Seafood allergy in children: a descriptive studyPaul Turner, PhD*†; Ian Ng, BSc†; Andrew Kemp, PhD*; and Dianne Campbell, PhD*†
Background: Food allergy and seafood (fish, mollusk, and crustacean) consumption have increased considerably over the past40 years. Seafood allergy is now a leading cause of anaphylaxis in both the United States and Australia. However, there is onlylimited published data describing the clinical presentation and management of seafood allergy.
Objectives: To describe the characteristics of a large cohort of children with seafood allergy.Methods: Using a retrospective chart review, we collected data on all children presenting to our Tertiary Allergy Service with
an allergic reaction to seafood between 2006 and 2009.Results: 167 children had a history of definite clinical reaction to seafood and/or positive food challenge (103 male, 62%).
94% had evidence of co-existent atopic disease. Prawn/shrimp was the most common seafood implicated. One-fifth presentedwith a history of anaphylaxis to seafood. Over 50% of crustacean-allergic children could tolerate non-crustacean fish.Sensitization to other fish species was very common in fish-allergic children, with one third reporting clinical reactions to at leasttwo species; 16% developed symptoms to fish vapours. In children with allergy to tuna and/or salmon, at least 21% were ableto tolerate the fish in a tinned form.
Conclusions: Seafood is a relatively common and important cause of food allergy in Australian children, presenting with ahigh rate of anaphylaxis.
Ann Allergy Asthma Immunol. 2011;106:494–501.
INTRODUCTIONThe consumption of seafood (crustacean, mollusk, and fish)has risen by approximately 50% over the last 40 years, bothin the United States and elsewhere,1 corresponding to anincrease in the incidence of seafood allergy over the sameperiod.2 The prevalence of self-reported seafood allergy as-sessed by telephone survey in the United States in 2002 was2.3% (shellfish 2.0%, fish 0.4%), with significantly lowerrates in children compared with adults3; similar rates havebeen reported in Canada.4 Prevalence is thought to be morecommon in countries with higher levels of seafood consump-tion. In children referred for allergy assessment, seafood wasthe third most common food sensitivity in Spain5 (after eggand cow’s milk) and the second most common in Singapore.6
Clinical reactions to seafood range from localized urticaria tolife-threatening anaphylaxis2 and can occur after exposure toseafood vapors.5,7,8 Shellfish may cause more severe allergicreactions compared with other food triggers.9 Seafood is nowone of the commonest causes of allergic reactions (includinganaphylaxis) presenting to emergency departments.10,11
Recent published data on children with seafood allergyhave used either self-reporting or evidence of sensitization asa surrogate for proven allergy,3-6 or they have been limited to
small case series,5,12 thus providing only limited informationon clinical presentation and management of true seafoodallergy. Although significant cross-reactivity occurs betweendifferent types of crustacean,2,12 the situation with fish is lesscertain, with reports of both polysensitization to multiplespecies13,14 and monosensitization to a single fish type.7,15
Cross-reactivity between crustacean and fish has not beenreported,16 so affected individuals are usually advised toavoid either fish or crustacean. Children and young adultswith fish allergy may be able to tolerate canned fish.17 Theobjective of this study was to clarify the clinical characteris-tics of seafood allergy among children, in order to facilitateimproved clinical management.
METHODSWe undertook a retrospective chart review of all patientspresenting to the Allergy Clinic at the Children’s Hospital atWestmead between 2006 and 2009. Records were assessedby two reviewers trained in the same methodology (P.J.T. andI.N.). Inclusion criteria used were as follows:• A convincing clinical history of immunoglobulin (Ig)
E–mediated symptoms within 2 hours of known seafoodexposure, as assessed by a pediatric allergist, together withevidence of sensitization on skin testing/serum specificIgE; or
• A positive food challenge to seafood performed undermedical supervision.
Children with evidence of sensitization to seafood but nohistory of clinical reaction were thus excluded. A total of2,999 charts were reviewed, from which 174 children withseafood allergy were identified. In 16 cases, the history wasnot convincing, and the children subsequently underwentopen oral food challenges (OFC), 7 of which were negative
Affiliations: * Department of Allergy and Immunology, Children’s Hos-pital at Westmead, Sydney, Australia; † Discipline of Paediatrics and ChildHealth, School of Medicine, University of Sydney, Sydney, Australia.
