Divers aliments

[1] - Lombardi C, Senna GE, Gatti B, Feligioni M, Riva G, Bonadonna P, et al. Allergic reactions to honey and royal jelly and their relationship with sensitization to compositae. Allergol Immunopathol (Madr) 1998;26:288-290

Honey and royal jelly are complex etherogeneous mixtures of flowers' nectar, sugars, proteins and bee's glandular secretions. The existence of a type I hypersensitivity to honey is still matter of debate, while an aetiological role of Compositae pollens in the clinical manifestations following honey ingestion has been envisaged. We describe two cases of severe systemic reactions (anaphylaxis and generalized urticaria/angioedema) due to honey and royal jelly ingestion in patients sensitized to compositae (mugwort). Both patients had a skin and RAST positivity to mugwort and a positive prick-by-prick to the offending foods. Moreover, in one of the two patients the RAST-inhibition assay showed the strong cross-reactivity between the proteins of honey and mugwort and the SDS-PAGE analysis showed that the major proteic bands from honey and mugwort extracts are largely superimposable. Both the clinical data and the laboratory analysis support the hypothesis of a strict link between sensitization to compositae and adverse reactions to honey and jelly.

↩

[2] - Fuiano N, Incorvaia C, Riario-Sforza GG, Casino G. Anaphylaxis to honey in pollinosis to mugwort: a case report. Eur Ann Allergy Clin Immunol 2006;38:364-365

A case of anaphylaxis to honey in a 19 year old female sensitized to Compositae pollen is described. The patient suffered from summer rhinoconjunctivitis since seven years; in January 2006, ten minutes after eating bread and honey she developed angioedema of the lips and tongue, runny nose, cough, dyspnoea, and collapse, requiring hospitalization and treatment with high dose corticosteroids and anti-histamines. After two weeks, skin prick tests (SPT) with a standard panel of inhalant allergens and prick + prick with a number of kinds of honey were performed. SPTs were positive to mugwort, ragweed, dandelion, and goldenrod. Concerning honey, the prick + prick was positive to "Millefiori" (obtained from bees foraging on Compositae) and also to sunflower, limetree, and gum tree honey, while was negative for other kinds of honey, including the frequently used chestnut honey and acacia honey. The allergenic component responsible of anaphylaxis in this case seems to be a molecule occurring in Compositae pollens, as previously reported for other three reports, but also in pollen from plants of different families.Honey contains a large number of components derived from bees, such as gland secretions and wax, as well as from substances related to their foraging activity, such flower nectar and pollens (1, 2). Honey as a food has been associated to allergic reactions and particularly to anaphylaxis (3-6). Among the pollens, the role of Compositae is somewhat controversial, since its responsibility is clear in some studies (3, 5, 6) but considered negligible in others (7). Here we present the case of a patient sensitized to Compositae pollen who had an anaphylactic reaction to the ingestion of honey obtained from bees foraging on Compositae flowers and was tested with a number of different varieties of honey.

↩

[3] - Pitsios C, Vartholomeos S, Ergazakis M, Kompoti E, Kontou-Fili K. Honey hypersensitivity in two atopic patients. EAACI 23th Congress, Amsterdam, 12-16 June, 2004, Poster n°973

Pollens, glandular glycoproteins and bee-body material are the constituents of honey, mainly responsible for rare food-induced reactions. Two cases of patients with mild systemic reactions after ingestion of honey are reported in this study. Methodology: The first case is a 21-years-old male with a history of seasonal rhinitis, conjunctivitis and mild asthma. Soon after the ingestion of honey he reported rhinitis, conjunctivitis and oral pruritus that were successfully treated with antihistamine p.o. The second case is a 24-years-old female with a history of seasonal rhinitis and asthma. She reported two episodes of generalized urticaria and gastrointestinal symptoms, ten minutes after the ingestion of a sweet containing honey and walnuts. Symptoms dissolved after treatment with corticosteroids and antihistamines. She used to eat tree-nuts with no signs of allergic reactions. Skin Prick Test (SPT) with commercial extracts of aeroallergens, food allergens and prick-to-prick (P-P) with two different in origin samples of honey were performed. SPT was also performed with homemade bee whole body extract (BWB). Serum specific IgE (sIgE) CAP to pollens, food allergens and bee venom was investigated. Double blind placebo controled food challenge (DBPCFC) was proposed to confirm the diagnosis. Results: Pat. 1: SPT and CAP were positive for Olea europea, Parietaria, Chenopodium and P-P were positive to both honeys. SPT to other foods, BWB and sIgE to bee venom was negative. DBPCFC was performed at our outpatient clinic using honey of local origin and corn syrup as placebo. Increasing doses were administered with intervals of 30 minutes. The challenge resulted positive at the total intake of 3,35g of honey. The patient presented sneezing, nasal pruritus, congestion, a 50% decrease of nasal peak flow and conjunctivitis. The symptoms dissolved 30 min after the administration of 10mg cetirizine. Pat. 2: SPT were positive for mixed Grasses extract and both honeys. sIgE confirmed hypersensitivity to Grasses. No positive reaction was shown to tree-nuts, other foods or BWB. Bee venom sIgE was negative. DBPCFC was not accepted by patient. She ever since avoids honey and honey sweets referring no problem. An emergency set (epinephrine, cetirizine and cortisone) was prescribed. Conclusions: Honey ingestion may cause mild allergic reactions. In our patients the pollen proteins contained in honey appear to be the responsible allergens.

↩

[4] - Bousquet J, Dhivert H, Clauzel AM, Hewitt B, Michel FB. Occupational allergy to sunflower pollen. J Allergy Clin Immunol 1985;75:70-74

Although the sunflower belongs to the Compositeae family, allergy to sunflower pollen is not common. The occurrence of occupational allergy to this pollen species made it possible to characterize cross-reactive patterns of Compositeae pollens in a human experimental model. A 24-yr-old man developed rhinitis and conjunctivitis over 5 yr of exposure to sunflower pollens, and asthma developed during the fifth year. All respiratory and occular symptoms disappeared after he was removed from exposure, but he had a food allergic reaction while he was eating honey containing 30% sunflower pollens. The diagnosis of occupational allergy was based on history, skin prick tests and RAST to the pollen. Bronchial provocation tests performed after removal from exposure confirmed the sensitivity to sunflower pollens but there was no nonspecific hyperreactivity. It was found by RAST inhibition that sunflower pollen does not cross-react with other Compositeae pollens tested or with sunflower seed. The honey that elicited food intolerance was demonstrated to inhibit significantly sunflower pollen RAST

↩

[5] - Bousquet J, Campos J, Michel FB. Food intolerance to honey. Allergy 1984;39:73-75

A 42 year-old beekeeper who had an inhalant allergy to Compositeae pollen presented an adverse reaction while eating a honey which contained large numbers of Compositeae pollens. As she was not intolerant to honey of own production, which contained no Compositeae pollen, the adverse reaction seems to be attributed to these pollens.

↩

[6] - Arbab E, Grims R. Bee-venom and honey allergy. Allergy 2007;62(suppl. 83):79-80

Background: Honey allergy is a very rare condition, which shows clinical pictures ranging from cough to anaphylaxis after ingestion of honey. Patients sensitized to bee venom and concomitantly allergic to honey are even scarcer and pose the following question: Does specific immunotherapy (SIT) with bee venom prevent allergic reactions after honey ingestion. Case: A 37-year-old woman had a history of systemic grade II reactions after bee stings since 5 years. The patient reported about two episodes of similar reactions after honey ingestion in the last couple of months. Results: Her specific IgE level for bee venom and honey was class 2 and class 1, respectively, counting a total IgE of 296 kU/l. Skin tests for bee venom were positive at 300µg/ml prick and at 0,1 µg/ml intradermal. Prick test with honey was also positive. Conclusion: Proteins responsible for honey allergy are derived from proteins secreted by bees and from proteins derived from plant pollens. In this case a SIT with bee venom was recently introduced on the one hand due to patient's sensitization to bee venom and as a possible therapy for the honey allergy on the other hand.

