Tromp APAM 2011;165:933 % children with eczema 605 preschool children. 40 – Timing of introduction 30 – 38% of cow’s milk, hen’s egg, peanuts, tree nuts, soy, 20 – and gluten collected by questionnaires at 6 and 10 – 20% 18% 12 months of age. 18% 0 2 3 4 age (years)
    • The introduction of allergenic foods and the development of reported wheezing and eczema in childhood Tromp APAM 2011;165:933 with cow’s milk introduction ≤6 mo OR for eczema at age 1.0 – 605 preschool children. 0.95 Timing of introduction 0.91 0.88 of cow’s milk, hen’s egg, peanuts, tree nuts, soy, 0.5 – and gluten collected by questionnaires at 6 and 12 months of age. 0.0 2 yrs 3 yrs 4 yrs
    • Effect of a partially hydrolyzed whey infant formulaat weaning risk of allergic disease in high-risk children: a randomized controlled trial Lowe JACI 2011;128:360BackgroundPartially hydrolyzed whey formula (pHWF)has been recommended for infants with a family historyof allergic disease at the cessation of exclusive breast-feedingto promote oral tolerance and prevent allergic disease.ObjectivesTo determine whether feeding infants pHWFreduces their risk of allergic disease.
    • Effect of a partially hydrolyzed whey infant formulaat weaning risk of allergic disease in high-risk children: a randomized controlled trial Lowe JACI 2011;128:360 To compare a conventional cow’s milk formula, a pHWF, or a soy formula. There was no evidence 620 infants with a family that infants allocated history of allergic disease to the pHWF were recruited and randomized or the soy formula to receive the allocated were at lower risk formula at cessation of breast-feeding. of allergic manifestations in infancy compared with Follow-up at 2 yrs, at 6 or 7 conventional formula. yrs.
    • Effect of a partially hydrolyzed whey infant formulaat weaning risk of allergic disease in high-risk children: a randomized controlled trial Lowe JACI 2011;128:360 To compare a conventional cow’s milk formula, ano evidence We found pHWF, support recommending to or a soy formula. There was no evidence the use of pHWF 620 infants with a family that infants allocated history of allergic disease the at weaning for to the pHWF were recruited and randomized prevention of allergic or the soy formula to receive the allocated were at lower risk disease in formula at cessation high-risk infants. of breast-feeding. of allergic manifestations in infancy compared with Follow-up at 2 yrs, at 6 or 7 conventional formula. yrs.
    • Soybean isoflavones regulate dendritic cell function and suppress allergic sensitization to peanut Masilamani, JACI 2011;128:1242Background:Although peanut and soybean proteins share extensiveamino acid sequence homology, the incidence and severity ofallergic reactions to soy are much less than those to peanut.Soybeans are rich in anti-inflammatory isoflavones andare the most common source of isoflavones in the human food supply.Objective:We hypothesized that the active isoflavones in the gut milieuare capable of modulating immune responses to dietary antigensby regulating dendritic cell (DC) function.
    • Soybean isoflavones regulate dendritic cell function and suppress allergic sensitization to peanut Masilamani, JACI 2011;128:1242 Sensitized and challenged with peanut Fed a diet fed containing a soy-free genistein dietand daidzein• Dietary isoflavones significantly reduced the anaphylactic symptoms and mast cell degranulation in vivo after peanut challenge.• Serum peanut-specific antibodies were markedly reduced in mice fed the isoflavone diet.
    • Soybean isoflavones regulate dendritic cell function and suppress allergic sensitization to peanut Masilamani, JACI 2011;128:1242 Activated with cholera toxin in the presence of isoflavonesHuman monocyte-derived dendritic cells Isoflavones inhibited cholera toxin–induced DC maturation and subsequent DC-mediated CD4+ T-cell function in vitro.
    • Soybean isoflavones regulate dendritic cell function and suppress allergic sensitization to peanut Masilamani, JACI 2011;128:1242 Chemical structure of the soybean isoflavones:• Isoflavones belong to a class of molecules related to flavonoids.• Soybeans are the most common source of isoflavones in the human diet.• Isoflavones, such as genistein, daidzein, and glycitein, have been shown to have anti-inflammatory and antioxidant properties. Barnes, Lymphat Res Biol 2010;8:89
    • Soybean isoflavones regulate dendritic cell function and suppress allergic sensitization to peanut Masilamani, JACI 2011;128:1242• The immune-regulatory effects of isoflavones, specifically genistein, have been extensively investigated. Sakai, J Med Invest 2008;55:167• The high intake of soy-containing foods and isoflavones is associated with reduced prevalence of allergic rhinitis and better lung function in asthmatic patients. Miyake, J Allergy Clin Immunol 2005;115:1176 Smith, J Asthma 2004;41:833• Dietary soy supplementation reduced: - antigen-induced eosinophilia in the lungs in a pig model of asthma; - eosinophil leukotriene C4 synthesis and eosinophilic airway inflammation ii in asthmatic patients. Regal, Proc Soc Exp Biol Med 2000;223:372 Kalhan, Clin Exp Allergy 2008;38:103
    • Take home
    • Take home
    • • Food allergy burden
    • Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets Ball Pediat Allergy Immunol 2011;22:808 In children allergic to peanut The challenge food was % reacting to treanut challenge 35 – administered by way of 30 – a homemade biscuit containing 8 g of each 25 – 31.2% nut given in increasing 20 – visually measured doses. 15 – 10 – 145 children peanut allergic or tree nut 05 – allergic. 00 0% (-) (+) Treanut SPTs
    • Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets Ball Pediat Allergy Immunol 2011;22:808 In children allergic to peanut The challenge food was % reacting to treanut challenge 35 – Children allergic administered by way of 30 – to peanuts with a homemade biscuit 31.2% containing 8 g of each negative allergy 25 – nut given in increasing tests to tree 20 – visually measured doses. nuts had no 15 – co-existing 145 children peanut 10 – allergy. allergic or tree nut 05 – 0% allergic. 00 (-) (+) Treanut SPTs
    • Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets Ball Pediat Allergy Immunol 2011;22:808 In children allergic to treanut The challenge food was % reacting to peanut challenge 40 – administered by way of 38.4% 35 – a homemade biscuit 30 – containing 8 g of each 25 – nut given in increasing 20 – visually measured doses. 15 – 145 children peanut 10 – allergic or tree nut allergic. 05 – 00 7.9% (-) (+) Peanut SPTs
    • Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets Ball Pediat Allergy Immunol 2011;22:808 In children allergic to treanut Children with tree The challenge food was % reacting to peanut challenge 40 – administered by were nut allergy way of 38.4% 35 – a homemade biscuit at risk of 30 – containing 8 g of each co-existing peanut nut given in increasing 25 – or other tree nut visually measured doses. 20 – allergy whether 15 – 145 children peanut SPTs were positive 10 – allergic or tree nut or negative. allergic. 05 – 00 7.9% (-) (+) Peanut SPTs
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720 % parents unable to correctly recall the dietary advice 30 – 94 children with 25 – seafood allergy. 20 – 15 – 25% Postal questionnaire 10 – 05 – 0
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720 % parents using a safe diet 90 – 89% 80 – 94 children with 70 – seafood allergy. 60 – 50 – 40 – Postal questionnaire 30 – 20 – 10 – 0
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720 % parents using a safe diet 90 – But over half 89% 80 – 94 children with more followed a 70 – seafood allergy. 60 – stringent 50 – elimination than 40 – Postal questionnaire that 30 – recommended. 20 – 10 – 0
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720Seafood triggers identified Size of skin prick test (SPT) wheal in relation to reaction severity
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720 Schema demonstrating study population and degree of cross-reactivity between crustacean, mollusc and fish. 94 children with seafood allergy. Postal questionnaire
    • Parental perceptions and dietary adherence in children with seafood allergy Ng Pediat Allergy Immunol 2011;22:720 A common scenario for the parents of crustacean-allergic children (who have previously tolerated finned fish) is to exclude all seafood and fish from the child’s diet, even though the child has no evidence of sensitization to non-crustacea and had previously tolerated finned fish. In view of our experience lack of reactions which can be accounted to ‘traces’ in the context of seafood allergy, avoidance of foods labelled ‘may contain traces’ has not been our universal recommendation with commercially produced foods of Australian origin. Is theoretically possible that overadherence may result in the development of sensitization owing to the avoidance of a previously tolerated allergen in an atopic child.