Disclosures: The authors have nothing to disclose.Funding Sources: Department of Allergy and Immunology, Children’s
Hospital at Westmead.Received for publication November 30, 2010; Received in revised form
Published by Elsevier Inc. All rights reserved.doi:10.1016/j.anai.2011.02.001
494
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(ie, no evidence of allergy). A total of 167 children weretherefore included in the study.
Data collected included patient demographics, details ofprevious reactions to seafood (including species, method ofpreparation, symptoms), sensitization to food and aeroaller-gens, presence of other atopy (including food allergy, definedas a previous clinical reaction rather than sensitization alone),management advice, prescription of adrenaline autoinjectordevice, compliance with advice, and subsequent reactions(whether accidental or not). Sensitization was assessed byskin prick testing (SPT) rather than detection of serum spe-cific IgE, because of the lack of commercial availability ofspecies-specific antibodies for most Australian fish, and inany event, cutoff levels predicting clinical reactivity for spe-cific IgE to seafood species except Gadus morhua (cod) havenot been published.18 Skin prick testing was performed ac-cording to standard guidelines, using commercial allergenextracts and histamine 10 mg/mL as a positive control (Hol-lister Stier Laboratories, Washington).19 A positive SPT wasdefined as a wheal size of at least 3 mm greater than a salinecontrol read at 15 minutes. The specific allergens tested weredetermined by clinicians on an individualized basis. In manychildren, SPT to fresh or canned fish was also performed,using raw or cooked fish pulverized in normal saline. If datawere ambiguous, families were contacted by telephone orletter to provide further information. Oral food challengeswere performed as deemed appropriate by the treating clini-cian after a protocol consistent with established guidelines.20
Prior reactions were classified as localized contact reac-tions, either mild–moderate (skin and subcutaneous tissueinvolvement, gastrointestinal symptoms) or anaphylaxis (re-
Table 1. Patient Characteristics
Characteristic
No. of patientsAge at first reaction, median (interquartile range)Duration of follow-up, median (interquartile range)Sex, no. (%)
MaleFemale
Other atopy, no. (%)AsthmaAllergic rhinitisEczema
Other food allergy besides seafoodEggCow’s milkPeanutTree nut
Initial symptoms of seafood allergy, no. (%)Gastrointestinal symptomsAnaphylaxis
History of reaction to vapors from seafood
Abbreviation: OFC, oral food challenge.
VOLUME 106, JUNE, 2011
piratory or cardiovascular symptoms), in line with the cri-eria suggested by the 2005 National Institute of Allergy andnfectious Disease/Food Allergy and Anaphylaxis Networkymposium.21 The diagnoses of asthma, allergic rhinitis, andczema were made by the attending physician.
Data analysis was performed using GraphPad Prism 5oftware (GraphPad Software, Inc, La Jolla, California). Sta-istical analysis was performed using two-tailed Mann-Whit-ey U test, with P � .05 considered significant. The studyas approved by the Ethics Committee at the Children’sospital at Westmead.
ESULTSne hundred sixty-seven patients were included in the study,
s described in Table 1. In 13 children, the diagnosis wasonfirmed at OFC (Table 2). Ninety-four percent of childrenad evidence of preexisting atopy. Prawn, “white fish,”almon, and tuna were the most common seafood allergensFig 1). In 14% of reactions, the type of seafood could not beecalled by the parent or identified retrospectively by thehysician on history. Thirty-five children (21%) had experi-nced an anaphylactic reaction to seafood before presenta-ion. One child developed symptoms consistent with foodrotein–induced enterocolitis syndrome approximately 4ours after consuming mackerel on 2 separate occasions. Theemainder developed symptoms consistent with IgE-mediatedood allergy, specifically angioedema, urticaria, and, in 20ases (12%), gastrointestinal symptoms (nausea, vomiting,nd abdominal pain). Twenty-six children (16%) had expe-ienced ocular or upper respiratory symptoms (rhinorrhea,asal pruritus) on exposure to vapors from seafood. In 19
Diagnosis made on the basis of:
linical history withence of sensitization
Positive OFC
154 13rs (10 months–4 years) 3.5 years (1–4 years)ars (2.3–5.6 years) 4.1 years (3.2–8.2 years)
(11%) cases, the child had previously tolerated the sensitizingseafood on at least 3 occasions before the first reaction.