↩

[7] - Sánchez Palacios A, Schamann F, Garcia Marreo JA, Figueroa J, Gallego M. Anaphylaxis induced by Matricaria chamomilla and honey in two asthmatic patients sensitized to Artemisia vulgaris pollen. Allergy 2007;62(suppl. 83):358

Introduction We describe 2 cases of severe anaphylaxis in 2 patients with allergic rhinitis and bronchial asthma sensitized to Artemisia vuglaris. These patients experienced the reactions after an eye wash with a chamomile solution and after the ingestion of honey. Material and Methods First case: 24 years old woman.Rhinitis and asthma seasonal allergy several minutes after an eye wash with a chamomile solution.Angioedema, shortness of breath. Lost of consciousness which required admission and treatment at the emergency. SPT: - Skin prick test aeroallergens and extract of M. chamomilla 5% w/v - Conjuntival provocation test (CPT) 0.001 - 100 UB/ml - IgE specific. - In vitro cross-reactivity between Artemisa vulgaris and chamomile ELISA inhibition. Second case: 36 years old male.Rhinitis and asthma seasonal allergy after ingestion of honey and fermented aqueous honey solution (hidromiel).Facial angioedema, bronchospasm and luss of consciousness. SPT acroallergens and extrac honey solution specificise. SDS - Page and inmunoblots RESULTS SPT positive: - L. peronne.A. vulgaris.Taraxacum officinali.M. chamomilla Specific IgE - ELISA inhibition - Chamomilla inhibited > 80%.Specific IgE binding to A. vulgaris Conclusions: 1.-The first case is severe anaphylaxis inouced by matricaria chamomilla wich show cross Reactivity to Artemisia vulgaris. 2.-The second case is severe anaphylaxis after the ingestion of honey and hidromiel. 3.-The microscopic exam of the honey and hidromiel revealed the presence of pollens of Composital and of eucalyptus spp. 4.-The patient had positive skin test to artemisa vulgaris,celery and honey. 5.-Pollen extracts of several compositae plants were able to inhibit IgE binding to hidromiel, Where Eucalyptus spp.Pollen did not inhibit.

↩

[8] - Ibero M, Castillo MJ, Pineda F, Palacios R, Martinez J. Whole bee for diagnosis of honey allergy. Allergy 2002;57:557-558

↩

[9] - Fuiano N, Incorvaia C, Riario-Sforza GG, Casino G. Anaphylaxis to honey in pollinosis to mugwort: a case report. Eur Ann Allergy Clin Immunol 2006;38:364-365

A case of anaphylaxis to honey in a 19 year old female sensitized to Compositae pollen is described. The patient suffered from summer rhinoconjunctivitis since seven years; in January 2006, ten minutes after eating bread and honey she developed angioedema of the lips and tongue, runny nose, cough, dyspnoea, and collapse, requiring hospitalization and treatment with high dose corticosteroids and anti-histamines. After two weeks, skin prick tests (SPT) with a standard panel of inhalant allergens and prick + prick with a number of kinds of honey were performed. SPTs were positive to mugwort, ragweed, dandelion, and goldenrod. Concerning honey, the prick + prick was positive to "Millefiori" (obtained from bees foraging on Compositae) and also to sunflower, limetree, and gum tree honey, while was negative for other kinds of honey, including the frequently used chestnut honey and acacia honey. The allergenic component responsible of anaphylaxis in this case seems to be a molecule occurring in Compositae pollens, as previously reported for other three reports, but also in pollen from plants of different families.Honey contains a large number of components derived from bees, such as gland secretions and wax, as well as from substances related to their foraging activity, such flower nectar and pollens (1, 2). Honey as a food has been associated to allergic reactions and particularly to anaphylaxis (3-6). Among the pollens, the role of Compositae is somewhat controversial, since its responsibility is clear in some studies (3, 5, 6) but considered negligible in others (7). Here we present the case of a patient sensitized to Compositae pollen who had an anaphylactic reaction to the ingestion of honey obtained from bees foraging on Compositae flowers and was tested with a number of different varieties of honey.

↩

[10] - Arbab E, Grims R. Bee-venom and honey allergy. Allergy 2007;62(suppl. 83):79-80

Background: Honey allergy is a very rare condition, which shows clinical pictures ranging from cough to anaphylaxis after ingestion of honey. Patients sensitized to bee venom and concomitantly allergic to honey are even scarcer and pose the following question: Does specific immunotherapy (SIT) with bee venom prevent allergic reactions after honey ingestion. Case: A 37-year-old woman had a history of systemic grade II reactions after bee stings since 5 years. The patient reported about two episodes of similar reactions after honey ingestion in the last couple of months. Results: Her specific IgE level for bee venom and honey was class 2 and class 1, respectively, counting a total IgE of 296 kU/l. Skin tests for bee venom were positive at 300µg/ml prick and at 0,1 µg/ml intradermal. Prick test with honey was also positive. Conclusion: Proteins responsible for honey allergy are derived from proteins secreted by bees and from proteins derived from plant pollens. In this case a SIT with bee venom was recently introduced on the one hand due to patient's sensitization to bee venom and as a possible therapy for the honey allergy on the other hand.

↩

[11] - Sánchez Palacios A, Schamann F, Garcia Marreo JA, Figueroa J, Gallego M. Anaphylaxis induced by Matricaria chamomilla and honey in two asthmatic patients sensitized to Artemisia vulgaris pollen. Allergy 2007;62(suppl. 83):358

Introduction We describe 2 cases of severe anaphylaxis in 2 patients with allergic rhinitis and bronchial asthma sensitized to Artemisia vuglaris. These patients experienced the reactions after an eye wash with a chamomile solution and after the ingestion of honey. Material and Methods First case: 24 years old woman.Rhinitis and asthma seasonal allergy several minutes after an eye wash with a chamomile solution.Angioedema, shortness of breath. Lost of consciousness which required admission and treatment at the emergency. SPT: - Skin prick test aeroallergens and extract of M. chamomilla 5% w/v - Conjuntival provocation test (CPT) 0.001 - 100 UB/ml - IgE specific. - In vitro cross-reactivity between Artemisa vulgaris and chamomile ELISA inhibition. Second case: 36 years old male.Rhinitis and asthma seasonal allergy after ingestion of honey and fermented aqueous honey solution (hidromiel).Facial angioedema, bronchospasm and luss of consciousness. SPT acroallergens and extrac honey solution specificise. SDS - Page and inmunoblots RESULTS SPT positive: - L. peronne.A. vulgaris.Taraxacum officinali.M. chamomilla Specific IgE - ELISA inhibition - Chamomilla inhibited > 80%.Specific IgE binding to A. vulgaris Conclusions: 1.-The first case is severe anaphylaxis inouced by matricaria chamomilla wich show cross Reactivity to Artemisia vulgaris. 2.-The second case is severe anaphylaxis after the ingestion of honey and hidromiel. 3.-The microscopic exam of the honey and hidromiel revealed the presence of pollens of Composital and of eucalyptus spp. 4.-The patient had positive skin test to artemisa vulgaris,celery and honey. 5.-Pollen extracts of several compositae plants were able to inhibit IgE binding to hidromiel, Where Eucalyptus spp.Pollen did not inhibit.

↩

[12] - Lombardi C, Senna GE, Gatti B, Feligioni M, Riva G, Bonadonna P, et al. Allergic reactions to honey and royal jelly and their relationship with sensitization to compositae. Allergol Immunopathol (Madr) 1998;26:288-290

Honey and royal jelly are complex etherogeneous mixtures of flowers' nectar, sugars, proteins and bee's glandular secretions. The existence of a type I hypersensitivity to honey is still matter of debate, while an aetiological role of Compositae pollens in the clinical manifestations following honey ingestion has been envisaged. We describe two cases of severe systemic reactions (anaphylaxis and generalized urticaria/angioedema) due to honey and royal jelly ingestion in patients sensitized to compositae (mugwort). Both patients had a skin and RAST positivity to mugwort and a positive prick-by-prick to the offending foods. Moreover, in one of the two patients the RAST-inhibition assay showed the strong cross-reactivity between the proteins of honey and mugwort and the SDS-PAGE analysis showed that the major proteic bands from honey and mugwort extracts are largely superimposable. Both the clinical data and the laboratory analysis support the hypothesis of a strict link between sensitization to compositae and adverse reactions to honey and jelly.

