Egg allergy is one of the most common food allergies. As there are many studies of allergy to egg, only some key articles are highlighted below.
As reviewed by Martorell Aragones et al. (2001) [1339], a wide range of symptoms have been observed with allergy to egg including 1. Cutaneous reactions: erythema, urticaria and angioedema. 2. Generalized reactions: anaphylaxis. 3. Gastrointestinal reactions: abdominal pain, nausea, vomiting and diarrhea. 4. Respiratory reactions: rhino-conjunctivitis, laryngeal edema and asthma.
Several studies have compared cooked versus raw eggs
Romeira et al. (2003) [1343] reported 4 children who had all developed tolerance for cooked eggs but remained sensitive to raw or partially cooked eggs. The reactions on eating raw or partially cooked egg were respectively generalized urticaria and labial angioedema, an anaphylactic reaction with laryngeal angioedema, generalized urticaria, and labial angioedema and facial urticaria.
Eigenmann (2000) [1342] reported 2 children who had similarly developed tolerance for cooked eggs but reacted to raw or partially cooked egg. The first suffered initially itching on her face and respiratory distress with severe urticaria of the face and signs of laryngeal edema developing later. The second child suffered a diffuse, severe urticarial reaction and profuse vomiting.
Certain egg allergies are associated with allergies to birds kept as pets in the so-called Bird - Egg syndrome.
Quirce et al. (2001) [1268] reported that 8 patients suffered rhinoconjunctivitis and 6 of these also asthma on exposure to feathers. All of these individuals also experienced itching and burning of the mouth immediately after eating fried egg yolk (usually undercooked), and sometimes with homemade mayonnaise. This was followed by swelling of the lips and oral mucosa, and sometimes facial angioedema. 2 patients also suffered shortness of breath and chest tightness after egg ingestion. Most patients tolerated well-cooked eggs.
Blanc et al. (2004) [1401] describe a patient with bird - egg syndrome and very severe symptoms despite tolerating a challenge with cooked egg white. Symptoms after eating egg included urticaria, angioedema and anaphylactic shock with loss of consiousnes and low blood presure.
Many individuals, especially young children can outgrow allergy to egg. Bernhisel-Broadbent et al (1994) [1269] compared 10 patients with persistent egg hypersensitivity with 11 patients in whom tolerance developed after an initial positive DBPCFC. All 21 patients were highly atopic; 14 had asthma, 20 had atopic dermatitis, and all had allergic rhinitis and a positive family history of atopic disease. The median age of those with persistent egg hypersensitivity was 2.6 years (range, 0.8 to 17.4 years) at the time of their initial positive DBPCFC, and 4.6 years at their most recent positive DBPCFC. For those becoming tolerant the ages were 3.5 years (range, 2.6 to 15.2 years) and 5.9 years (range, 3.3 to 18.2 years) at the negative DBPCFC. Patients with persistent egg allergy were more likely to have symptoms involving multiple target organs during their first DBPCFC (8 of 10 patients) compared with children who became clinically tolerant (3 of 11 patients).
The types of symptoms experienced by egg allergic individuals may be associated with sensitisation to specific allergens although the studies to date have only described a small number of patients. Mine & Zhang (2002) [1245] reported that 4 patients with anaphylaxis differed from 2 patients with atopic dermatitis and asthma and 2 with cutaneous and gasterintestinal symptoms in that IgE in sera from the patients with anaphylaxis bound ovotransferrin (and ovomucoid) rather than ovalbumin (and ovomucoid).
Skin Prick Test
Number of Studies:
>20
Food/Type of allergen:
Hansen et al. (2004) [1294] used extract of fresh egg.
Sporik et al. (2000) [1322] (Hill et al. 2001 [662] and Hill et al. 2004) [1317]) performed skin prick tests using commercial extracts.
Osterballe & Bindslev-Jensen (2003) [1175] used the prick-prick method.