Risk Factors for Anaphylaxis to SeafoodConcurrent asthma (physician diagnosed) was found to beassociated with anaphylaxis to seafood (odds ratio 2.4,95% CI 1.1–5.4, P � .03, Fisher exact test). History ofreactions to fish vapors and previous food anaphylaxis tononseafood triggers were not found to be significant asso-ciations (Table 3).
Table 2. Characteristics of Children with Seafood Allergy Diagnosed
Agea (yrs),sex
SeafoodSPT(mm)
Amount eaten
2, M Salmon (canned) 0 ¼ tsp Lip an12, M Crab 3 ¼ tsp Periora7, M Tuna 4 1/8 tsp Periora
7, F Salmon 10 1/8 tsp Itchy t13, F Crab 6 1/16 tsp Facial
urtic2, F Flathead 0 Smear to cheek Localiz5, F Prawn 2 2 tsp Genera6, F Crab 6 Smear to lip Facial
angi6, M Tuna 2 2 tsp Genera
4, M Prawn 3 ½ tsp Vomite
5, M Barramundi 5 8 tsp Facial3, M Crab 9 1/8 tsp Facial1, M Tuna (canned) 3 ¼ tsp Genera
Abbreviations: SPT, skin prick test; tsp, teaspoon.a At time of OFC.
Figure 1. Common seafood triggers in
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rustacean Allergy
eventy-one children were diagnosed with crustacean al-ergy, most commonly to prawn/shrimp in 87%. Fifteen21%) presented with anaphylaxis, and 11 (15%) developedontact urticaria. Six children had experienced previous re-ctions to both prawn and crab, whereas a further 57 (80%)ad evidence of cross-sensitization to another crustacean. Theize of the SPT was not related to severity of reaction (P �10, Mann-Whitney U test) (data not shown). Five children
ia Nil Cod (8), snapper (4)ia Nil Prawn (8), –ve to fishody urticaria Barramundi Barramundi (10), cod (9),
salmon (5), prawn (3)
at Ora
Sym
gioedel urtical urtica
hroat,angioeariaed urtlized b
urticaroedemlized b
d after
urticarurticarlized b
children with seafood allergy.
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with convincing history of crustacean allergy with negativeSPT to commercial extracts tested positive to SPT performedusing fresh crustacean. Thirty-five children (49%) were alsosensitized to noncrustacean seafood (cod, salmon, or tuna),with 21 having had a previous clinical reaction to at least 1fish species. However, at least 50% of crustacean-allergicchildren could tolerate fish. Aeroallergen sensitivity was de-termined in 57 children. Forty-eight (84%) were sensitized tohouse dust mite, 16 (28%) to rye grass, and 13 (23%)to cockroach.
Allergy to MollusksNine children were allergic to mollusks (7 to squid, 2 tooyster); none had experienced anaphylaxis to mollusk. Cross-sensitization to crustacean was common in this group: 7 weresensitized to crustacean (2 with clinical allergy), and 5 chil-dren tolerated fish.
Fish AllergyA total of 95 children were diagnosed with IgE-mediatedallergy to fish, of which 19 (20%) had experienced anaphy-laxis to fish. The size of the SPT was not related to severityof reaction (P � .39, Mann-Whitney U test) (data not shown).Cross-sensitization between fish species was common; 88(93%) were sensitized to at least one other fish type, whereas28 (29%) had experienced a previous allergic reaction toanother species of fish. Although 21 children (22%) were alsoallergic to crustacean, at least 16 could tolerate crustacean (all
Table 3. Risk Factors for Anaphylaxis to Seafood
Risk factor OR 95% CI P valuea
Asthma (physician diagnosed) 2.44 1.11–5.35 .03Eczema 1.66 0.67–4.12 .39Reaction to vapors 1.56 0.59–4.07 .43Previous anaphylaxis to
nonseafood trigger1.15 0.47–2.83 .82
1st Reaction under 2 years of age 1.41 0.66–3.00 .441st Reaction over 5 years of age 1.40 0.56–3.46 .63
a By Fisher exact test.
Figure 2. Size of skin prick test (SPT) wheal in relation to outcome of oral
fish. P values by Mann-Whitney U test.