↩

[13] - Codreanu F. L'activité du réseau Allergo-Vigilance: allergies alimentaires. Alim'Inter 2007;12:239-242

↩

[14] - Garcia Ortiz JC, Cosmes Martin P, Lopez-Asunsolo A. Allergy to foods in patients monosensitized to Artemisia pollen. Allergy 1996;51:927-931

It is known that patients with pollinosis may display clinical characteristics caused by allergy to certain fruits and vegetables, but subjects allergic to Artemisia seem to show particularly peculiar characteristics. The clinical features of 84 patients with rhinitis, asthma, urticaria, and/or anaphylaxis whose inhalant allergy was exclusively to Artemisia vulgaris were studied and compared with a control group of 50 patients monosensitized to grass pollen. The mean age for the beginning of symptoms was 30.2 years, and this was higher than in the control group (P < 0.05). We found the main incidence to be in women (70.2%). Some 42.3% had family history of atopia, lower than in the control group (P < 0.05), while the prevalence of asthma and urticaria was significantly higher (P < 0.05). Food hypersensitivity was reported by 23 patients (27.3%) allergic to Artemisia. The foods responsible (with respective numbers of cases) were honey (14), sunflower seeds (11), camomile (four), pistachio (three), hazelnut (two), lettuce (two), pollen (two), beer (two), almond (one), peanut (one), other nuts (one), carrot (one), and apple (one). None of the patients monosensitized to grass had food allergy. CAP inhibition experiments were carried out on a single patient. Results showed the existence of common antigenic epitopes in pistachio and Artemisia pollen for this patient. We concluded that mugwort hay fever can be associated with the Compositae family of foods, but that it is not normally associated with other foods.

↩

[15] - Pitsios C, Chliva C, Mikos N, Kompoti E, Nowak-Wegrzyn A, Kontou-Fili K. Bee pollen sensitivity in airborne pollen allergic individuals. Ann Allergy Asthma Immunol 2006;97:703-706

BACKGROUND: Physicians who practice alternative medicine often prescribe bee pollen as a food supplement and a treatment for various ailments. OBJECTIVES: To determine the qualitative and quantitative composition of bee pollen and to investigate the cutaneous reactivity of atopic patients to bee pollen extracts. METHODS: The absolute number of pollen grains per gram of bee pollen was calculated, and morphologic identification of the botanical family was performed. Five extracts of bee pollen were prepared for skin prick testing, according to standard methods. Two hundred two volunteers participated in the study; 145 were atopic patients with respiratory allergy. The remaining 57 were healthy volunteers or nonatopic patients and served as a control group. All participants underwent skin prick testing with a standard battery of 6 aeroallergens (olive, grasses mix, Parietaria, mugwort, Dermatophagoides pteronyssinus, and Dermatophagoides farinae) and with all homemade bee pollen extracts. RESULTS: All samples of bee pollen contained Oleaceae pollen in high concentrations. Small amounts of anemophilous pollen (Compositeae, Chenopodiaceae) were detected in various samples. A strong positive correlation was observed between cutaneous reactivity to bee pollen extracts and olive, grasses, and mugwort. CONCLUSIONS: Bee pollen contains a large amount of pollen, which belongs to various allergenic families of plants. Bee pollen retains its allergenic potential as demonstrated by strong cutaneous responses to bee pollen extracts observed in atopic patients in contrast to nonatopic subjects. Regarding pollen allergic individuals, further studies are needed to evaluate the safety of ingesting large amounts of bee pollen.

↩

[16] - Martín Muñoz M, Bartolomé B, Caminoa M, Bobolea I, Quirce S. Bee pollen allergy in a young child. Allergy 2009;64(Suppl. 90):200-201

Background: A 4-years-old boy developed, intense itching on his lips, mouth, pharynx, ears and tongue immediately after bee pollen ingestion. A few minutes later he experienced changes in his voice with edema on his uvula and pharynx. It was the first time he had taken pollen or honey bee. Material and Methods: We realized A prick by prick test with pollen bee. Skin prick tests (SPTs) were performed with important local pollens, house dust mites, common fungi and animal dander. The composition of pollen bee was investigated. Serum tryptasa and total and specific serum IgE to bee pollen, Lolium perenne, Ole europaea, Platanus acerifolia, Cupresus arizonica, Taraxacum and Artemisia vulgaris and to specific allergens (n Art v 1, n Ole e2, n Lol p1, Pla a2, Pla a1 and pesch LTP) were determinated. SDS-PAGE immunoblotting and SDS-PAGE immunobloting inhibition were carried out to determine the responsible allergens of reaction. Results: Skin prick test resulted positives to all pollens and negative with rest of allergens. The pollen bee composition was about 25% Quercus pollen, 16% Rosaceae pollen, 12% Compositae pollen. Total IgE was 435 ku/l. Serum specific IgE to bee pollen was 6 ku/l. Specific serum IgE to Artemisia vulgaris, Taraxacum, Cupressus arizónica, Olea europaea, Platanus acerifolia, Lolium perenne and Art v 1, Ole e 1, Lol p1 and Pla a 2 resulted mayor than 0,35 ku/L in each case. Tryptasa levels were normal. SDS-PAGE immunoblotting and SDSPAGE immunoblotting inhibition confirmed Artemisia vulgaris as responsible of reaction to bee pollen. Conclusion: Bee and honey pollen, royal jelly or propolis should not be used in patients with an allergic predisposition, in particular in people with pollen allergy. Warning labels of possible adverse reactions should be presented on the packaging of these products to protect the public from this hazard.

↩

[17] - Pitsios C, Vartholomeos S, Ergazakis M, Kompoti E, Kontou-Fili K. Honey hypersensitivity in two atopic patients. EAACI 23th Congress, Amsterdam, 12-16 June, 2004, Poster n°973

Pollens, glandular glycoproteins and bee-body material are the constituents of honey, mainly responsible for rare food-induced reactions. Two cases of patients with mild systemic reactions after ingestion of honey are reported in this study. Methodology: The first case is a 21-years-old male with a history of seasonal rhinitis, conjunctivitis and mild asthma. Soon after the ingestion of honey he reported rhinitis, conjunctivitis and oral pruritus that were successfully treated with antihistamine p.o. The second case is a 24-years-old female with a history of seasonal rhinitis and asthma. She reported two episodes of generalized urticaria and gastrointestinal symptoms, ten minutes after the ingestion of a sweet containing honey and walnuts. Symptoms dissolved after treatment with corticosteroids and antihistamines. She used to eat tree-nuts with no signs of allergic reactions. Skin Prick Test (SPT) with commercial extracts of aeroallergens, food allergens and prick-to-prick (P-P) with two different in origin samples of honey were performed. SPT was also performed with homemade bee whole body extract (BWB). Serum specific IgE (sIgE) CAP to pollens, food allergens and bee venom was investigated. Double blind placebo controled food challenge (DBPCFC) was proposed to confirm the diagnosis. Results: Pat. 1: SPT and CAP were positive for Olea europea, Parietaria, Chenopodium and P-P were positive to both honeys. SPT to other foods, BWB and sIgE to bee venom was negative. DBPCFC was performed at our outpatient clinic using honey of local origin and corn syrup as placebo. Increasing doses were administered with intervals of 30 minutes. The challenge resulted positive at the total intake of 3,35g of honey. The patient presented sneezing, nasal pruritus, congestion, a 50% decrease of nasal peak flow and conjunctivitis. The symptoms dissolved 30 min after the administration of 10mg cetirizine. Pat. 2: SPT were positive for mixed Grasses extract and both honeys. sIgE confirmed hypersensitivity to Grasses. No positive reaction was shown to tree-nuts, other foods or BWB. Bee venom sIgE was negative. DBPCFC was not accepted by patient. She ever since avoids honey and honey sweets referring no problem. An emergency set (epinephrine, cetirizine and cortisone) was prescribed. Conclusions: Honey ingestion may cause mild allergic reactions. In our patients the pollen proteins contained in honey appear to be the responsible allergens.