Bernhisel-Broadbent et al (1994) [1269] used egg white extract and purified ovomucoid, ovalbumin, and lysozyme.
Protocol:
(controls, definition of positive etc)
Sporik et al. (2000) [1322] (as well as Hill et al. 2001 [662] and Hill et al. 2004 [1317]) used histamine (1 mg/mL) as positive control and also a negative control solution. Skin tests were performed on the backs of infants and on the forearm of older children. The skin weal diameter (mm) to histamine was measured between 10 and 15 min and to allergen between 15 and 20 min.
Hansen et al. (2004) [1294] and Osterballe & Bindslev-Jensen (2003) [1175] tested patients with a 1-mm lancet (ALK-ABELLÓ) at the volar surface of the forearm with fresh pasteurized whole egg, histamine standard (10 mg/mL) and diluent as negative control. The skin prick test was done in duplicate according to the EAACI (European Academy of Allergology and Clinical Immunology) guidelines, and wheals were read after 15 minutes. Hansen et al. (2004) [1294] also compared a skin application test and an atopy patch test.
Bernhisel-Broadbent et al (1994) [1269] counted a wheal diameter of 3 mm than negative control as a positive skin prick test response.
Number of Patients:
Hansen et al. (2004) [1294] tested 10 egg allergic children, 10 atopic and 10 normal controls.
Kim et al. (2002) [1361] tested 97 children with atopic dermatitis.
Sporik et al. (2000) [1322] reported SPT reactions for 106 patients with egg out of a group of 467 children with suspected food allergies with median age 3.0 years.
Rance et al. (1997) [1360] tested 128 children with egg.
Bernhisel-Broadbent et al (1994) [1269] reported SPT results for 18 patients with egg allergy, 13 diagnosed by DBPCFC and 5 by a recent episode of anaphylaxis to egg.
Summary of Results:
Hansen et al. (2004) [1294] found that SPT was the most effective method for diagnosis of egg allergy with 100% sensitivity and 85% specificity.The skin application and atopy patch tests were less useful and caused more severe reactions.
Osterballe & Bindslev-Jensen (2003) [1175] report that all children who gave a positive oral challenge also gave a positive skin prick test with a mean wheal diameter of 5.7 ± 2.4 mm.
Kim et al. (2002) [1361] report that the accuracy of SPT for diagnosis of egg allergy in children with atopic dermatitis was improved by using an extract of boiled egg rather than commercial extracts (sensitivites 63.8% and 55.6%, specificities 81% and 53.3%).
Hill et al. (2001) [662] suggested that a wheal diameter >5 mm was able to give a '100% diagnostic SPT level' for egg. They reported that SPT was more effective than measuring serum IgE levels (by EAST or CAP) but that combining CAP and SPT results could improve the diagnosis and thus avoid the need for some food challenges. Subsequent studies by the same group (Hill et al. 2004) [1317] analysed the diagnostic accuracy of different SPT weal diameters in children 0-2yr, and children 2 yr and older, regarding sensitivity, specificity, positive and negative predictive value as a function of diameter. They revised their earlier conclusion that SPT was more sensitive than food-specific serum lgE antibody testing in the diagnosis of food allergy, noting that with age-specific cut-offs the difference was less significant. They also investigated the diagnostic accuracy of SPT in children who had never directly ingested a particular food item. At 6 months of age, 13 infants had a negative SPT (0 mm) to egg, but 12 months later, at the time of open challenge, 10 of these infants had developed positive SPT (≥5 mm) above the diagnostic SPT threshold. All children with an SPT above the age-specific diagnostic cut-off level subsequently reacted to egg on open challenge.
Sporik et al. (2000) [1322] found that wheals larger than 6 mm were associated with only positive challenges in a study of 86 oral challenge positive egg allergic individuals and 20 oral challenge negative individuals.