VOLUME 106, JUNE, 2011
f whom had either negative or borderline SPTs to thesellergens). Thirty-eight children were allergic to eitheralmon or tuna. Twelve (32%) of these children developedymptoms after eating the tinned fish, including 2 childrenho had anaphylaxis. Of the remaining 26 children, at least(31%) were able to tolerate the tinned fish even though theyould develop symptoms to the fresh variety.
pen Oral Food Challenges to Seafoodinety-five open OFCs were undertaken during the studyeriod, either to confirm the diagnosis of seafood allergy (13ases) or to confirm tolerance to a different species of seafoodo the known allergen. Thirty-eight (40%) children underwentFC to crustacean, 3 to mollusk, and the remainder to fish. In2 (23%) cases, the OFC was positive. Common symptomsere localized skin symptoms (61%), widespread skin symp-
oms (33%), and vomiting (6%). No child experienced ana-hylaxis. The SPT had a high negative predictive valueNPV) for challenge outcome (NPV 91%, P � .03, Mann-
hitney U test) but a low positive predictive value of 42%Fig 2). The SPT was not predictive of outcome where thehallenge was performed to the tinned fish (NPV 67%, P �31, Mann-Whitney U test). Five children with noncrustaceanish allergy underwent challenge to shark meat; 4 had nega-ive challenges, including 3 children with a history of allergyo tuna.
tility of Skin Prick Testing in Determining Potentialross-Reactivitycohort of children underwent SPT to fresh, raw seafood
ither to provide further diagnostic information or to clarifyotential cross-reactivity to other species when commercialxtracts were not available. In general, SPT to fresh extractesulted in increased wheal size compared with extract butas not related to severity of reaction (P � .59, Mann-hitney U test) (Fig. 2). Table 4 shows the probability of a
atient having a positive SPT to a species of seafood depend-ng on whether they have evidence of sensitization to anothereafood species. Rates of sensitization to noncrustacean fish
allenges performed to seafood (all challenges), crustacean only, and canned
food ch
497
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DS
an fish
was fairly uniform across the 3 species assessed (tuna,salmon, and cod).
Management of Seafood AllergyIn general, children allergic to 1 seafood type were advised toavoid all seafood in their diet unless they were alreadytolerating another species or they had passed an OFC per-formed under medical supervision. All children with a historyof anaphylaxis to seafood were prescribed an adrenalineautoinjector device. Eighteen children were also prescribedthis on the basis of significant risk factors (frequent exposure,asthma, concerns about avoidance), and a further 89 had beenprescribed an autoinjector for the management of other foodallergies. Twenty-seven (16%) children subsequently experi-enced a clinical reaction to seafood that their family had received
Table 4. Cross-Sensitization between Allergens on Skin Prick Testing
Prawn Cr
Crustacean allergyOverall rate of sensitization .90 .7Prawn
SPT� .8SPT– .1
CrabSPT� .98SPT– .56
CodSPT� .88 .7SPT– .86 .7
SalmonSPT� .87 .8SPT– .87 .6
TunaSPT� .87 .8SPT– .86 .6
Noncrustacean Fish ALLERGYOverall rate of sensitization .62 .5Prawn
SPT� .8SPT– .0
CrabSPT� .94SPT– .17
CodSPT� .60 .5SPT– .67 .6
SalmonSPT� .61 .5SPT– .58 .5
TunaSPT� .62 .5SPT– .55 .5
Abbreviation: HDM, house dust mite.Data represent probability of a positive SPT to the seafood listed, denegative, in children with crustacean allergy (n � 73) or noncrustace
advice to avoid; in 2 cases, the reaction was anaphylaxis. l
498
Seafood allergy was found to resolve in 7 (4%) children. Inchildren, a reduction in SPT to the causative agent was seen
fter 5 to 7 years; 3 children subsequently passed OFC underedical supervision, whereas in 1 the seafood was introduced
y the family against medical advice before planned OFC.he remaining 3 children tolerated exposure 2 to 3 years after
nitial reaction; in 2 cases the child had been intentionallyxposed to the implicated seafood by their families on aemiregular basis. These 3 children continued to demonstrateildly positive SPT to the seafood despite developing toler-
nce.