↩

[18] - Rosmilah M, Shahnaz M, Patel G, Lock J, Rahman D, Masita A et al. Characterization of major allergens of royal jelly Apis mellifera. Trop Biomed 2008;25:243-251

Abstract Royal jelly is widely consumed in the community and has perceived benefits ranging from promoting growth in children and improvement of general health status to enhancement of longevity for the elderly. However, royal jelly consumption has been linked to contact dermatitis, acute asthma, anaphylaxis and death. High prevalence of positive skin tests to royal jelly have been reported among atopic populations in countries with a high rate of royal jelly consumption. The present study is aimed to identify the major allergens of royal jelly. Royal jelly extract was separated by sodium dodecyl polyacrylamide gel electrophoresis (SDS-PAGE) and 2-dimensional electrophoresis (2-D). Immunoblotting of the SDS-PAGE and 2-D profiles were performed to identify the allergenic spots. Spots were then excised from the 2-D gel, digested with trypsin and analyzed by mass spectrometry. The SDS-PAGE of royal jelly extract revealed 18 bands between 10 to 167 kD. Western blot of the fractionated proteins detected 15 IgE-binding band s between 14 to 127 kD with seven major allergens of 32, 40, 42, 49, 55, 60 and 67 kD using serum from 53 subjects with royal jelly allergy. The 2-D gel fractionated the royal jelly proteins to more than 50 different protein spots. Out of these, 30 spots demonstrated specific IgE affinity to the sera tested. Eight spots of the major royal jelly allergens were selected for mass-spectrometry analysis. Digested tryptic peptides of the spots were compared to the amino acid sequence search in protein databases which identified the fragments of royal jelly homologus to major royal jelly protein 1 (MRJ1) and major royal jelly protein 2 (MRJ2). In conclusion, the major allergens of royal jelly are MRJ1 and MRJ2 in our patients' population

↩

[19] - Kimura Y, Miyagi C, Kimura M, Nitoda T, Kawai N, Sugimoto H. Structural features of N-glycans linked to royal jelly glycoproteins: structures of high-mannose type, hybrid type, and biantennary type glycans. Biosci Biotechnol Biochem 2000;64:2109-2120

The structures of N-glycans of total glycoproteins in royal jelly have been explored to clarify whether antigenic N-glycans occur in the famous health food. The structural feature of N-glycans linked to glycoproteins in royal jelly was first characterized by immunoblotting with an antiserum against plant complex type N-glycan and lectin-blotting with Con A and WGA. For the detail structural analysis of such N-glycans, the pyridylaminated (PA-) N-glycans were prepared from hydrazinolysates of total glycoproteins in royal jelly and each PA-sugar chain was purified by reverse-phase HPLC and size-fractionation HPLC. Each structure of the PA-sugar chains purified was identified by the combination of two-dimensional PA-sugar chain mapping, ESI-MS and MS/MS analyses, sequential exoglycosidase digestions, and 500 MHz 1H-NMR spectrometry. The immunoblotting and lectinblotting analyses preliminarily suggested the absence of antigenic N-glycan bearing beta1-2 xylosyl and/or alpha1-3 fucosyl residue(s) and occurrence of beta1-4GlcNAc residue in the insect glycoproteins. The detailed structural analysis of N-glycans of total royal jelly glycoproteins revealed that the antigenic N-glycans do not occur but the typical high mannose-type structure (Man(9 to approximately 4)GlcNAc2) occupies 71.6% of total N-glycan, biantennary-type structures (GlcNAc2Man3 GlcNAc2) 8.4%, and hybrid type structure (GlcNAc1 Man4GlcNAc2) 3.0%. Although the complete structures of the remaining 17% N-glycans; C4, (HexNAc3 Hex3HexNAc2: 3.0%), D2 (HexNAc2Hex5HexNAc2: 4.5%), and D3 (HexNAc3Hex4HexNAc2: 9.5%) are still obscure so far, ESI-MS analysis, exoglycosidase digestions by two kinds of beta-N-acetylglucosaminidase, and WGA blotting suggested that these N-glycans might bear a beta1-4 linkage N-acetylglucosaminyl residue.

↩

[20] - Katayama M, Aoki M, Kawana S. Case of anaphylaxis caused by ingestion of royal jelly. J Dermatol 2008;35:222-224

Anaphylaxis is a severe form of allergic disease. Royal jelly is widely consumed in Japan, but a few cases of anaphylaxis caused by royal jelly have been reported. We encountered a 26-year-old Japanese woman who developed anaphylaxis after drinking a beverage of crude royal jelly including honey. She had a history of bronchial asthma, allergic rhinitis, allergic conjunctivitis, atopic dermatitis and food allergy (abalone). Prick tests were performed with the beverage of crude royal jelly including honey and with two other beverages including honey. Only the crude royal jelly beverage showed a positive reaction. An oral challenge test with the crude royal jelly beverage was not performed, but a similar test with a beverage including honey caused no symptoms. A positive response to the beverage of crude royal jelly was not observed in normal volunteers. A positive diagnosis of anaphylaxis due to royal jelly was made based on the positive prick test, systemic clinical symptoms and the negative prick tests in healthy volunteers. Moreover, the patient had no symptoms when taking lemon and orange, which were present as essences in the crude royal jelly beverage, and also had no response to honey after anaphylaxis. Increased consumption of royal jelly in health food supplements may increase the incidence of royal jelly-related allergic reactions. Therefore, royal jelly should be considered as a causative allergen in food-induced anaphylaxis.

↩

[21] - Arroabarren E, Echechipía S, Aldunate MT, Garrido S, Goienetxe E, García BE, et al. Allergy to Royal jelly: 2 cases. EAACI 23th Congress, Amsterdam, 12-16 June, 2004, Poster n°974

Background: Royal jelly (RJ) is secreted by worker bees hypopharingeal glands and approximately 50% of its dry weight consists of proteins. In recent years asthma and anaphylaxis cases related to royal jelly ingestion haven been described and frequent sensitisation in pollen allergic patients has been observed. So far there are no data about possible cross-reactivity between D. pteronyssinus and RJ. We describe 2 asthmatic, dust-mite allergic patients, who presented, respectively, an anaphylaxis (generalized urticaria, dyspnea and vomiting) and an asthma attack after the ingestion of RJ containing compounds. Methods: SPT with the responsible compound, as well as with every single component and RJ extract of our own were performed, and so were with common inhalants and pollens including compositae and honey. Intradermal tests with bee venom were done. SPT with RJ extract were performed to healthy individuals and pollen, dust-mite and bee venom allergic patients. RJ powder was checked under a microscope. Specific IgE (CAP-Pharmacia) to bee venom and honey was determined. CAP-inhibition of D. pteronyssinus with RJ extract, performed separately with 2 patients' sera and one positive control serum, were carried out Results: Both patients presented positive tests with the suspected compound but only RJ extracts tests were positive. Four out of 10 dust mite allergic patients had positive test to RJ extract being negative rest of controls. Specific IgE to honey was observed in one patient. We observed no mites contamination of the RJ powder. CAP-inhibition of D. pteronyssinus with RJ were negative. Conclusion: We report 2 mite allergic patients with allergy to RJ. We discarded possible mite contamination of our RJ sample. Our results do not support a possible cross-reactivity between D. pteronyssinus and RJ. Although cosensitization is possible, being dust mite one of our most frequent allergens, it doesn´t explain the lack of sensitisation of the other controls, such as pollen allergic patients.

↩

[22] - Lombardi C, Senna GE, Gatti B, Feligioni M, Riva G, Bonadonna P, et al. Allergic reactions to honey and royal jelly and their relationship with sensitization to compositae. Allergol Immunopathol (Madr) 1998;26:288-290

Honey and royal jelly are complex etherogeneous mixtures of flowers' nectar, sugars, proteins and bee's glandular secretions. The existence of a type I hypersensitivity to honey is still matter of debate, while an aetiological role of Compositae pollens in the clinical manifestations following honey ingestion has been envisaged. We describe two cases of severe systemic reactions (anaphylaxis and generalized urticaria/angioedema) due to honey and royal jelly ingestion in patients sensitized to compositae (mugwort). Both patients had a skin and RAST positivity to mugwort and a positive prick-by-prick to the offending foods. Moreover, in one of the two patients the RAST-inhibition assay showed the strong cross-reactivity between the proteins of honey and mugwort and the SDS-PAGE analysis showed that the major proteic bands from honey and mugwort extracts are largely superimposable. Both the clinical data and the laboratory analysis support the hypothesis of a strict link between sensitization to compositae and adverse reactions to honey and jelly.