Rance et al. (1997) [1360] reported that the correlation between SPT results with fresh egg and oral challenge results was much better than for SPT performed with commercial extract (for egg white, 79.3% v. 43% ). However, the fresh food gave more false positives (sensitivites 100% and 56%, specificities 10% and 80%).
Bernhisel-Broadbent et al (1994) [1269] reported a study of 18 patients with a positive skin prick test response to egg white (median, 8 mm; range, 3 to 18 mm) and their responses to individual allergens. 7/18 patients had negative skin prick test responses to lysozyme, 4/18 had negative responses to ovalbumin, and 2/18 had negative responses to ovomucoid. Ovomucoid produced the largest skin prick test wheal in 14 of 18 patients (78%) while ovomucoid and ovalbumin wheals were equal largest in a further patient, indication that ovomucoid is the most significant egg white allergen. One patient with egg allergy had negative skin test responses to all extracts tested.
IgE assay (by RAST, CAP etc)
Number of Studies:
>20
Food/Type of allergen:
Commercial extracts were used in most studies. Commercially available purified proteins have also been used. However, Bernhisel-Broadbent et al (1994) [1269] note that some preparations of ovalbumin used in the past often contained ovomucoid and recommended repurified proteins.
Walsh et al (1988) [1215] used purified apovitellenins I and VI, phosvitin and ovomucin.
Celik-Bilgili et al. (2005) [1309] measured IgE levels to egg in 227 children who were subjected to oral challenge with hen's egg.
Perry et al. (2004) [1218] measured IgE levels to egg in 138 children who were subjected to oral challenge with egg.
Shek et al. (2004) [1214] repeatedly measured IgE levels in 88 children who were also subjected to oral challenge with egg.
Osterballe & Bindslev-Jensen (2003) [1175] measured serum IgE levels to egg in 56 children with Magic Lite system of whom 32 were reanalysed with the CAP system.
Cooke & Sampson (1997) [1274] tested sera from 45 patients selected with >20 kU/l IgE to egg and who were DBPCFC positive to egg.
Fremont et al. (1997) [1341] tested sera from 52 egg allergic patients.
Szepfalusi (1994) compared sera from 13 patients with bird-egg syndrome, 13 with egg white allergy without bird allergy and 5 with bird allergy without egg allergy.
Bernhisel-Broadbent et al (1994) [1269] tested sera from the 18 patients with egg allergy used for SPT, 10 additional egg allergic patients and 11 who had become tolerant to egg.
Walsh et al (1988) [1215] reported results from sera from 27 egg sensitive patients.
Summary of Results:
Celik-Bilgili et al. (2005) [1309] report that out of a total of 227 children, 44 had <0.35 kU/l of egg specific IgE, 17 had 0.35 to 0.7 kU/l, 61 had 0.7 to 3.5 kU/l, 69 had 3.5 to 17.5 kU/l, 26 had 17.5 to 50.0 kU/l, 5 had 50.0 to 100 kU/l and 5 had >100.0 kU/l.
Perry et al. (2004) [1218] found that the median IgE level of patients showing a clinical response was 1.2 kU/l and 0.7 kU/l for those tolerating the challenge. The number of children tolerating or reacting to challenge are listed below as a function of egg specific IgE divided into those with and without a history clearly suggesting IgE mediated allergy (groups 1 and 2)
Egg Specific IgE level
Group 1
Group 2
Tolerant
Allergic
Tolerant
Allergic
<0.35kU/l
16
8
3
2
0.36 to <1kU/l
19
11
8
2
1 to 2kU/l
14
15
7
6
>2kU/l
5
7
3
5
From this data, it was recommended that patients with <2 kU/l IgE to egg should be given an oral challenge with egg.