ISCUSSIONeafood is now a common cause of food allergy and anaphy-
Probability of positive SPT to:
Cod Salmon Tuna HDM
.44 .42 .44 .84
.42 .41 .42 .84
.44 .44 .44 .86
.44 .42 .47 .86
.44 .33 .33 .79
.91 .94 .85
.07 .07 .83
.93 .97 .85
.10 .07 .82
.94 .94 .85
.07 .03 .81
.86 .87 .86 .77
.85 .87 .88 .86
.88 .85 .82 .56
.84 .86 .85 .89
.89 .86 .86 .56
.96 .96 .79
.29 .31 .60
.96 .93 .78
.23 .42 .67
.95 .94 .76
.31 .46 .75
g on whether the SPT to the seafood listed on the left is positive or(n � 97).
(SPT)
ab
7
41
52
07
16
8
99
67
88
78
pendin
axis. This study provides important new perspectives on
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confirmed seafood allergy in children. We have found thatseafood allergy is relatively common in our population ofallergic children and that these children present with a highrate of anaphylaxis compared with other common food aller-gens. We observed a rate of 21% to seafood, 5-fold greaterthan our observed rate for anaphylaxis in children presentingto our service with a history of clinical allergy to peanut(4.2%). We also report a high degree of cross-sensitizationbetween crustacean and noncrustacean (fish) allergy. Chil-dren with seafood allergy appear to have higher rates of otheratopy (asthma, allergic rhinitis, eczema) compared with pea-nut-allergic children in Australia,22 which might account forthese observations. However, no difference was found inrates of atopy between children allergic to both crustaceanand fish compared with those with allergy to a single species.
The high rate of anaphylaxis documented in this study maybe an overestimate, because children with mild symptomsmight not be referred to a specialist service for assessment.This would, however, affect all children presenting to ourservice irrespective of the causative food. In line with previ-ous reports for other food allergens, asthma was a significantrisk factor for anaphylaxis,23 whereas the degree of sensiti-zation on SPT to seafood was not predictive of reactionseverity.24 Reassuringly, a history of reaction to vapors fromcooked seafood was not associated with an increased riskof anaphylaxis.
Dietary avoidance is essential in the management of foodallergy. However, conflicting information exists regardingcross-reactivity between different seafood species. Our find-ings of significant cross-sensitization in children with crus-tacean allergy agree with those of Wu et al,25 who reported ahigh degree of cross-sensitization between different speciesof shellfish, thought to be attributable to significant homol-ogy in tropomyosins found in all crustaceans and mollusk. Ittherefore seems prudent for shellfish-allergic patients toavoid all shellfish in the absence of evidence of tolerance.
The major allergens responsible for cross-reactivityamongst noncrustacean fish are the parvalbumins, found inthe muscular sarcoplasm.26,27 However, other allergensalso may contribute to cross-sensitization.28 It has beensuggested that the parvalbumin Gad c 1 present in cod canbe used as a panallergen to detect sensitization.26 However,in our cohort, 14% of fish-allergic individuals were nega-tive on SPT to cod extract containing Gad c 1. Previousreports have estimated that more than 50% of fish-allergicsubjects are sensitized to other species.29 We observed amuch higher rate of at least 93%, with similar rates ofsensitization to tuna as to cod and salmon, in contrast toreports that members of the Scombridae family (whichincludes tuna) are best tolerated with lower rates of sen-sitization.17,26 Skin sensitization to seafood does not nec-essarily equate with clinical reactivity.7,30 Although thisstudy is therefore limited in its ability to determine cross-reactivity, more than one third of fish-allergic children hadexperienced a previous clinical reaction to at least 1 other
fish species. Food challenges, ideally under double-blind, p
VOLUME 106, JUNE, 2011
lacebo-controlled conditions, would provide valuableata on cross-reactivity, but in reality, parents are reluctanto consent to their child having multiple food challenges,articularly with a history of anaphylaxis or reactions to aumber of different fish species. Diagnostic testing usingecombinant allergens and inhibition assays is limited byhe range of allergens commercially available (For exam-le, most common Australian fish do not have an equiva-ent recombinant allergen available) and in any event doesot correlate with clinical reactivity. Physicians are there-ore likely to rely on SPT to determine cross-sensitization.he SPT has a high NPV and is therefore useful in deter-ining a low likelihood of clinical reaction to other spe-
ies. Fish-allergic individuals may be more likely to tol-rate those species that are taxonomically remote from thepecies to which they are allergic.13 In this regard, sharkeat (known locally as flake and Sweet William) is tax-
nomically distant from other fish (particularly tuna) ands readily available commercially in Australia, where it isommonly used for “fish-and-chips.” Our cohort includedchildren with allergy to tuna who were able to tolerate
hark meat. Assessing the degree of cross-sensitization andolerance of fish-allergic patients to shark meat thereforeould be interesting.General opinion and teaching in the allergy/immunology
ommunity appears to be that no significant cross-reactivityccurs between crustacean and fish allergy. The 2006 Foodllergy Guidelines from the American College of Allergy,sthma and Immunology state that “crustaceans do not cross-
eact with vertebrate fish,”31 presumably on the basis ofAST inhibition studies. However, epidemiological evidenceould suggest the opposite. Sicherer et al3 reported that 43%f fish-allergic individuals (adults and children) were alsollergic to shellfish on telephone interview.3 In our cohort, ateast 21% of children with fish allergy were also allergic torustacean in our study. This rate is probably an underesti-ate, given the high rate of sensitization to crustacean ob-
erved and that parents of fish-allergic children generally fearhat their child also may react to crustacean. In our experi-nce, in such a scenario, few parents are prepared to introducehellfish into the diet even in the absence of sensitization.