    • Parents report better health-related quality of life for their food-allergic children than children themselves van der Velde CEA 2011;41:1431 To compare child- and parent-proxy reports on FAQLQ score HRQL in food-allergic 4.0 – children (8–12 years). 3.0 – 3.74 Food Allergy Quality of Life Questionnaire-Child Form (FAQLQ-CF), and 2.0 – 2.68 Parent Form (FAQLQ-PF). 1.0 – Where 1 indicates no impairment and 7 indicates 0 0 extreme impairment) Child Parents
    • Parents report better health-related quality of life for their food-allergic children than children themselves van der Velde CEA 2011;41:1431 To compare child- and parent-proxy reports on FAQLQ score Parents reported HRQL in food-allergic 4.0 – significantly less children (8–12 years). impact of food 3.0 – 3.74 Food Allergy Quality of Lifeallergy on the Questionnaire-Child 2.0 – 2.68 childs HRQL than Form (FAQLQ-CF), and children Parent Form (FAQLQ-PF). 1.0 – themselves. Where 1 indicates no impairment and 7 indicates 0 0 extreme impairment) Child Parents
    • Inadvertent exposures in children with peanut allergy Nguyen-Luu, Pediatr Allergy Immunol 2012;23:133 % children with accidental exposures 1411 children mean age 15 – 7.1 yr parents of children with a physician-confirmed 10 – 12.5% peanut allergy questionnaires about accidental exposures 05 – over the preceding year 0
    • Inadvertent exposures in children with peanut allergy Nguyen-Luu, Pediatr Allergy Immunol 2012;23:133 OR for accidental exposure 1411 children mean age 03 – 7.1 yr parents of children with 2.33 a physician-confirmed peanut allergy 02 – 2.04 questionnaires about 01 – accidental exposures over the preceding year 0.88 0 severe increasing Age ≥13 yr previous reaction disease duration to peanut
    • Inadvertent exposures in children with peanut allergy Nguyen-Luu, Pediatr Allergy Immunol 2012;23:133 OR for accidental exposure 1411 children mean age 03 – 7.1 yr Children with a parents of children with 2.33 recent diagnosis and a physician-confirmed peanut allergyare at 02 – 2.04 adolescents higher risk questionnaires about 01 – accidental exposures over the preceding year 0.88 0 severe increasing Age ≥13 yr previous reaction disease duration to peanut
    • Inadvertent exposures in children with peanut allergy Nguyen-Luu, Pediatr Allergy Immunol 2012;23:133 Annual incidence rate of accidental exposure stratified by disease duration 1411 children mean age 7.1 yr parents of children with a physician-confirmed peanut allergy questionnaires about accidental exposures over the preceding year
    • Restaurant staffs knowledge of anaphylaxis and dietary care of people with allergies Bailey CEA 2011;41:713 Telephone 100 – % staff member reporting questionnaire to 90 – a member of staff at 90 table-service 80 – 70 – 90% restaurants in 60 – Brighton. 50 – 40 – 30 – 20 – 33% 10 – 0 Food hygiene Specific food training allergy training.
    • Restaurant staffs knowledge of anaphylaxis and dietary care of people with allergies Bailey CEA 2011;41:713 % staff members believing Telephone 40 – questionnaire to a member of staff 38% 30 – at 90 table-service restaurants in Brighton. 20 – 23% 10 – 16% 00 An individual Consuming a Cooking food experiencing a small amount prevents it reaction should of an allergen causing allergy drink water to is safe dilute the allergen
    • The high prevalence of peanut sensitization in childhood is due to cross-reactivity to pollen Niggemann, Allergy 2011;66:979 Point prevalence of sensitization to peanut in general and to peanut without birch and/or grass 13 100 children aged 3-17 years. Specific IgE concentrations to common aeroallergens and foods;
    • The high prevalence of peanut sensitization in childhood is due to cross-reactivity to pollen Niggemann, Allergy 2011;66:979 Point prevalence of sensitization to peanut in general and to peanut Our data indicate without birch and/or grass that the high Specific IgE sensitization of concentrationspeanut 10.9 % to to common aeroallergens and is predominantly foods;due to cross- reactivity to 13 100 children aged 3- pollen irrespective 17 years. age of the of the children
    • The high prevalence of peanut sensitization in childhood is due to cross-reactivity to pollen Niggemann, Allergy 2011;66:979 Point prevalence of sensitization to peanut in general and to peanut The observed without birch and/or grass high peanut Specific IgE sensitization concentrations to therefore does common aeroallergens and not indicate a foods; high risk for the development of 13 100 children aged 3- primary allergy 17 years. to peanut
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk  Immediate IgE-mediated allergic reactions to corticosteroids are rather uncommon, whereas causative agents usually involve the native steroid molecule or a pharmaceutical excipient, in most cases as succinate ester bound to methyl-prednisolone or hydrocortisone;  We here report two cases of immediate reaction to methyl-prednisolone, attributed to milk allergen contamination.
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk 1) A 9 yrs old boy with severe persistent cow’s milk allergy (CMA) was seen for asthma exacerbation; 2) The boy was administered 40 mg of methyl-prednisolone by intravenous injection; 3) Paradoxically, wheezing deteriorated; 4) The boy was given another course of the same medication on assumption of clinical under-responsiveness; 5) Within a few minutes the patient acutely collapsed.
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk a) Another patient, a 7-year-old boy with severe CMA was similarly treated with intravenous administration of 40 mg methyl-prednisolone; b) The therapeutic intervention resulted in a full-blown anaphylactic reaction; c) Both children were evaluated within the next 6 months for assumed IgE-mediated reactivity to methyl-prednisolone.