Shek et al. (2004) [1214] determined the probability of developing tolerance to egg based on the % decrease in specific IgE over 12 months for children diagnosed with egg allergy before age 4. Fitting by logistic regression predicted that individuals with a 99% reduction in IgE had a 0.95 probability of loosing their allergy while 90%, 75% and 50% reductions gave probabilities of 0.78, 0.65 and 0.52 respectively. In all 28 children became tolerant and 60 remained allergic. Fewer children first diagnosed older than 4 years were studied and no clear relationships predicting tolerance were seen.
Osterballe & Bindslev-Jensen (2003) [1175] report the cut-off level of a positive IgE response (0.35 kUA/L and 1.43 SU/mL, respectively) for the CAP and the Magic Lite tests. They report that a specific IgE concentration to egg white exceeding 10.8 SU/mL (ML) or 1.5 kUA/L (CAP) correlated to a greater than 95% likelihood of the patient having egg allergy. On the basis of published data the variability in the specific IgE level predicting clinical egg allergy varied from 0.35 KUA/L (Boyano Martinez et al 2001 [1324]), 6 kUA/L (Sampson & Ho, 1997 [652]; Sampson, 2001 [651]) to 17.5 KUA/L (Roehr et al 2001 [1325]). Thus Osterballe & Bindslev-Jensen (2003) [1175] concluded that data obtained in one population cannot readily be transferred to others. They attributed at least part of the differences observed in these studies to the median ages of the patients which were 16 months (Boyano Martinez et al 2001 [1324]), 13 months (Roehr et al 2001 [1325]), 2.2 years (Osterball & Bindslev-Jensen, 2003 [1175]) and 5.2 years (Sampson, 2001 [651]).
Boyano Martinez et al (2002) [1327] reported that the specific IgE level was useful in prediction for children who only had cutaneous symptoms. Half of the children younger than 2 years of age with egg allergy were able to tolerate the food after 35 months rising to 66% after 5 years.
Cooke & Sampson (1997) [1274] found that 42/45 patients had serum IgE that bound ovomucoid (Gal d 1).
Fremont et al. (1997) [1341] found that 16/52 patients had specific anti-lysozyme serum IgE.
Bernhisel-Broadbent et al (1994) [1269] found that 18 patients, who were SPT positive for egg, all had detectable serum IgE antibodies to purified ovomucoid but only 12/18 had detectable serum IgE antibodies to repurified ovalbumin (limit of assay 0.02 ng/ml). The median concentration of IgE antibodies to ovomucoid was significantly greater at the time of initial DBPCFC in 10 patients with persistent egg allergy as compared with 11 patients in whom clinical tolerance later developed (median, 44.5 ng/ml vs 3.5 ng/ml; p < 0.01). The concentration of IgE antibody to ovomucoid was also significantly greater at the time of rechallenge in the 10 patients with persistent egg hypersensitivity (median, 28.0 ng/ml vs 3.2 ng/ml, p < 0.01). There was no significant difference in the IgE antibody levels to ovalbumin in the children with persistent egg allergy compared to those who became tolerant.
Bernhisel-Broadbent et al. (1991) [1306] found that 15 of 28 egg-allergic patients had specific IgE binding against one or more of the egg yolk-derived antiviral chicken immunoglobulins.
Walsh et al (1988) [1215] found that apovitellenins I and VI, phosvitin and ovomucin all bound IgE from sera of egg allergic patients. Apovitellenins I and VI and phosvitin inhibited IgE binding to egg yoke. Ovomucin inhibited IgE binding to egg white. The percentage inhibitions are 60-70% for several patients for these allergens.
Immunoblotting
Immunoblotting separation:
Quirce et al. (2001) [1268] used 1D SDS-PAGE in reducing conditions with 2.67-12% acrylamide separating gels.
Aabin et al. (1996) [1216] used 1D SDS-PAGE by the method of Sutton et al. (1982) [1400] with 0.75 mm thickness gels and used 40 mM DTT for reduction. Ebbehoj et al. (1995) [1355] state that separating gels were 10% acryamide.