↩

[23] - Leung R, Ho A, Chan J, Choy D, Lai CKW. Royal jelly consumption and hypersensitivity in the community. Clin Exp Allergy 1997;27:333-336

Prevalence of royal jelly (RJ) hypersensitivity as related to RJ use in Hong Kong was examined, using questionnaires sent to 2000 hospital employees. Respondents were asked to undergo skin prick testing to RJ and common inhalant allergens, and a further 300 asthma clinic attendees were skin tested. Clinic attendees positive to skin tests to RJ also completed the questionnaire and results were analysed together with the hospital sample. >30% of respondents consumed RJ. Nearly all Chinese subjects with positive skin tests to RJ were atopic and 37.1% had a history of clinical allergy. Subjects with adverse reactions to RJ were more likely to have other clinical allergic manifestations. The precise relationship between RJ use, positive RJ skin test and clinical manifestations of adverse reactions to RJ is yet to be established

↩

[24] - Arroabarren E, Echechipía S, Aldunate MT, Garrido S, Goienetxe E, García BE, et al. Allergy to Royal jelly: 2 cases. EAACI 23th Congress, Amsterdam, 12-16 June, 2004, Poster n°974

Background: Royal jelly (RJ) is secreted by worker bees hypopharingeal glands and approximately 50% of its dry weight consists of proteins. In recent years asthma and anaphylaxis cases related to royal jelly ingestion haven been described and frequent sensitisation in pollen allergic patients has been observed. So far there are no data about possible cross-reactivity between D. pteronyssinus and RJ. We describe 2 asthmatic, dust-mite allergic patients, who presented, respectively, an anaphylaxis (generalized urticaria, dyspnea and vomiting) and an asthma attack after the ingestion of RJ containing compounds. Methods: SPT with the responsible compound, as well as with every single component and RJ extract of our own were performed, and so were with common inhalants and pollens including compositae and honey. Intradermal tests with bee venom were done. SPT with RJ extract were performed to healthy individuals and pollen, dust-mite and bee venom allergic patients. RJ powder was checked under a microscope. Specific IgE (CAP-Pharmacia) to bee venom and honey was determined. CAP-inhibition of D. pteronyssinus with RJ extract, performed separately with 2 patients' sera and one positive control serum, were carried out Results: Both patients presented positive tests with the suspected compound but only RJ extracts tests were positive. Four out of 10 dust mite allergic patients had positive test to RJ extract being negative rest of controls. Specific IgE to honey was observed in one patient. We observed no mites contamination of the RJ powder. CAP-inhibition of D. pteronyssinus with RJ were negative. Conclusion: We report 2 mite allergic patients with allergy to RJ. We discarded possible mite contamination of our RJ sample. Our results do not support a possible cross-reactivity between D. pteronyssinus and RJ. Although cosensitization is possible, being dust mite one of our most frequent allergens, it doesn´t explain the lack of sensitisation of the other controls, such as pollen allergic patients.

↩

[25] - Sánchez Palacios A, Schamann F, Garcia Marreo JA, Figueroa J, Gallego M. Anaphylaxis induced by Matricaria chamomilla and honey in two asthmatic patients sensitized to Artemisia vulgaris pollen. Allergy 2007;62(suppl. 83):358

Introduction We describe 2 cases of severe anaphylaxis in 2 patients with allergic rhinitis and bronchial asthma sensitized to Artemisia vuglaris. These patients experienced the reactions after an eye wash with a chamomile solution and after the ingestion of honey. Material and Methods First case: 24 years old woman.Rhinitis and asthma seasonal allergy several minutes after an eye wash with a chamomile solution.Angioedema, shortness of breath. Lost of consciousness which required admission and treatment at the emergency. SPT: - Skin prick test aeroallergens and extract of M. chamomilla 5% w/v - Conjuntival provocation test (CPT) 0.001 - 100 UB/ml - IgE specific. - In vitro cross-reactivity between Artemisa vulgaris and chamomile ELISA inhibition. Second case: 36 years old male.Rhinitis and asthma seasonal allergy after ingestion of honey and fermented aqueous honey solution (hidromiel).Facial angioedema, bronchospasm and luss of consciousness. SPT acroallergens and extrac honey solution specificise. SDS - Page and inmunoblots RESULTS SPT positive: - L. peronne.A. vulgaris.Taraxacum officinali.M. chamomilla Specific IgE - ELISA inhibition - Chamomilla inhibited > 80%.Specific IgE binding to A. vulgaris Conclusions: 1.-The first case is severe anaphylaxis inouced by matricaria chamomilla wich show cross Reactivity to Artemisia vulgaris. 2.-The second case is severe anaphylaxis after the ingestion of honey and hidromiel. 3.-The microscopic exam of the honey and hidromiel revealed the presence of pollens of Composital and of eucalyptus spp. 4.-The patient had positive skin test to artemisa vulgaris,celery and honey. 5.-Pollen extracts of several compositae plants were able to inhibit IgE binding to hidromiel, Where Eucalyptus spp.Pollen did not inhibit.

↩

[26] - Callejo A, Armentia A, Lombardero M, Martínez C, Rebollo S, Sedano E, et al. Hypersensitivity to propolis. Alergol Immunol Clin 2001;16:113-116

Background: Propolis is a recognised cause of occupational contact dermatitis in beekeepers. Although delayed hypersensitivity to propolis has been reported, not case of immediate hypersensitivity has been reported before. We described two cases of propolis allergy: in the first case, we demonstrated a delayed-hypersen-sitivity mechanism; in the second case, we described an IgE-mediated response. Methods: Delayed hypersensitivity to propolis was assessed by epicutaneous tes-ting and immediate hypersensitivity to propolis was assessed by prick to prick testing and detection of specific IgE by RAST. Results: In the first patient, the epicutaneous testing showed hypersensitivity to propolis. In the second case, IgE-mediated hypersensitivity was demonstrated by prick to prick and detection of specific IgE (RAST). Delayed hypersensitivity and specific IgE detection to propolis was not observed in any of the 6 patients used as control. Conclusions: The first case of IgE-mediated hypersensitivity to propolis is reported. This resi-nous substance should be taken into account in beekeepers, in addition to contact dermatitis, because of its frequent use and its allergenic potential.

↩

[27] - Florido-Lopez JF, Gonzalez-Delgado P, Saenz de San Pedro B, Perez-Miranda C, Arias de Saavedra JM, Marin-Pozo JF. Allergy to natural honeys and camomile tea. Int Arch Allergy Immunol 1995;108:170-174

Precipitation of food allergy reactions is well known in some patients with pollinosis when they consume natural food, such as honey or camomile tea. We present 9 patients with hay fever, with or without asthma, who experienced systemic allergic reactions after ingestion of natural honeys from two local areas (Andujar and Granada) and/or camomile tea. Pollen analysis showed a high level in sunflower pollen (23.6% of pollen grains) in the honey from Andujar but not in that from Granada. The diagnosis of food and respiratory allergy was based on history, skin prick tests and specific IgE activity against pollen from Compositae. Conjunctival challenge with camomile extract also gave positive results. The above allergological tests and the inhibition studies carried out, suggest that pollen of Compositae may be responsible for allergic reactions to certain natural foods and that the reactions are mediated by an IgE-related mechanism.

↩

[28] - Fuiano N, Incorvaia C, Riario-Sforza GG, Casino G. Anaphylaxis to honey in pollinosis to mugwort: a case report. Eur Ann Allergy Clin Immunol 2006;38:364-365

A case of anaphylaxis to honey in a 19 year old female sensitized to Compositae pollen is described. The patient suffered from summer rhinoconjunctivitis since seven years; in January 2006, ten minutes after eating bread and honey she developed angioedema of the lips and tongue, runny nose, cough, dyspnoea, and collapse, requiring hospitalization and treatment with high dose corticosteroids and anti-histamines. After two weeks, skin prick tests (SPT) with a standard panel of inhalant allergens and prick + prick with a number of kinds of honey were performed. SPTs were positive to mugwort, ragweed, dandelion, and goldenrod. Concerning honey, the prick + prick was positive to "Millefiori" (obtained from bees foraging on Compositae) and also to sunflower, limetree, and gum tree honey, while was negative for other kinds of honey, including the frequently used chestnut honey and acacia honey. The allergenic component responsible of anaphylaxis in this case seems to be a molecule occurring in Compositae pollens, as previously reported for other three reports, but also in pollen from plants of different families.Honey contains a large number of components derived from bees, such as gland secretions and wax, as well as from substances related to their foraging activity, such flower nectar and pollens (1, 2). Honey as a food has been associated to allergic reactions and particularly to anaphylaxis (3-6). Among the pollens, the role of Compositae is somewhat controversial, since its responsibility is clear in some studies (3, 5, 6) but considered negligible in others (7). Here we present the case of a patient sensitized to Compositae pollen who had an anaphylactic reaction to the ingestion of honey obtained from bees foraging on Compositae flowers and was tested with a number of different varieties of honey.