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk Skin testing results in both patients with acute reaction to lactose-containing succinylated methyl-prednisolone
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk Sensitization to theresultssteroid molecule andwith acute Skin testing native in both patients to the succinate reaction to lactose-containing succinylated ester was ruled out by negative skin tests, while both patients exhibited positive skin response exclusively to lactose-containing preparations. methyl-prednisolone
    • Cow’s milk allergy as a cause of anaphylaxis to systemic corticosteroids Savvatianos, Siragakis, Allergy 2011;66:983 milk Subsequent drug provocation tests were negative in both patients Skin a full therapeuticboth patients with acute reaction for testing results in dose (125 mg) of non-lactose to lactose-containing succinylated methyl-prednisolone containing, otherwise identical to the one that elicited the reaction, succinylated methyl-prednisolone preparation (Solu-Medrol 125 mg, Pfizer)
    • Hypersensitivity to total parenteral nutrition fat-emulsion component in an egg-allergic child Lunn Pediatrics 2011;128:e1025 Intravenous fat emulsions (IFEs) are a vital component of total parental nutrition, because they provide essential fatty acids. IFE is a sterile fat emulsion that contains egg-yolk phospholipids. Although egg allergy is listed as a contraindication, adverse reactions are uncommon.
    • Hypersensitivity to total parenteral nutrition fat-emulsion component in an egg-allergic child Lunn Pediatrics 2011;128:e1025 2-year-old patient with previously undocumented egg allergy. Placed on total parental nutrition and a 20% IFE postoperatively and developed diffuse pruritus 14 days after initiation of therapy.
    • Hypersensitivity to total parenteral nutrition fat-emulsion component in an egg-allergic child Lunn Pediatrics 2011;128:e1025 2-year-old patient with previously undocumented egg allergy. Placed on total parental nutrition and a 20% IFE postoperatively and developed diffuse pruritus 14 days after initiation of therapy. She showed transient improvement with intravenous antihistamine, but her symptoms did not resolve until the IFE was stopped.
    • Hypersensitivity to total parenteral nutrition fat-emulsion component in an egg-allergic child Lunn Pediatrics 2011;128:e1025 2-year-old patient with previously undocumented egg allergy. Placed on total parental nutrition and a 20% IFE postoperatively and developed diffuse pruritus 14 days after initiation of therapy. She showed transient improvement with intravenous antihistamine, but her symptoms did not resolve until the IFE was stopped. On the basis of clinical history, including aversion to egg, we performed skin-prick testing, the results of which were positive for egg white allergy.
    • Hypersensitivity to total parenteral nutrition fat-emulsion component in an egg-allergic child Lunn Pediatrics 2011;128:e1025 2-year-old patient with previously undocumented egg allergy. Placed on total parental nutrition and a 20% IFE postoperatively Although ingestion of egg lecithin and developed diffuse pruritus 14 days after initiation of in cooked food therapy. is generally tolerated by egg-allergic people, She showed transient improvement with intravenous administration of antihistamine, but her symptoms did not resolve until the IFE intravenous egg-containing lipid was stopped. On the basis of clinical may cause significant egg, emulsions history, including aversion to adverse reactions. we performed skin-prick testing, the results of which were positive for egg white allergy.
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 1) Carrot (Daucus carota) allergy is one of the most common types of birch pollen-related food allergy in central Europe. 2) Approximately 24% of food allergic subjects suffer from allergic symptoms after ingestion of carrots. 3) Adverse reactions to carrots are elicited due to cross-reactive IgE-epitopes between the major birch pollen allergen, Bet v 1 and homologous food proteins. 4) Bet v 1 and the major carrot allergen Dau c 1 belong to the family of pathogenesis related proteins 10 (PR-10).
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 •The Dau c PRPlike proteinObjective To investigate was identified as a newpotential allergenic properties allergenic isoform, Dau cof a Dau c PRPlike protein, 1.03, in carrot roots.a novel isoform of thepathogenesis related proteins •68% of carrot allergic10 (PR-10) protein family in patients were sensitized tocarrot. rDau c 1.03.
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 Dau c 1.03 appears •The Dau c PRPlike protein to contribute to the was identified as a newObjective To investigate allergenicity allergenic isoform, Dau cpotential carrots and should of allergenic properties 1.03, in carrot roots.of a Dau cbe considered PRPlike protein,a novel isoform ofsilencing for gene the PR-10 •68% of carrot allergicprotein family in carrot. of carrot allergens. patients were sensitized to rDau c 1.03.
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643BackgroundTomatoes (Solanum lycopersicum) are consumed worldwide andtheir amount of consumption is associated with the prevalenceof tomato allergy. Therefore, identification of tomato cultivarswith reduced allergenicity would potentially increase the qualityof life of affected subjects.ObjectiveIn this study, we examined the allergenic and biological activityof two different tomato cultivars in tomato allergic subjects.
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 SPT reactions to ‘Reisetomate’ (RT) and ‘Matina’ (MT). The median is depicted as 25 subjects with black line, and outliers are shown as dots. tomato allergy. A Skin prick test and DBPCFC to investigate the clinical differences between two tomato cultivars (‘Reisetomate’ and ‘Matina’).
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 Symptom severity expressed as sum scores, no clinical relevant allergy ×0, mild allergy ×1, 25 subjects with moderate allergy ×2 and severe allergy ×3. tomato allergy. B Skin prick test and DBPCFC to investigate the clinical differences between two tomato cultivars (‘Reisetomate’ and ‘Matina’).
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 Symptom severity expressed as sum scores, no clinical relevant allergy ×0, mild 25 subjects cultivars Tomato with allergy ×1, moderate allergy ×2 and severe allergy promote a distinct tomato allergy. ×3. clinical reactivity in B Skin tomato allergic prick test and DBPCFC to might be subjects. This investigate the due to instabilities of clinical differences physicochemical sensitive two tomato between proteins and/or cultivars different isoform (‘Reisetomate’ expression of allergens. and ‘Matina’).
    • •Labelling•identification
    • How do peanut and nut-allergic consumers use information on the packaging to avoid allergens? Barnett , Allergy 2011;66:969 1) Some participants used the ingredients list as their primary check for allergens, 32 participants were but most used the allergy recorded during their advice box. normal food shop; 2) Package-based information was generally Followed by a semi considered reliable, but some supermarket and brand structured interview; labels were trusted more than others. During the interview they 3) Food labels were used in were given 13 potentially conjunction with nonpacket- problematic packaged based strategies foods. (e.g. previous experience) to make choices.
    • The ability of adults and children to visually identify peanuts and tree nutsHostetler, Ann Allergy Asthma Immunol 2012;108:25 1, Cashew, without shell; 2, Hazelnut (filbert), in shell; 3, Pistachio, without shell; 4, Brazil nut, without shell; 5, Almond, slivered; 6, Pecan, in shell; 7, Walnut, crushed; 8, Peanut, without shell; 9, Pecan, crushed; 10, Pine nut (Pignolia), without shell; 11, Almond, without shell; 12, Peanut, in shell; 13, Macadamia nut, without shell; 14, Pistachio, in shell; 15, Brazil nut, in shell; 16, Pecan, without shell; 17, Walnut, in shell; 18, Hazelnut (filbert), without shell; 19, Walnut, without shell.