Holen & Elsayed (1990) [1354] used 1D SDS PAGE with 4% stacking and 12% separating gels, IEF from pH 4-6 and 3.5-10.5 and also 2D SDS PAGE with 10% acrylamide. 1% mercaptoethanol was present in the IEF gels and samples were reduced.
Immunoblotting detection method:
Quirce et al. (2001) [1268] electrotransferred proteins to Immobilon-Pmembranes (Millipore, Bedford, MA, USA) by the method of Towbin. Unreacted membrane sites were blocked with PBS containing 3% (w/v) human serum albumin and 0.05% (v/v) Tween-20. The membrane was then incubated with the patient's serum diluted 1:50 (v/v) in 10 mM PBS containing 0.1% (v/v) Tween-20 (PBS-T). After washing with PBS-T, the membranes were incubated with monoclonal antihuman IgE conjugated with peroxidase at a concentration of 1 µg/ml (Ingenasa SA, Madrid, Spain). The protein bands were developed with 3-3',5-5' tetramethylbencidine and oxygen peroxide as substrate.
Aabin et al. (1996) [1216] and Ebbehoj et al. (1995) [1355] electrotransferred proteins to nitro cellulose or PVDF by semidry blotting with 10 mM CAPS (N-Cyclohexyl-3-aminopropanesulfonic acid) buffer, pH 11 with 10% methanol. The membranes were blocked by soaking for 5 minutes in 150 mM NaCl, 0.2% (v/v) Tween 20, 50 mM Tris pH 10.3. IgE binding was revealed by soaking in 150 mM NaCl, 0.2% (v/v) Tween 20, 50 mM Tris pH 7.4, 0.01% (w/v) NaN3 (TSBT) and 3% (w/v) skimmed milk powder followed by incubation with sera diluted 1:10 with TSBT and then 125I-labeled rabbit anti-human IgE. Autoradiography was at -80°C and used intensifying screens.
Holen & Elsayed (1990) [1354] electrotransferred proteins to nitro cellulose. These were washed in 70 mM NaCl - phosphate buffer and blocked with 10% BSA in PBS. IgE binding was revealed with 125I-anti-IgE.
Immunoblotting results:
Several egg allergens were identified by the early 1980's. Hoffman (1983) [1332] and Langeland (1983) [1333] used electrophoresis and RAST with purified proteins to show that ovomucoid (Gal d 1) and ovalbumin (Gal d 2) were major allergens and that conalbumin (Gal d 3) and Lysozyme (Gal d 4) were minor allergens. Bernhisel-Broadbent et al (1994) [1269] suggested that early studies did not always use highly purified protein preparations to raise IgG antibodies and may have misidentified some IgE specific for ovomucoid as anti-ovalbumin IgE. Similarly, Ebbehoj et al. (1995) [1355] show that misleading results can arise using impure allergen preparations.
Quirce et al. (2001) [1268] found strong serum IgE binding at 65-70 kDa in 5/7 and weak binding in 2/7 individuals with egg allergy.
Aabin et al. (1996) [1216] report that serum IgE from 18 out of 34 individuals reacted with ovotransferrin, 13 with ovomucoid, 11 with ovalbumin and 5 with lysozyme. The appearance of the blots with unfolded protein agreed with results from dot blotting at several dilutions and suggested that the amounts of IgE bound to ovalbumin and lysozyme were generally lower than the amounts bound to ovotransferrin and ovomucoid.
Bernhisel-Broadbent et al (1991) [1306] report that 15/28 egg allergic children showed IgE against anti-viral IgY by immunodot blotting. They also show IgE binding to heavy and light chains of IgY, which were identified by specific antibodies, on immunoblots using pooled sera.
Holen & Elsayed (1990) [1354] found IgE binding at 45, 27-28, 66-70 and 14.3 kDa. Ovomucoid ran as two bands at 27-28 kDa and pH 4.4-4.6. Ovomucoid, lysozyme, ovalbumin and ovotransferrin were identified as allergens.