↩

[29] - Sánchez Palacios A, Schamann F, Garcia Marreo JA, Figueroa J, Gallego M. Anaphylaxis induced by Matricaria chamomilla and honey in two asthmatic patients sensitized to Artemisia vulgaris pollen. Allergy 2007;62(suppl. 83):358

Introduction We describe 2 cases of severe anaphylaxis in 2 patients with allergic rhinitis and bronchial asthma sensitized to Artemisia vuglaris. These patients experienced the reactions after an eye wash with a chamomile solution and after the ingestion of honey. Material and Methods First case: 24 years old woman.Rhinitis and asthma seasonal allergy several minutes after an eye wash with a chamomile solution.Angioedema, shortness of breath. Lost of consciousness which required admission and treatment at the emergency. SPT: - Skin prick test aeroallergens and extract of M. chamomilla 5% w/v - Conjuntival provocation test (CPT) 0.001 - 100 UB/ml - IgE specific. - In vitro cross-reactivity between Artemisa vulgaris and chamomile ELISA inhibition. Second case: 36 years old male.Rhinitis and asthma seasonal allergy after ingestion of honey and fermented aqueous honey solution (hidromiel).Facial angioedema, bronchospasm and luss of consciousness. SPT acroallergens and extrac honey solution specificise. SDS - Page and inmunoblots RESULTS SPT positive: - L. peronne.A. vulgaris.Taraxacum officinali.M. chamomilla Specific IgE - ELISA inhibition - Chamomilla inhibited > 80%.Specific IgE binding to A. vulgaris Conclusions: 1.-The first case is severe anaphylaxis inouced by matricaria chamomilla wich show cross Reactivity to Artemisia vulgaris. 2.-The second case is severe anaphylaxis after the ingestion of honey and hidromiel. 3.-The microscopic exam of the honey and hidromiel revealed the presence of pollens of Composital and of eucalyptus spp. 4.-The patient had positive skin test to artemisa vulgaris,celery and honey. 5.-Pollen extracts of several compositae plants were able to inhibit IgE binding to hidromiel, Where Eucalyptus spp.Pollen did not inhibit.

↩

[30] - Lombardi C, Senna GE, Gatti B, Feligioni M, Riva G, Bonadonna P, et al. Allergic reactions to honey and royal jelly and their relationship with sensitization to compositae. Allergol Immunopathol (Madr) 1998;26:288-290

Honey and royal jelly are complex etherogeneous mixtures of flowers' nectar, sugars, proteins and bee's glandular secretions. The existence of a type I hypersensitivity to honey is still matter of debate, while an aetiological role of Compositae pollens in the clinical manifestations following honey ingestion has been envisaged. We describe two cases of severe systemic reactions (anaphylaxis and generalized urticaria/angioedema) due to honey and royal jelly ingestion in patients sensitized to compositae (mugwort). Both patients had a skin and RAST positivity to mugwort and a positive prick-by-prick to the offending foods. Moreover, in one of the two patients the RAST-inhibition assay showed the strong cross-reactivity between the proteins of honey and mugwort and the SDS-PAGE analysis showed that the major proteic bands from honey and mugwort extracts are largely superimposable. Both the clinical data and the laboratory analysis support the hypothesis of a strict link between sensitization to compositae and adverse reactions to honey and jelly.

↩

[31] - Pitsios C, Vartholomeos S, Ergazakis M, Kompoti E, Kontou-Fili K. Honey hypersensitivity in two atopic patients. EAACI 23th Congress, Amsterdam, 12-16 June, 2004, Poster n°973

Pollens, glandular glycoproteins and bee-body material are the constituents of honey, mainly responsible for rare food-induced reactions. Two cases of patients with mild systemic reactions after ingestion of honey are reported in this study. Methodology: The first case is a 21-years-old male with a history of seasonal rhinitis, conjunctivitis and mild asthma. Soon after the ingestion of honey he reported rhinitis, conjunctivitis and oral pruritus that were successfully treated with antihistamine p.o. The second case is a 24-years-old female with a history of seasonal rhinitis and asthma. She reported two episodes of generalized urticaria and gastrointestinal symptoms, ten minutes after the ingestion of a sweet containing honey and walnuts. Symptoms dissolved after treatment with corticosteroids and antihistamines. She used to eat tree-nuts with no signs of allergic reactions. Skin Prick Test (SPT) with commercial extracts of aeroallergens, food allergens and prick-to-prick (P-P) with two different in origin samples of honey were performed. SPT was also performed with homemade bee whole body extract (BWB). Serum specific IgE (sIgE) CAP to pollens, food allergens and bee venom was investigated. Double blind placebo controled food challenge (DBPCFC) was proposed to confirm the diagnosis. Results: Pat. 1: SPT and CAP were positive for Olea europea, Parietaria, Chenopodium and P-P were positive to both honeys. SPT to other foods, BWB and sIgE to bee venom was negative. DBPCFC was performed at our outpatient clinic using honey of local origin and corn syrup as placebo. Increasing doses were administered with intervals of 30 minutes. The challenge resulted positive at the total intake of 3,35g of honey. The patient presented sneezing, nasal pruritus, congestion, a 50% decrease of nasal peak flow and conjunctivitis. The symptoms dissolved 30 min after the administration of 10mg cetirizine. Pat. 2: SPT were positive for mixed Grasses extract and both honeys. sIgE confirmed hypersensitivity to Grasses. No positive reaction was shown to tree-nuts, other foods or BWB. Bee venom sIgE was negative. DBPCFC was not accepted by patient. She ever since avoids honey and honey sweets referring no problem. An emergency set (epinephrine, cetirizine and cortisone) was prescribed. Conclusions: Honey ingestion may cause mild allergic reactions. In our patients the pollen proteins contained in honey appear to be the responsible allergens.

↩

[32] - Bousquet J, Dhivert H, Clauzel AM, Hewitt B, Michel FB. Occupational allergy to sunflower pollen. J Allergy Clin Immunol 1985;75:70-74

Although the sunflower belongs to the Compositeae family, allergy to sunflower pollen is not common. The occurrence of occupational allergy to this pollen species made it possible to characterize cross-reactive patterns of Compositeae pollens in a human experimental model. A 24-yr-old man developed rhinitis and conjunctivitis over 5 yr of exposure to sunflower pollens, and asthma developed during the fifth year. All respiratory and occular symptoms disappeared after he was removed from exposure, but he had a food allergic reaction while he was eating honey containing 30% sunflower pollens. The diagnosis of occupational allergy was based on history, skin prick tests and RAST to the pollen. Bronchial provocation tests performed after removal from exposure confirmed the sensitivity to sunflower pollens but there was no nonspecific hyperreactivity. It was found by RAST inhibition that sunflower pollen does not cross-react with other Compositeae pollens tested or with sunflower seed. The honey that elicited food intolerance was demonstrated to inhibit significantly sunflower pollen RAST

↩

[33] - Bousquet J, Campos J, Michel FB. Food intolerance to honey. Allergy 1984;39:73-75

A 42 year-old beekeeper who had an inhalant allergy to Compositeae pollen presented an adverse reaction while eating a honey which contained large numbers of Compositeae pollens. As she was not intolerant to honey of own production, which contained no Compositeae pollen, the adverse reaction seems to be attributed to these pollens.

↩

[34] - Lombardi C, Senna GE, Gatti B, Feligioni M, Riva G, Bonadonna P, et al. Allergic reactions to honey and royal jelly and their relationship with sensitization to compositae. Allergol Immunopathol (Madr) 1998;26:288-290

Honey and royal jelly are complex etherogeneous mixtures of flowers' nectar, sugars, proteins and bee's glandular secretions. The existence of a type I hypersensitivity to honey is still matter of debate, while an aetiological role of Compositae pollens in the clinical manifestations following honey ingestion has been envisaged. We describe two cases of severe systemic reactions (anaphylaxis and generalized urticaria/angioedema) due to honey and royal jelly ingestion in patients sensitized to compositae (mugwort). Both patients had a skin and RAST positivity to mugwort and a positive prick-by-prick to the offending foods. Moreover, in one of the two patients the RAST-inhibition assay showed the strong cross-reactivity between the proteins of honey and mugwort and the SDS-PAGE analysis showed that the major proteic bands from honey and mugwort extracts are largely superimposable. Both the clinical data and the laboratory analysis support the hypothesis of a strict link between sensitization to compositae and adverse reactions to honey and jelly.