hether this cross-reactivity is a consequence of the in-reased atopic predisposition of these children or attributableo some other mechanism remains unclear. Certainly, tropo-yosins are not an allergen in noncrustacean fish,15 but no
ata exist regarding other potential candidate proteins. In theirst instance, analyzing data from the prevalence studies tossess whether subjects allergic to noncrustacean fish areore likely to also have allergy to shellfish compared with
ther allergens would be desirable.Approximately 30% of seafood consumed in developed
ountries is from canned fish.1 The canning process typicallyesults in the fish being cooked for up to 7 hours underressure, which may result in a conformational change in theish protein, rendering it less allergenic.32 In a study of 18
atients with fish allergy (some of whom had positive SPT to
499
1
1
1
1
1
1
1
1
1
1
2
2
2
2
2
2
2
2
tuna), all were able to tolerate canned tuna, although none hadactually experienced a previous reaction to this fish.17 Theauthors suggest that “children and young adults allergic tofish appear to be able to safely eat canned tuna.” A further 2patients with salmon allergy were able to tolerate the cannedfish. However, Kelso et al33 subsequently reported a 19-year-old man with allergy to canned tuna. In our cohort, 12children developed symptoms of IgE-mediated food allergyafter eating canned fish, including 2 who had anaphylaxis.Physicians therefore must recommend avoidance of cannedfish in individuals with seafood allergy, unless tolerance tocanned fish has been demonstrated. Performing OFC tocanned fish is a useful strategy allowing the canned fish to beintroduced when negative. We found that more than 20% ofchildren allergic to salmon or tuna were able to tolerate thefish in canned form, and this was associated with a reductionin SPT size in most, implying that consumption of cannedfish may have resulted in the induction of tolerance in thesepatients. The SPT to either allergen extracts or the cannedfish was not predictive of challenge outcome; thus, a formalOFC under medical supervision is warranted.
Tropomyosin found in both shellfish and house dust mite(HDM) accounts for the high rates of sensitization (up to90%) to HDM in patients with crustacean allergy.25 In thisstudy, approximately 80% of subjects were sensitized toHDM. However, approximately half of fish-allergic childrenwith negative SPT to crustacean were also sensitized toHDM, implying that in our population sensitization to HDMmay be a marker of atopy rather than a consequence ofcross-sensitization to tropomyosin.
In summary, we report a rate of anaphylaxis in childrenpresenting with seafood allergy of over 20%. These childrendemonstrate a significant degree of clinical cross-reactivity(and even higher levels of cross-sensitization) not just be-tween different types of fish or crustacean but also betweenfish and crustacean, a finding that has not been previouslyreported. Finally, although many children are able to toleratecanned fish, anaphylaxis can occur even to this, and, there-fore, contrary to previous reports, challenges should alwaysbe performed under medical supervision.
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equests for reprints should be addressed to:r. Paul Turnerepartment of Allergy and Immunologyhildren’s Hospital at Westmeadocked Bag 4001, Westmead, NSW 2145, Australia-mail: [email protected]
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