Oral provocation
Number of Studies:
6-10
Food used and oral provocation
vehicle
Celik-Bilgili et al. (2005) [1309] gave 0.04, 0.11, 0.38, 1.14, 3.8, 11.4 & 38.0 ml. of fresh whisked egg-white (54.9 ml. total) in total volumes of 0.2 to 200ml.
Perry et al. (2004) [1217] gave the food in escalating doses every 15 minutes until 4 g (<5 years old) or 8 g (>5 years old) of food protein had been ingested. The challenge was terminated on objective symptoms or when subjective symptoms such as abdominal pain worsened. Patients were observed in the clinic for a minimum of 4 hours or until signs of clinical reactivity subsided for those patients who failed the challenge and were instructed before discharge to contact a physician on possible late-phase reactions.
Osterballe & Bindslev-Jensen (2003) [1175] used an open food challenge with dose steps of 0.011, 0.044, 0.25, 0.5, 1, 2.5, 5, and 40 g of pasteurized whole egg, in total 49.305 g (approximately 1 egg). The dose interval was 15 minutes. The criterion for a positive outcome of challenge (egg allergy) was an immediate (maximum 2 hours after the last dose) objective reaction.
Morrisset et al. (2003) [613] gave doses of 5, 10, 50, 200 and 700 mg of raw egg white every 20 min during a period of 3 h. Stewed apples or mashed potatoes were commonly chosen as placebo.
Quirce et al. (2001) [1268] reconstituted chicken serum albumin, CSA, in saline at a concentration of 20 mg/ml, and several twofold dilutions were prepared. 1 ml. of either placebo (normal saline) or freshly prepared solutions of CSA containing 0.16, 0.31, 0.62, 1.25, 2.5, 5, and 10 mg/ml was administered orally. The dose was doubled at 30-min intervals until the patient experienced allergic symptoms, or a maximum amount of 20 mg of CSA was reached. Spirometry was performed before each oral challenge and at 10-min intervals for the first 30 min after the challenge. Patients were observed for 2 h after the last dose was administered.
Sporik et al. (2000) [1322] used egg white of a lightly boiled egg (boiled for approximately 2 min). Day 1: a drop was smeared on the buccal mucosa of the lower lip, then 1/8, 1/4, 1/2 and 1 teaspoon at 30 minute intervals. Day 2: 1 teaspoon, 2 teaspoons (approximately 1 egg white) at 30 minute intervals. Day 3: 1 egg white per day continued for a week. The procedure was repeated for egg yolk by challenge at home. 1/8 of a level (5 mL) teaspoon of egg white contains approximately 0.1 g of egg protein.
Bernhisel-Broadbent et al (1994) [1269], Sampson & Ho (1997) [652] and Sampson (2001) [651] administered up to 10 gm of dehydrated powdered egg (equivalent to 75% of an egg) and placebo disguised in juice, infant formula, or moist food (e.g., cream of rice cereal) over a 90-minute period in sequentially increasing doses until persistent objective symptoms developed or until the entire challenge dose was ingested.
Blind?
Perry et al. (2004) [1217], Osterballe & Bindslev-Jensen (2003) [1175] and Sporik et al. (2000) [1322] used open challenges.
Quirce et al. (2001) [1268], Roehr et al. (2001) [1325], Bernhisel-Broadbent et al (1994) [1269], Sampson & Ho (1997) [652] and Sampson (2001) [651] used DBPCFC.
Morrisset et al. (2003) [613] used double or single blind challenges.
Celik-Bilgili et al. (2005) [1309] used open challenges for patients below age 1 year with history of immediate type reactions and blind challenges for other patients.
Number of Patients?
Celik-Bilgili et al. (2005) [1309] reported 227 challenges with hen's egg.
Perry et al. (2004) [1217] report 133 challenges with egg and 56 "failed" challenges (42%). The median age was 5.5 years for the 56 allergic children.