↩

[35] - Bousquet J, Dhivert H, Clauzel AM, Hewitt B, Michel FB. Occupational allergy to sunflower pollen. J Allergy Clin Immunol 1985;75:70-74

Although the sunflower belongs to the Compositeae family, allergy to sunflower pollen is not common. The occurrence of occupational allergy to this pollen species made it possible to characterize cross-reactive patterns of Compositeae pollens in a human experimental model. A 24-yr-old man developed rhinitis and conjunctivitis over 5 yr of exposure to sunflower pollens, and asthma developed during the fifth year. All respiratory and occular symptoms disappeared after he was removed from exposure, but he had a food allergic reaction while he was eating honey containing 30% sunflower pollens. The diagnosis of occupational allergy was based on history, skin prick tests and RAST to the pollen. Bronchial provocation tests performed after removal from exposure confirmed the sensitivity to sunflower pollens but there was no nonspecific hyperreactivity. It was found by RAST inhibition that sunflower pollen does not cross-react with other Compositeae pollens tested or with sunflower seed. The honey that elicited food intolerance was demonstrated to inhibit significantly sunflower pollen RAST

↩

[36] - Helbling A, Peter C, Berchtold E, Bogdanov S, Müller U. Allergy to honey: relation to pollen and honey bee allergy. Allergy 1992;47:41-49

To identify the allergenic components of honey we studied 22 patients with a history of systemic allergic symptoms following honey ingestion. The group of honey-allergic patients was compared with three control groups: 10 subjects sensitized to artemisia, 10 with honey bee venom allergy and 10 without a history of atopy or bee sting reactions. The allergological tests included skin tests and RAST with three different kinds of Swiss honey (dandelion, forest and rape), pollen of compositae species, celery tuber, extract of bee pharyngeal glands, honey bee venom and bee whole body extract. The results show that 3/4 of honey-allergics are sensitive to dandelion honey and 13 of 22 also to compositae pollen. Nine of the honey allergic patients were sensitized to honey bee venom, 3 also to bee pharyngeal glands and to bee whole body extract. Analysis of diagnostic tests and RAST inhibition studies suggest that besides compositae pollen other allergens, most likely of bee origin are important. In honey allergics primary sensitization may be due either to the honey itself, to airborne compositae pollen or even to cross-reacting bee venom components.

↩

[37] - Fernandez C, Martin-Esteban M, Fiandor A, Pascual CY, Lopez Serrano C, Martinez Alzamora F, et al. Analysis of cross-reactivity between sunflower pollen and other pollens of the Compositae family. J Allergy Clin Immunol 1993;92:660-667

The sera of 20 patients with Compositae pollen allergy were investigated for the presence of IgE antibodies reacting against sunflower pollen by means of RAST and immunoblotting studies. Thirteen IgE-binding bands were detected with molecular weights ranging from 14.4 to 94 kd. Two of these bands, with molecular weights of 24 and 25 kd, contained major allergens that reacted strongly with 100% (24 kd) and 95% (25 kd) of the sera, respectively. Cross-reactivity between sunflower and other Compositae pollens (mugwort, marguerite, dandelion, golden rod, and short ragweed) was revealed by RAST and immunoblotting inhibition experiments. Mugwort pollen exhibited the greatest degree of allergenic homology (cross-reactivity) with sunflower pollen, whereas at the other end of the spectrum, short ragweed showed less cross-reactive epitopes.

↩

[38] - Garcia Ortiz JC, Cosmes Martin P, Lopez-Asunsolo A. Allergy to foods in patients monosensitized to Artemisia pollen. Allergy 1996;51:927-931

It is known that patients with pollinosis may display clinical characteristics caused by allergy to certain fruits and vegetables, but subjects allergic to Artemisia seem to show particularly peculiar characteristics. The clinical features of 84 patients with rhinitis, asthma, urticaria, and/or anaphylaxis whose inhalant allergy was exclusively to Artemisia vulgaris were studied and compared with a control group of 50 patients monosensitized to grass pollen. The mean age for the beginning of symptoms was 30.2 years, and this was higher than in the control group (P < 0.05). We found the main incidence to be in women (70.2%). Some 42.3% had family history of atopia, lower than in the control group (P < 0.05), while the prevalence of asthma and urticaria was significantly higher (P < 0.05). Food hypersensitivity was reported by 23 patients (27.3%) allergic to Artemisia. The foods responsible (with respective numbers of cases) were honey (14), sunflower seeds (11), camomile (four), pistachio (three), hazelnut (two), lettuce (two), pollen (two), beer (two), almond (one), peanut (one), other nuts (one), carrot (one), and apple (one). None of the patients monosensitized to grass had food allergy. CAP inhibition experiments were carried out on a single patient. Results showed the existence of common antigenic epitopes in pistachio and Artemisia pollen for this patient. We concluded that mugwort hay fever can be associated with the Compositae family of foods, but that it is not normally associated with other foods.

↩

[39] - Bilo B, Czarnobilska E, Obtulowicz K. Specific immunotherapy and oral allergy syndrome (OAS) in pollen allergy. EAACI 25th Congress, Vienna, 10-14 June, 2006, Poster n°1366

Intolerance of plant-derived foods is an increasing problem in patients with pollen allergy. Aim of this study was to determine the relationship between specific immunotherapy (SIT) with pollen allergens and OAS prevalence. The study population included 57 subjects (31 M, 26 F, mean age 26.5 years) undergoing subcutaneous SIT in the Department of Clinical and Environmental Allergology in Cracow, in whom a detailed information on reactions to plant-derived foods was obtained. Results of skin tests with inhalant and food allergens (Allergopharma) as well as total and specific IgE levels (before SIT) were analysed. The average SIT duration before enrolment was 3 years. In 30 out of 41 subjects with SIT lasting over 1 year, a marked improvement of symptoms was observed. The mean duration of pollinosis symptoms was 10.8 years. In 17 patients OAS symptoms developed (mean duration 6.2 years): in one subject prior to the occurrence of pollinosis, in 12 before SIT was initiated and in 4 during SIT; in 3 subjects OAS symptoms improved during SIT (apple tolerance appeared). The predominant symptoms included itching in the mouth, throat irritation, less frequently lip, palate or tongue oedema; they occurred after the consumption of apple (14 subjects), celery (12), hazelnut (11), less frequently after carrots, peaches or other fruit.. Compared to subjects with a good food tolerance, OAS subjects were characterized by older age (30.6 vs. 23.5 years), longer duration of symptoms (11.6 vs. 10.4 years), higher rate of female gender (59% vs. 40%, NS), more frequent tree pollen allergy (88% vs. 45%, p<0.005), less frequent grass (70% vs. 98%, p<0.005) or weed pollen allergy (41% vs. 53%, NS). OAS symptoms occur most commonly in patients allergic to tree pollen (or to several groups of pollens, including trees). SIT does not appear to increase OAS incidence and it may be associated with a transitional improvement in food tolerance.

↩

[40] - Bauer L, Kohlich A, Hirschwehr R, Siemann U, Ebner H, Scheiner O, et al. Food allergy to honey: pollen or bee products ? J Allergy Clin Immunol 1996;97:65-73

To characterize the allergenic components of honey, 23 patients allergic to honey were investigated. All displayed allergic symptoms after ingestion of honey or honey-containing products, ranging from itching in the oral mucosa to severe systemic symptoms to anaphylactic shock. METHODS AND RESULTS: Immunoblot analyses of the patients' sera revealed IgE binding to proteins at a molecular mass of 54 kd, 60 kd, 72 kd, or to a 30 kd/33 kd double band, or to both in sunflower honey extracts. The three bands corresponding to higher molecular mass proteins could also be detected in the three other kinds of honey (locust tree, European chestnut and forest honey) that were tested and represented bee products because IgE binding to these proteins was inhibited by extracts of honeybee heads and extracts of isolated bee venom sacs. The 30 kd/33 kd bands could be identified as sunflower honey-specific. When testing sera from patients allergic to bee venom with honey extracts, in seven of 10 cases IgE binding to bee-specific components could be observed. CONCLUSION: Both proteins derived from secretions of pharyngeal and salivary glands of honeybee heads and pollen proteins contained in the honey cause allergic reactions to honey.

↩

[41] - Helbling A, Peter C, Berchtold E, Bogdanov S, Müller U. Allergy to honey: relation to pollen and honey bee allergy. Allergy 1992;47:41-49

To identify the allergenic components of honey we studied 22 patients with a history of systemic allergic symptoms following honey ingestion. The group of honey-allergic patients was compared with three control groups: 10 subjects sensitized to artemisia, 10 with honey bee venom allergy and 10 without a history of atopy or bee sting reactions. The allergological tests included skin tests and RAST with three different kinds of Swiss honey (dandelion, forest and rape), pollen of compositae species, celery tuber, extract of bee pharyngeal glands, honey bee venom and bee whole body extract. The results show that 3/4 of honey-allergics are sensitive to dandelion honey and 13 of 22 also to compositae pollen. Nine of the honey allergic patients were sensitized to honey bee venom, 3 also to bee pharyngeal glands and to bee whole body extract. Analysis of diagnostic tests and RAST inhibition studies suggest that besides compositae pollen other allergens, most likely of bee origin are important. In honey allergics primary sensitization may be due either to the honey itself, to airborne compositae pollen or even to cross-reacting bee venom components.