    • The ability of adults and children to visually identify peanuts and tree nuts Hostetler, Ann Allergy Asthma Immunol 2012;108:25 Percentage of peanuts and nuts correctly identified by item, form, and age group.A nut display.A total of 19 different forms.Persons ≥ 6 years completed a worksheet to name the items.
    • The ability of adults and children to visually identify peanuts and tree nuts Hostetler, Ann Allergy Asthma Immunol 2012;108:25 Distribution of the totalA nut display. number of correct responsesA total of 19 different forms.Persons ≥ 6 years completed a worksheet to name the items.
    • The ability of adults and children to visually identify peanuts and tree nuts Hostetler, Ann Allergy Asthma Immunol 2012;108:25 Distribution of the totalA nut display. Both number of correct responses children andA total of adults are 19 different unreliable forms. at visually identifyingPersons ≥ 6 years completed nuts. most a worksheet to name the items.
    • Take home
    • Chronic palpable purpura mediated by Kiwi antigen Act c 1-induced immune complex vasculitis Gutermuth, Allergy 2011;66:982 For 3 months, a 61 years old female developed recurrent palpable purpura with multiple erythematous and hyperpigmented papules and macules on the dorsum of the feet, lowerand upper legs. Multiple erythematous macules and papules on the lower extremities
    • Chronic palpable purpura mediated by Kiwi antigen Act c 1-induced immune complex vasculitis Gutermuth, Allergy 2011;66:982 Detailed history was taken concerning the circumstances under which new purpuric lesions occurred and the patient reported the ingestion of fruit salads preceding the active rashes; To verify or rule out foodstuff as elicitor of vasculitis, the patient was put on elimination diet and then orally challenged to 40 g of fresh fruits that she consumes regularly, including apple, banana, kiwi and pineapple; Six to ten hours after consumption of kiwi she reproducibly developed an itchy rash consisting of confluent 3–5 mm purpuric macules and papules on the legs, lower trunk and forearms with consecutive bleeding in the central part of the lesions.
    • Anaphylactic reactions caused by oil body fraction lipoproteins Pineda, Allergy 2011;66:7011) Allergies to olive fruit and derivative product have seldom been reported;2) Few cases of contact dermatitis and contact urticaria caused by olive oil or olives have been documented, and only three cases of allergy caused by olive ingestion have been described;3) Thaumatin-like protein and other proteins with a 10–15 kDa molecular mass are those described as allergenic in the patients with olive allergy.
    • Anaphylactic reactions caused by oil body fraction lipoproteins Pineda, Allergy 2011;66:7011) A 20-year-old man was admitted to our allergy unit for investigation into recurrent food-induced anaphylaxis;2) Skin prick test was positive for Platanus and Parietaria pollen and only positive for hazelnut, walnut, peach peel, sunflower seed, and mustard food extracts when testing the panel of plant food allergens;3) Further, SPTs were performed using home-made extract of liposoluble proteins from olives and prick to prick with olive. A wheal diameter of 13.9 and 10 mm was obtained from olive and liposoluble proteins from olive fruit respectively.
    • Anaphylactic reactions caused by oil body fraction lipoproteins Pineda, Allergy 2011;66:7011) The basophil activation test (BAT) was performed;2) The stimuli used were lipoproteins from olive;3) The test was positive for olive fruit (30,5%);4) The BAT was performed in parallel with two nonallergic individuals obtaining a negative result with the Basophil activation test (BAT) to oil body fraction proteins from stimuli tested. hazelnut, olive and sesame.
    • Food Proteins Induced Enterocolitis
    • Food protein–induced enterocolitis syndrome: an update on natural history and review of management Leonard Ann Allergy Asthma Immunol 2011;107:951) FPIES is a non–IgE-mediated gastrointestinal food hypersensitivity thought to be cell-mediated.2) In a recent birth cohort, the incidence of cows milk FPIES was 0.34% in the first year of life compared with 0.5% for IgE-mediated cows milk allergy.3) FPIES typically presents before 6 months of age in formula-fed infants with repetitive emesis, diarrhea, dehydration, and lethargy 1 to 5 hours after ingesting the offending food.4) Four cases of FPIES in breastfed infants have recently been reported.5) The most common offending foods are cows milk, soy, and rice.6) FPIES is usually outgrown by school age.
    • Eosinophilicesophagitiseosinophilic gastritis multiple rings associated with eosinophilic esophagitis
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477 Symptoms reported by pediatric & adult patients with eosinophilic esophagitis
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477 Endoscopic pictures illustrating the major endoscopic signs of eosinophilic esophagitis. All pictures are from adult patients. (A) represents an acute and severe inflamed esophagus. (B) Shows an acute but only moderate inflamed organ. White exudates, furrowing and edema with the loss of vascular visibility are the leading signs of inflammation.
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477 Endoscopic pictures illustrating the major endoscopic signs of eosinophilic esophagitis. All pictures are from adult patients. (C) & (D) illustrate signs associated with remodeling, such as fixed esophageal rings (=trachealization or corrugated rings) and crêpe-paper esophagus with deep laceration after minimal trauma.
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477 Biopsies from a child (A) and an adult (B) who have eosinophilic esophagitis show similar features. In each picture, black arrows point to numerous intraepithelial eosinophils in esophageal squamous epithelium. The asterisk rests on thickened collagen fibers.
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477 Simplified scheme on the immunopathogenesis of eosinophilic esophagitis (EoE) • EoE is believed to be triggered by aero- and food-allergens. • The epithelial cells (EC) of the esophagus that are activated by IL-13 actively contribute to the inflammatory process. • Dendritic cell (DC)-mediated Th2 differentiation. • Eotaxin-3 attracts eosinophils. • IL-9 activates mast-cells (MC). • IL-5 activates eosinophils. • Eos generates TGF-β, which stimulates fibroblasts (F) to produce extracellular matrix proteins.
    • Pediatric and adult eosinophilic esophagitis: similarities and differences. Straumann, Allergy 2012;67:477Distinction between pediatric and adult eosinophilic esophagitis (EoE)
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037Background:Recent research shows that both pediatric and adult patients witheosinophilic esophagitis (EoE) experience esophageal remodelingmarked by increased collagen deposition in which TGF-β playsan important role.However, limited data are available on the intensity and reversibilityof fibrous remodeling in adults with EoE.Objective:We sought to analyze differences in collagen deposition in thelamina propria (LP) and profibrogenic cytokine gene expression alongwith other changes induced by prolonged treatment withfluticasone propionate in adults with EoE.
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037 10 adults with EoE. Intraepithelial eosinophils: Deep esophageal biopsy Cells/mm2 before and after 1 yr 400 – of treatment with 308.0 p<0.001 fluticasone propionate. 300 – 400 µg of fluticasone propionate 200 – in a 2 mL volume to swallow 2/day 100 – after breakfast and 1.5 0 dinner and to avoid eating 00 Patients with Patients with Healthy or drinking in the EoE GERD subjects subsequent 3 h.
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037 Density of intraepithelial and lamina propria (LP) eosinophils in patients with EoE before and after treatment with fluticasone propionate compared with that seen in patients with GERD and healthy subjects.* p< 0.05 before and after treatment in patients with EoE. # p< 0.05 between patients with EoEbefore treatment and those with GERD. + p<0 .05 between patients with EoEbefore treatment and normal esophagi.