Osterballe & Bindslev-Jensen (2003) [1175] challenged 56 children with suspected egg allergy.
Roehr et al. (2001) [1325] challenged 42 children with egg.
Sporik et al. (2000) [1322] reported 121 oral challenges with egg.
Bernhisel-Broadbent et al (1994) [1269] reported 13 challenges to confirm allergy and repeated challenges on 21 children to follow the development of tolerance.
Dose response
Perry et al. (2004) [1217] did not report a detailed dose response but note that severe symptoms tended to occur with low doses.
Osterballe & Bindslev-Jensen (2003) [1175] report that children aged <2 years showed a mean LOAEL (lowest observed adverse effect level) of 1.6 g. and mean NOAEL (no observed adverse effect level) of 1.0 g. Children aged >2 years showed a mean LOAEL of 6.1 g. and mean NOAEL of 2.2 g. (the mean LOAEL was reduced to 3.4 g. if a single patient reacting to 49 g. was removed). The range of LOAELs was from 0.011 to 49 g and there was no significant relationship between the threshold level and the age of the patients.
Morrisset et al. (2003) [613] reported a threshold ≤15 mg of solid food in 5.6% of egg allergies. The lowest reactive threshold was observed at less than 2 mg of crude egg.
Taylor et al. (2002) [639] have collected data from several studies with the aim of defining thresholds for reaction to egg (281 patients in total). The lowest provoking dose was 1 mg of liquid whole egg, which was seen with 2 patients.
Symptoms
Celik-Bilgili et al. (2005) [1309] report that 12%, 42%, 67%, 93% and 96% of children with <0.35, 0.35 to 0.7 kU/l, 0.7 to 3.5, 3.5 to 17.5 kU/l and 17.5 to 50.0 kU/l, of egg specific IgE respectively reacted to oral egg challenges as did all those with >50.0 kU/l.
Perry et al. (2004) [1217] report that the symptoms of the 56 patients reacting to egg were associated with skin (43 patients, 77%), oral (12 patients, 21%), upper respiratory (15 patients, 27%), lower respiratory (19 patients, 34%) and gasterointestinal (31 patients, 55%). Symptoms were described as mild (18, 32%), moderate (17, 30%) or severe (21, 38%). There was no significant correlation between symptom severity and IgE level to egg.
Morrisset et al. (2003) [613] reported the frequency of serious clinical reactions on egg challenge as 2% drop in blood pressure (and/or tachycardia) and 12% severe respiratory symptoms.
Quirce et al. (2001) [1268] reported that ten minutes after oral administration of 15 mg of CSA, patient 1 experienced severe ocular injection, chemosis, and ocular itching, as well as angioedema of the oral mucosa, tongue, and eyelids. Patient 5 suffered intense itching in the oropharynx and ears 5 min after 10 mg of CSA was administered, followed by abdominal pain and coughing 10 min after the challenge.
Osterballe & Bindslev-Jensen (2003) [1175] reported that 36 out of 56 children reacted to the challenge with egg. The symptoms elicited during challenge consisted of immediate urticaria in 95% of patients and rhinoconjunctivitis in 5% of patients.
Roehr et al. (2001) [1325] reported that 28/44 (67%) challenges with egg were positive.
Sporik et al. (2000) [1322] reported that 77% of challenges with egg were positive with 72% immediate reactions and 5% delayed reactions.
Bernhisel-Broadbent et al (1994) [1269] reported that patients with persistent egg allergy were more likely to have symptoms involving multiple target organs during their first DBPCFC (8 of 10 patients) compared with children who became clinically tolerant (3 of 11 patients).
IgE cross-reactivity and Polysensitisation
Eggs from several other species of birds are eaten and these generally cause reactions in individuals allergic to hen's eggs. These include turkey, duck, goose, seagull (Langeland, 1983) [1212] and quail (Alessandri et al., 2005) [1213]. However, Añíbarro et al. (2000) [1281] report that allergy to duck and goose eggs may not always involve allergy to hen's eggs.
Chicken meat also contains some of the known egg allergens and cross-reactivity is observed with both meat and bird feathers (Anibarro Bausela et al. 1991 [1283]; Szepfalusi et al. 1994 [1275]; Anibarro Bausela et al. 1997 [1267]).
Other Clinical information
Eggesbo et al. (2001) [1329] calculated the prevalence of allergy to egg at 1.6% in children aged 2.5 years, and egg allergy occurs in more than 35% of children with atopic dermatitis (Oehling et al, 1998 [1330]; Kim et al. 2002 [1361]). Lever et al. (1998) [1337] and Aoki et al. (1992) [1338] have used exclusion diets to demonstrate the importance of egg allergy in children with atopic dermatitis. By contrast, egg allergy is rare in adults (Zuberbier et al. 2004 [1051]).
Urisu et al. (1999) [1254] reported that subjects with high IgE-binding activity to pepsin treated ovomucoid are unlikely to outgrow egg white allergy.
Diagnosis of egg allergy by the atopy patch test (APT) has led to apparently conflicting results. Osterballe et al. (2004) [1340] (also Hansen et al. (2004) [1294]) conclude that the APT cannot be recommended in daily practice for the diagnosis of hypersensitivity to cow's milk and hen's egg in children 3 years of age. By contrast, Roehr et al. (2001) [1325] suggest that the combination of positive APT results and measurement of levels of specific IgE makes double-blind, placebo-controlled, food challenges superfluous for suspected cow's milk and hen's egg allergy. Yamada et al (2000) [1353] suggest that some egg challenge negative patients with positive APT have IgE reactive to proteolytically labile peptides.
Escudero et al. (2003) [1331] report that egg white proteins can cause baker's asthma and that 3 of these patients became food allergic to egg after occupational exposure.
As many vaccines are produced using hen's eggs, there is a potential for adverse reaction in patients with egg allergy. Kelso & Yunginger (2003) [1645] discuss differences in vaccine preparation and the quantitation of residual egg-derived protein in each vaccine. The frequency and severity of vaccine-induced allergic reactions are reviewed, and an algorithm is described for the preimmunization evaluation of egg-sensitive individuals.
Vlieg-Boerstra et al (2004) [1661] report the development and validation of recipes for double blind oral challenge with several allergenic foods including egg.
General surveys of methods used for oral challenges in hospitals have been published such as Martelli et al. (2005) [1504].
Although Walsh et al (1988) [1215] and Walsh et al (2005) [1646] report phosvitin derived from Vitellogenin I, II and III precursors, P87498, P02845 and Q91025, as an allergen, only 2 sera showed >10% uptake in RAST. Thus this allergen has not yet been given a biochemical entry.
Reviews (2)
Martorell Aragones A, Bone Calvo J, Garcia Ara MC, Nevot Falco S, Plaza Martin AM; Food Allergy Committee of the Spanish Society of Pediatric Clinical Immunology and Allergy.
Allergy to egg proteins. Food Allergy Committee of the Spanish Society of Pediatric Clinical Immunology and Allergy. Allergol Immunopathol (Madr). 29(2):72-95.
2001
PUBMED ID:
11420031
Aabin B, Poulsen LK, Ebbehoj K, Norgaard A, Frokiaer H, Bindslev-Jensen C, Barkholt V.
Identification of IgE-binding egg white proteins: comparison of results obtained by different methods. Int Arch Allergy Immunol. 109(1):50-57. 1996
PUBMED ID:
8527951
Añíbarro B, Seoane FJ, Vila C, Lombardero M.
Allergy to eggs from duck and goose without sensitization to hen egg proteins. J Allergy Clin Immunol. 105(4):834-836. 2000
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