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037 Density of intraepithelial and lamina propria (LP) Prolonged eosinophils fluticasone propionate in patients with EoE treatment before and after treatment reversed intraepithelial with fluticasone propria and lamina propionate compared with infiltration eosinophilic that seen in patients with GERD and and downregulated healthy subjects. profibrogenic cytokine* p< 0.05 before and after treatment in patients with EoE. gene expression… # p< 0.05 between patients with EoEbefore treatment and those with GERD. + p<0 .05 between patients with EoEbefore treatment and normal esophagi.
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037 Mean fibrosis scores in healthy subjects, patients with GERD, and patients with EoE before and after 1 yr of topical treatment with fluticasone propionate.
    • Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study. Lucendo, JACI 2011;128:1037 Mean fibrosis scores in healthy subjects, patients with …However, no significant change in subepithelial collagen GERD, and patients withwas observed. deposition EoE before and after 1 yr of topical treatment with fluticasone propionate.
    • Tissue remodeling in patients with eosinophilic esophagitis: What lies beneath the surface? Editorial Aceves, JACI 2011;128:1047 Potentialpathogenesis and effects oftissue remodeling in patients with EoE.
    • Food allergy Diagnostic aspects Cross-ReactivityOral Allergy Syndrome
    • Secondary soy allergy in children with birch pollen allergy may cause both chronic and acute symptoms De Swert, Pediatr Allergy Immunol 2012;23:117 Children with birch •8 of them proved to be soy allergic (SA). pollen allergy •3/8 subjects also had been SPT with soy extract suffering from severe chronic and with soy flour complaints because of soy allergy. sIgE to Gly m4, Gly •SPT with commercial soy extract m5, and Gly m6 was negative in all SA and ST 15 subjects with birch subjects tested. pollen allergy and •SPT with soy flour was positive suspected of soy in 8/8 SA and in 5/6 ST allergy subjects, but negative in all 8 controls (p < 0.0001).
    • Secondary soy allergy in children with birch pollen allergy may cause both chronic and acute symptoms De Swert, Pediatr Allergy Immunol 2012;23:117 Children with birch •8 of them proved to be soy allergic (SA). pollenmedian IgE level The allergy to rGly m 4 using CAP •3/8 subjects also had been SPTand ISAC was, with soy extract suffering from severe chronic and with soy flour respectively, 32.4 complaints because of soy allergy. sIgE to Gly4.0 ISU in kU/l and m4, Gly •SPT with commercial soy extract SA subjects, m5, and Gly m6 was negative in all SA and ST compared to 6.2 kU/l 15and 0.4 ISU in ST subjects with birch subjects tested. pollen allergy and subjects (p<0.05) •SPT with soy flour was positive suspected of soy in 8/8 SA and in 5/6 ST allergy subjects, but negative in all 8 controls (p < 0.0001).
    • Secondary soy allergy in children with birch pollen allergy may cause both chronic and acute symptoms De Swert, Pediatr Allergy Immunol 2012;23:117 SPT with Children with birch •8 of them proved to be soy soy flour is a sensitive allergic (SA). pollen allergy tool in and specific detecting soy •3/8 subjects also had been SPT with soy extract suffering from severe chronic sensitization. and with soy flour CAP rGly m 4, and complaints because of soy allergy. sIgE to Gly m4, 4 are ISAC rGLY m Gly •SPT with commercial soy extract m5, valuable m6 in and Gly tools was negative in all SA and ST the diagnosis of 15 subjects with birch subjects tested. birch-pollen-associated pollen allergy and secondary •SPT with soy flour was positive suspected allergy soy of soy in 8/8 SA and in 5/6 ST subjects, allergy but negative in all 8 controls (p < 0.0001).
    • Correlation of anti-pru p 3 IgE levels with severity of peach allergy reactions in children Novembre, Ann Allergy Asthma Immunol 2012;108:271 Peach allergy is regarded as one of the most important fresh fruit allergies. Most patients allergic to peaches present with an associated pollen allergy and exhibit other food allergies, mainly to other Rosaceae species ( apples, apricots, plums..) but also to taxonomically unrelated vegetables. Data are available on the state-of-the-art diagnosis, including food challenges, and a component-resolved diagnosis. However, the roles played by different peach allergens with respect to symptom severity are not completely understood.
    • Correlation of anti-pru p 3 IgE levels with severity of peach allergy reactions in children Novembre, Ann Allergy Asthma Immunol 2012;108:271 Mean specific IgE levels to Pru p 3, Pru p 1, and Pru p 4 in patients with systemic symptoms (SS), patients with oral allergic syndrome (OAS), and controls (not shown). 44 children with peach allergy. 2 groups : mild oral allergy syndrome (OAS) and systemic symptoms (SS). Presence of specific IgE to peach and rPru p 1, rPru p 3, and rPru p 4.
    • Correlation of anti-pru p 3 IgE levels with severity of peach allergy reactions in children Novembre, Ann Allergy Asthma Immunol 2012;108:271 Mean specific IgE levels to Pru p 3, Pru p 1, and Pru p 4 in patients with systemic Only symptoms (SS), patients with oral allergic syndrome (OAS), and controls (not shown). 44anti-rPru p 4 children with peach allergy IgE levels 2 groupswere : mild oral allergy significantly syndrome (OAS) and higher in systemic symptoms (SS). patients with Presence of specific IgE OAS, p 1, to peach and rPru rPru p 3, and rPru p 4.
    • Pollen-food syndrome is related to Bet v 1/PR-10 protein sensitization, but not all patients have spring rhinitis Rashid, Allergy 2011;66:1391  The pollen-food syndrome (PFS) results from sensitisation to panallergens that are common to pollen and edible plant products, typically manifesting as oral symptoms upon exposure to Rosaceae fruits.  The panallergen molecules comprise three protein clusters: Bet v 1/PR-10; profilins; non-specific lipid transfer proteins (nsLTP).
    • Pollen-food syndrome is related to Bet v 1/PR-10 protein sensitization, but not all patients have spring rhinitis Rashid, Allergy 2011;66:1391 Foods reported to cause symptoms in 24 patients with pollen-food syndrome
    • Pollen-food syndrome is related to Bet v 1/PR-10 protein sensitization, but not all patients have spring rhinitis Rashid , Allergy 2011;66:1391 Component-resolved diagnosis demonstrated ubiquitous Foods reported to cause symptoms in 24 patients sensitisation to the Bet v 1/PR-10 protein cluster with pollen-food syndrome
    • Pollen-food syndrome is related to Bet v 1/PR-10 protein sensitization, but not all patients have spring rhinitis Rashid , Allergy 2011;66:1391 Component-resolved diagnosis demonstrated ubiquitous sensitisation to the Bet v 1/PR-10 protein cluster Despite this finding, 4 of 24 had no history (past or present) of spring rhinitis: of these, 2 had symptoms restricted to the summer months only, 1 had chronic rhinitis with house dust mite allergy and 1 had no history of rhinitis
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. 504 serum samples. sIgE to shrimp, cockroach (Blattella germanica) and Dermatophagoides farinae.
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. High exposure 504 serum samples. to B. Germanica in sIgE to shrimp, cockroach the home was (Blattella germanica) and Dermatophagoides farinae. significantly correlated with higher shrimp IgE levels.
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. In contrast, 504 serum samples. high exposure sIgE to shrimp, cockroach (Blattella germanicamite to dust ) and in the home Dermatophagoides farinae. was not correlated with shrimp IgE levels.
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834Conclusions•For children with evidence of IgE-mediated sensitization to cockroach and shrimp,having high exposure to cockroach in the home can contribute to higher shrimp IgElevels, which might not correlate with clinical reactivity.•Further patient evaluations with clinical historiesof shrimp exposure and reactions, as well as oral food challenges, would have to beperformed to confirm these findings.
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth cohort. 1.0 – Fruit and vegetable consumption. 0.5 – 0.62 Allergic diseases by parental questionnaires p=0.002 0.0 at the 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth cohort. Whereas no 1.0 – association was Fruit and vegetable observed for consumption. total vegetable 0.5 – 0.62 Allergic diseases by intake. parental questionnaires p=0.002 0.0 at the 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth of Intake cohort. 1.0 – apples/pears and carrots was Fruit and vegetable consumption. associated inversely with rhinitis, 0.5 – 0.62 Allergic diseases atopic asthma, and by parental questionnaires p=0.002 sensitization. 0.0 at the 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 50% of the children with Cross-sectional data from rhinitis were sensitized OR for Rhinitis a Swedish birch pollen, which against birth cohort. 1.0 – may cross-react with apples Fruit and and carrots. vegetable After exclusion of children consumption. food-related who reported allergic symptoms, most of 0.5 – 0.62 Allergic diseases by the observed inverse parental questionnaires p=0.002 associations moved toward 0.0 at the the null and became 8-year follow-up. Total fruit nonsignificant. (highest vs lowest quartile)
    • Vitamin D levels and food and environmental allergies in the United States: Results from the National Health and Nutrition Examination Survey 2005-2006 Sharief JACI 2011;127:1195 In children and adolescents in those with 25(OH)D levels <15 ng/mL 5.0 – OR for Serum 25-hydroxyvitamin 4.75 4.5 – D deficiency (<15 ng/mL) 4.0 – and insufficiency 3.5 – p<0.01 for all (15-29 ng/mL). 3.0 – 2.5 – Allergic sensitization 2.0 – serum IgE levels. 2.39 1.5 – 1.0 – 1.83 3136 children and 0.5 – adolescents 0.0 Peanut Ragweed Oak and 3454 adults. Allergies
    • Vitamin D levels and food and environmental allergies in the United States: Results from the National Health and Nutrition Examination Survey 2005-2006 Sharief JACI 2011;127:1180 In children and adolescents in those with 25(OH)D levels <15 ng/mL 5.0 – OR for Serum 25-hydroxyvitamin 4.75 4.5 – D deficiency (<15 ng/mL) There were no 4.0 – and insufficiency 3.5 – p<0.01 for all consistent associations (15-29 ng/mL). 3.0 – seen between 25(OH)D 2.5 – levels and allergic Allergic sensitization 2.0 – sensitization in adults. serum IgE levels. 2.39 1.5 – 1.0 – 1.83 3136 children and 0.5 – adolescents 0.0 Peanut Ragweed Oak and 3454 adults. Allergies
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 % children with 649 children enrolled at birth; 50 – Vitamin D deficiency as cord blood 25(OH)D < 11 ng/ml; 40 – 44% Food sensitization: 30 – 37% sIgE ≥ 0.35 kUA/l to any of 8 common food allergens; 20 – Single-nucleotide polymorphisms (SNPs) in 11 10 – genes known to be involved in regulating IgE and 25(OH)D 0 concentrations. Vitamin D deficiency Food sensitization
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; 2 – Food sensitization: sIgE ≥ 0.35 kUA/l to any 1.79 of 8 common food allergens; Single-nucleotide 1 – polymorphisms (SNPs) in 11 genes known to be involved in regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes 0
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Similar but weaker Vitamin D deficiency as cord deficiency interactions were blood 25(OH)D < 11 ng/ml; observed for SNPs 2 – in MS4 A2 Food sensitization: sIgE ≥ 0.35 kUA/l to any (rs512555), FCERIG 1.79 of 8 (rs2070901), and common food allergens; CYP24A1 Single-nucleotide (rs2762934). 1 – polymorphisms (SNPs) in 11 genes known to be involved in regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes 0
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D all four SNPs When deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; were simultaneously 2 – Food sensitization:strong considered, a gene-VSS interaction sIgE ≥ 0.35 kUA/l to any 1.79 of 8 commonevident was food allergens; (pinteraction=9x10-6) Single-nucleotide 1 – polymorphisms (SNPs) in 11 genes known to be involved in regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes 0
    • Significance of ovomucoid- and ovalbumin-specific IgE/IgG4 ratios in egg allergy Caubet, JACI 2012;129:739 IgE/IgG4 ratio to O V A L B U 107 egg-allergic children M I (mean age 6.9 years) N Challenged to baked egg Specific IgE and IgG4 to O V ovomucoid (OVM) and O ovalbumin (OVA) M U C O I D
    • Significance of ovomucoid- and ovalbumin-specific IgE/IgG4 ratios in egg allergy Caubet, JACI 2012;129:739 IgE/IgG4 ratio to O V A The balance L B between IgE U 107 egg-allergic children M and IgG4 to (mean age 6.9 years) I N OVA and Challenged to baked egg OVM has Specific IgE and IgG4 to functional O V ovomucoid (OVM) and O consequences ovalbumin (OVA) M U C O I D
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125BackgroundThe majority (approximately 75%) of children with cow’s milkallergy tolerate extensively heated (baked) milk products.Long-term effects of inclusion of dietary baked milk have notbeen reported.ObjectiveWe report on the outcomes of children who incorporated bakedmilk products into their diets.
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125 88 children evaluated Among 65 subjects initially for tolerance to baked tolerant to baked milk milk (muffin) underwent 60 – sequential food challenges to baked cheese (pizza) followed 50 – 40 – 60% by unheated milk. 30 – Natural history of 20 – development of tolerance. 10 – A median of 37 months 00 follow-up. Tolerate unheated milk during follow-up
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125 Development of tolerance in the active group stratified by initial baked milk challenge: tolerant versus reactive.
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125 88 children evaluated Among the baked milk– for tolerance to baked reactive subgroup (n=23) milk (muffin) underwent 100 – 90 – sequential food 80 – challenges to baked 70 – cheese (pizza) followed 60 – by unheated milk. 50 – Natural history of 40 – 9% 30 – development of 20 – tolerance. 10 – A median of 37 months 0 follow-up. Tolerate unheated milk during follow-up
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125 88 children evaluated Among the baked milk– for tolerance to baked reactive subgroup (n=23) milk Subjects underwent (muffin) who were 100 – 90 – sequential food to baked initially tolerant 80 – challenges to baked more milk were 28 times 70 – cheeseto become unheated likely (pizza) followed 60 – bymilk tolerant compared unheated milk. 50 – Natural history of with baked milk–reactive 40 – 9% 30 – development of 0.001 ). subjects (P< 20 – tolerance. 10 – A median of 37 months 0 follow-up. Tolerate unheated milk during follow-up
    • Dietary baked milk accelerates the resolution of cow’s milk allergy in children. Kim JACI 2011;128:125Conclusions•Tolerance of baked milk is a marker of transient IgE-mediatedcow’s milk allergy, whereas reactivity to baked milk portends amore persistent phenotype.•The addition of baked milk to the diet of children toleratingsuch foods appears to accelerate the development of unheatedmilk tolerance compared with strict avoidance.
    • A longitudinal study of resolution of allergy to well-cooked and uncooked egg Clark CEA 2011;41:706 Years to develop tolerance 11 – 10 – 9 – p<0.0001 10.3 95 egg-allergic children 8 – yrs from 2004 to 2010. 7 – 6 – Annual challenges and 5 – egg-specific IgE 4 – 5.6 measurement. 3 – yrs 2 – 1 – 0 Well-cooked Uncooked EGGS
    • A longitudinal study of resolution of allergy to well-cooked and uncooked egg Clark CEA 2011;41:706 Years to develop tolerance 11 – 10 – 9 – p<0.0001 10.3 95 egg-allergic children Nearly 1/3 had 8 – yrs from 2004 allergy to resolved to 2010. 7 – well-cooked egg 6 – Annual 3 years and challenges and 5 – at egg-specific IgE 2/3 at 6 years. 4 – 5.6 measurement. 3 – yrs 2 – 1 – 0 Well-cooked Uncooked EGGS
    • A longitudinal study of resolution of allergy to well-cooked and uncooked egg Clark CEA 2011;41:706 % symptoms during the challenge with well-cooked 70 – 95 egg-allergic children 60 – 65% 68% from 2004 to 2010. 50 – 40 – Annual challenges and egg-specific IgE 30 – 39% measurement. 20 – 10 – 00 Cutaneous G-I Rhinitis
    • A longitudinal study of resolution of allergy to well-cooked and uncooked egg Clark CEA 2011;41:706 % symptoms during the challenge with well-cooked 70 – 95 egg-allergic children 60 – 65% 68% Adrenaline from 2004 to 2010. 50 – was not and Annual challenges 40 – required. egg-specific IgE 30 – 39% measurement. 20 – 10 – 00 Cutaneous G-I Rhinitis
    • A longitudinal study of resolution of allergy to well-cooked and uncooked egg Clark CEA 2011;41:706 Cumulative persistence of allergy to well-cooked and uncooked egg 95 egg-allergic children from 2004 to 2010. Annual challenges and egg-specific IgE measurement.
    • •Induction of tolerance (SOTI)
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280Background: Patients with birch pollen allergy(major allergen: Bet v 1) have often an associatedoral allergy syndrome (OAS) to apple, which containsthe cross-reactive allergen Mal d 1.As successful birch pollen immunotherapy does notconsistently improve apple related OAS symptoms,we evaluated whether regular apple consumption hasan effect on OAS and immune parameters of Mal d 1or Bet v 1 allergy.
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280 40 patients with clear history of birch pollen rhinoconjunctivitis 17 of 27 patients and associated oral allergy in active group syndrome (OAS) to apple. and 0 of 13 patients 27 patients consumed in control group daily defined amount of apple (p=0.0001) (1-128g), doubling the amount could tolerate a whole every 2-3 weeks. apple after the 13 patients remained untreated. intervention. Follow up 8 mo.
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280 40 patients with clear history of birch pollen rhinoconjunctivitis 17 of 27 patients and associated oral with OAS In patients allergy in active group syndrome apple,to apple. to (OAS) tolerance and 0 of 13 patients 27 patients consumed induced can be safely in control group daily with slowly, gradually defined amount of apple (p=0.0001) increasing (1-128g), doubling the amount could tolerate a whole every 2-3 weeks. consumption apple after the of apple. 13 patients remained untreated. intervention. Follow up 8 mo.
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280Background: Patients with birch pollen allergy(major allergen: Bet v 1) have often an associatedoral allergy syndrome (OAS) to apple, which containsthe cross-reactive allergen Mal d 1.As successful birch pollen immunotherapy does notconsistently improve apple related OAS symptoms,we evaluated whether regular apple consumption hasan effect on OAS and immune parameters of Mal d 1or Bet v 1 allergy.
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280 40 patients with clear history of birch pollen rhinoconjunctivitis 17 of 27 patients and associated oral allergy in active group syndrome (OAS) to apple. and 0 of 13 patients 27 patients consumed in control group daily defined amount of apple (p=0.0001) (1-128g), doubling the amount could tolerate a whole every 2-3 weeks. apple after the 13 patients remained untreated. intervention. Follow up 8 mo.
    • Continuous apple consumption induces oral tolerance in birch-pollen-associated apple allergy Kopac, Allergy 2012;67:280 40 patients with clear history of birch pollen rhinoconjunctivitis 17 of 27 patients and associated oral with OAS In patients allergy in active group syndrome apple,to apple. to (OAS) tolerance and 0 of 13 patients 27 patients consumed induced can be safely in control group daily with slowly, gradually defined amount of apple (p=0.0001) increasing (1-128g), doubling the amount could tolerate a whole every 2-3 weeks. consumption apple after the of apple. 13 patients remained untreated. intervention. Follow up 8 mo.
    • Oral immunotherapy for IgE-mediated cow’s milk allergy: a systematic review and meta-analysis Brožek, Clin Exp Allergy 2012;42:363 RR of achieving full tolerance of cow’s milk 100 – 090 – 10.0• Systematic review of 080 – randomized controlled trials 070 – –RCTs- (n=5, 218 patients) 060 – & observational studies (n=5). 050 – 040 –• Use of oral immunotherapy in 030 – IgE-mediated cow’s milk allergy. 020 – 010 – 00 RCTs on immunotherapy, compared to elimination diet alone
    • Oral immunotherapy for IgE-mediated cow’s milk allergy: a systematic review and meta-analysis Brožek, Clin Exp Allergy 2012;42:363 RR of achieving full tolerance of cow’s milk 100 – 090 – 10.0 Results• Systematic review of 080 – randomized controlled trials of observational 070 – –RCTs- (n=5, 218 patients) 060 – studies were (n=5). 050 – & observational studies consistent 040 –• Use of oral immunotherapy in 030 – with those milk allergy. IgE-mediated cow’s of RCTs. 020 – 010 – 00 RCTs on immunotherapy, compared to elimination diet alone
    • Oral immunotherapy for IgE-mediated cow’s milk allergy: a systematic review and meta-analysis Brožek, Clin Exp Allergy 2012;42:363 In oral immunotherapy RR for14 –13 –12 – 12.9 11.311 –10 –09 –08 –07 –06 –0504 – – 5.80302 – – 3.801 –00 – Mild Mild asthma Reactions Reactions laryngospasm requiring oral requiring epinephrine glucocorticosteroids injection
    • Oral immunotherapy for IgE-mediated cow’s milk allergy: a systematic review and meta-analysis Brožek, Clin Exp Allergy 2012;42:363 In oral immunotherapy RR for14 –13 –12 – 12.9 11.311 –10 –09 –08 – A potentially large benefit of oral immunotherapy07 – in patients with cow’s milk allergy may be conterbalanced by06 – frequent and sometimes serious adverse effects.0504 – – 5.80302 – – 3.801 –00 – Mild Mild asthma Reactions Reactions laryngospasm requiring oral requiring epinephrine glucocorticosteroids injection
    • Allergy to goat’s and sheep’s milk in a population of cow’s milk-allergic children treated with oral immunotherapy Del Rio, Pediatr Allergy Immunol 2012;23:128 % children allergic to either goat’s or sheep’s milk by oral challenge 30 – Cow’s milk oral immunotherapy 25.9% 20 – 47% as (CMOIT) 15/58 anaphylactic successfully reactions performed in 58 10 – CM-allergic patients 0
    • Allergy to goat’s and sheep’s milk in a population of cow’s milk-allergic children treated with oral immunotherapy Del Rio, Pediatr Allergy Immunol 2012;23:128 % children allergic to either goat’s or sheep’s milk by oral challenge 30 – Although CM oral Cow’simmunotherapy milk oral 25.9% is a specific treatment immunotherapy 20 – for CM allergy, 15/58 47% as (CMOIT) anaphylactic successfully not be it may reactions effective against performed in 58 10 – CM-allergic patients of allergy to the milk other mammals 0
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155• Oral immunotherapy (OIT) with food isone of the most widely researchedtreatments for food allergy.• Immediate adverse reactions during therapy have been widelydescribed, and most of them were mild.• We describe 3 cases of esophageal eosinophilia in 110 patientstreated with milk OIT at our outpatient clinic during the last 5years.
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 1After 14 months of daily milk intake and dairy productsconsumption, he began to eat slowly and experienced generalweakness, low physical activity, sleep disturbances, and slow growthfor 5 months.Esophageal endoscopy showed rings and whitemucosal exudates with a peak of 35, 35, and 40eosinophils/hpf in mucosa from the upper, middle,and lower esophagus, respectively.
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 1After 14 months of daily milk intake and dairy products Milk-freeconsumption, he began to eat slowly and experienced general diet for 3 months,weakness, low physical activity, sleep disturbances, and slow growthfor 5 months. he wasEsophageal endoscopy showed rings and white asymptomatic andmucosal exudates with a peak of 35, 35, and 40 endoscopy andeosinophils/hpf in mucosa from the upper, middle,and lower esophagus, respectively. biopsy findings were normal
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 2Successfully achieved a daily intake of 200 mL in 19 weeks.Three months later, he began to experience retrosternal pain anddysphagia related to food ingestion.A complete blood cell count revealed 1270 eosinophils/mm3, andesophageal endoscopy disclosed rings and white mucosal exudateswith a peak of 30, 25, and 25 eosinophils/hpf in mucosa from theupper, middle, and lower esophagus.
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 2Successfully achieved a daily intake of 200 mL in 19endoscopy After the 3-month milk-free diet, weeks.Three months later, he began to experience retrosternaland and findings were macroscopically normal paindysphagia related to food ingestion. biopsies showed a peak of 7, 5, and 5A complete blood cell count revealed 1270 eosinophils/mm3, and eosinophils/hpf from the upper, middle, andesophageal endoscopy disclosed rings and white mucosal exudateswith a peak of 30,lower esophagus, respectively from the 25, and 25 eosinophils/hpf in mucosaupper, middle, and lower esophagus.
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 3He successfully achieved a 200 mL intake after 39 weeks.After 3 months of taking at least 200 mL of milk per day, he beganto experience abdominal pain immediately after ingestion of milkand other foods, anorexia, and weight loss (6 kg) for 4 months.A complete blood cell count revealed 920 eosinophils/mm3, andesophageal endoscopy showed rings and white mucosal exudates witha peak of 100 eosinophils/hpf in mucosa from the upper, middle, andlower esophagus.
    • Possible eosinophilic esophagitis induced by milk oral immunotherapy Sanchez-Garcia, JACI 2012;129:1155Case 3He successfully achieved a 200 mL intake after 39 weeks.After 3 months of taking at least 200 mL of milk per day, he beganto experience abdominal pain immediatelymilk-free diet. milk He was treated with a after ingestion ofand other foods, anorexia, and weight loss was asymptomatic. After 8 months, the patient (6 kg) for 4 months.A complete blood cell count showed 920 improvement. and Endoscopy revealed an eosinophils/mm3,esophageal endoscopy showed rings and white mucosal exudates witha peak of 100 eosinophils/hpf in mucosa from the upper, middle, andlower esophagus.
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2) and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259• Food allergy is a common and increasing health concern in westernized countries.• No effective treatment is available, and accidental ingestion can be life-threatening.• Food Allergy Herbal Formula-2 (FAHF-2) blocks peanut-induced anaphylaxis in a murine model of peanut-induced anaphylaxis.• It was found to be safe and well tolerated in an acute phase I study of patients with food allergy.
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2) and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259 Patients in an open-label study No significant received 3.3 g (6 tablets) drug-associated of FAHF- differences in 2, laboratory 3 times/day for 6 mo. parameters, pulmonary function or Basophil activation and electrocardiographic basophil and eosinophil findings numbers were evaluated before and after by using CCR3/CD63 staining treatment and flow cytometry. were found.
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2)and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259 Suppression of allergen-stimulated basophil activation by FAHF-2in a 6-mo phase I clinical study. Patients’ blood before treatment (0 mo) and at consecutive 2-mo time points during 6-mo was stimulated with increasing doses of allergen in the presence of stimulation buffer. Months of FAHF-2
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2)and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259 Suppression of allergen-stimulated basophil activation by FAHF-2in a 6-mo phase I clinical study. Patients’ reduction (p<0.01) There was a significant blood before treatment (0 mo) and in basophil CD63 expression (basophil activation) at consecutive 2-mo time points during 6-mo was stimulated with increasing in response to ex the presence of stimulation buffer. doses of allergen in vivo stimulation at month 6. Months of FAHF-2
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2)and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259 Effect of FAHF-2 treatment on basophil and eosinophil percentages. Patients’ blood at baseline and after 6 mo of a clinical phase I study.
    • Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2)and inhibitory effect on basophils from patients with food allergy: Extended phase I study. Patil, JACI 2011;128:1259 Effect of FAHF-2 treatment on basophil and eosinophil percentages. Patients’ blood at baseline a trend toward a clinical phase I study. There was and after 6 mo of reduction in eosinophil and basophil numbers after treatment.
    • take home
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955 Symptoms of food-inducedallergic reactions (1).
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955 Symptoms of food-inducedallergic reactions (2).
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955 Conducting an oral challenge.
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955 Recommendation for administering egg-containing vaccines to egg-allergic patients.
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955 Diagnostic criteria for anaphylaxis
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955Pharmacologic managementof anaphylaxis (1).
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955Pharmacologic managementof anaphylaxis (2).
    • NIAID-Sponsored 2010 Guidelines for Managing Food Allergy: Applications in the Pediatric Population Burks Pediatrics 2011;128:955Pharmacologic managementof anaphylaxis (3).