↩

[42] - Kiistala R, Hannuksela M, Makinen-Kiljunen S, Niinimaki A, Haahtela T. Honey allergy is rare in patients sensitive to pollens. Allergy 1995;50:844-847

We challenged in a double-blind manner 46 pollen-allergic patients with 30 g of honey and another 32 patients with a placebo (30 g of syrup). Minor, mostly subjective, symptoms were seen in or reported by 26% of those challenged with honey and 41% of those challenged with placebo. In no case could the symptoms with certainty be related to the challenge. Eight commercially available honeys were examined for allergen activity by RAST inhibition and immunospot methods. Both pollen and insect allergen activity was found in all honeys, and they could cause allergic reactions. However, no serious or even obvious reaction occurred in pollen-allergic patients challenged with honey.

↩

[43] - Fuiano N, Incorvaia C, Riario-Sforza GG, Casino G. Anaphylaxis to honey in pollinosis to mugwort: a case report. Eur Ann Allergy Clin Immunol 2006;38:364-365

A case of anaphylaxis to honey in a 19 year old female sensitized to Compositae pollen is described. The patient suffered from summer rhinoconjunctivitis since seven years; in January 2006, ten minutes after eating bread and honey she developed angioedema of the lips and tongue, runny nose, cough, dyspnoea, and collapse, requiring hospitalization and treatment with high dose corticosteroids and anti-histamines. After two weeks, skin prick tests (SPT) with a standard panel of inhalant allergens and prick + prick with a number of kinds of honey were performed. SPTs were positive to mugwort, ragweed, dandelion, and goldenrod. Concerning honey, the prick + prick was positive to "Millefiori" (obtained from bees foraging on Compositae) and also to sunflower, limetree, and gum tree honey, while was negative for other kinds of honey, including the frequently used chestnut honey and acacia honey. The allergenic component responsible of anaphylaxis in this case seems to be a molecule occurring in Compositae pollens, as previously reported for other three reports, but also in pollen from plants of different families.Honey contains a large number of components derived from bees, such as gland secretions and wax, as well as from substances related to their foraging activity, such flower nectar and pollens (1, 2). Honey as a food has been associated to allergic reactions and particularly to anaphylaxis (3-6). Among the pollens, the role of Compositae is somewhat controversial, since its responsibility is clear in some studies (3, 5, 6) but considered negligible in others (7). Here we present the case of a patient sensitized to Compositae pollen who had an anaphylactic reaction to the ingestion of honey obtained from bees foraging on Compositae flowers and was tested with a number of different varieties of honey.

↩

[44] - Arbab E, Grims R. Bee-venom and honey allergy. Allergy 2007;62(suppl. 83):79-80

Background: Honey allergy is a very rare condition, which shows clinical pictures ranging from cough to anaphylaxis after ingestion of honey. Patients sensitized to bee venom and concomitantly allergic to honey are even scarcer and pose the following question: Does specific immunotherapy (SIT) with bee venom prevent allergic reactions after honey ingestion. Case: A 37-year-old woman had a history of systemic grade II reactions after bee stings since 5 years. The patient reported about two episodes of similar reactions after honey ingestion in the last couple of months. Results: Her specific IgE level for bee venom and honey was class 2 and class 1, respectively, counting a total IgE of 296 kU/l. Skin tests for bee venom were positive at 300µg/ml prick and at 0,1 µg/ml intradermal. Prick test with honey was also positive. Conclusion: Proteins responsible for honey allergy are derived from proteins secreted by bees and from proteins derived from plant pollens. In this case a SIT with bee venom was recently introduced on the one hand due to patient's sensitization to bee venom and as a possible therapy for the honey allergy on the other hand.

↩

[45] - Helbling A, Peter C, Berchtold E, Bogdanov S, Müller U. Allergy to honey: relation to pollen and honey bee allergy. Allergy 1992;47:41-49

To identify the allergenic components of honey we studied 22 patients with a history of systemic allergic symptoms following honey ingestion. The group of honey-allergic patients was compared with three control groups: 10 subjects sensitized to artemisia, 10 with honey bee venom allergy and 10 without a history of atopy or bee sting reactions. The allergological tests included skin tests and RAST with three different kinds of Swiss honey (dandelion, forest and rape), pollen of compositae species, celery tuber, extract of bee pharyngeal glands, honey bee venom and bee whole body extract. The results show that 3/4 of honey-allergics are sensitive to dandelion honey and 13 of 22 also to compositae pollen. Nine of the honey allergic patients were sensitized to honey bee venom, 3 also to bee pharyngeal glands and to bee whole body extract. Analysis of diagnostic tests and RAST inhibition studies suggest that besides compositae pollen other allergens, most likely of bee origin are important. In honey allergics primary sensitization may be due either to the honey itself, to airborne compositae pollen or even to cross-reacting bee venom components.

↩

[46] - Bauer L, Kohlich A, Hirschwehr R, Siemann U, Ebner H, Scheiner O, et al. Food allergy to honey: pollen or bee products ? J Allergy Clin Immunol 1996;97:65-73

To characterize the allergenic components of honey, 23 patients allergic to honey were investigated. All displayed allergic symptoms after ingestion of honey or honey-containing products, ranging from itching in the oral mucosa to severe systemic symptoms to anaphylactic shock. METHODS AND RESULTS: Immunoblot analyses of the patients' sera revealed IgE binding to proteins at a molecular mass of 54 kd, 60 kd, 72 kd, or to a 30 kd/33 kd double band, or to both in sunflower honey extracts. The three bands corresponding to higher molecular mass proteins could also be detected in the three other kinds of honey (locust tree, European chestnut and forest honey) that were tested and represented bee products because IgE binding to these proteins was inhibited by extracts of honeybee heads and extracts of isolated bee venom sacs. The 30 kd/33 kd bands could be identified as sunflower honey-specific. When testing sera from patients allergic to bee venom with honey extracts, in seven of 10 cases IgE binding to bee-specific components could be observed. CONCLUSION: Both proteins derived from secretions of pharyngeal and salivary glands of honeybee heads and pollen proteins contained in the honey cause allergic reactions to honey.

↩

[47] - Ibero M, Castillo MJ, Pineda F, Palacios R, Martinez J. Whole bee for diagnosis of honey allergy. Allergy 2002;57:557-558

↩

[48] - Bauer L, Kohlich A, Hirschwehr R, Siemann U, Ebner H, Scheiner O, et al. Food allergy to honey: pollen or bee products ? J Allergy Clin Immunol 1996;97:65-73

To characterize the allergenic components of honey, 23 patients allergic to honey were investigated. All displayed allergic symptoms after ingestion of honey or honey-containing products, ranging from itching in the oral mucosa to severe systemic symptoms to anaphylactic shock. METHODS AND RESULTS: Immunoblot analyses of the patients' sera revealed IgE binding to proteins at a molecular mass of 54 kd, 60 kd, 72 kd, or to a 30 kd/33 kd double band, or to both in sunflower honey extracts. The three bands corresponding to higher molecular mass proteins could also be detected in the three other kinds of honey (locust tree, European chestnut and forest honey) that were tested and represented bee products because IgE binding to these proteins was inhibited by extracts of honeybee heads and extracts of isolated bee venom sacs. The 30 kd/33 kd bands could be identified as sunflower honey-specific. When testing sera from patients allergic to bee venom with honey extracts, in seven of 10 cases IgE binding to bee-specific components could be observed. CONCLUSION: Both proteins derived from secretions of pharyngeal and salivary glands of honeybee heads and pollen proteins contained in the honey cause allergic reactions to honey.

↩

[49] - Helbling A, Peter C, Berchtold E, Bogdanov S, Müller U. Allergy to honey: relation to pollen and honey bee allergy. Allergy 1992;47:41-49

To identify the allergenic components of honey we studied 22 patients with a history of systemic allergic symptoms following honey ingestion. The group of honey-allergic patients was compared with three control groups: 10 subjects sensitized to artemisia, 10 with honey bee venom allergy and 10 without a history of atopy or bee sting reactions. The allergological tests included skin tests and RAST with three different kinds of Swiss honey (dandelion, forest and rape), pollen of compositae species, celery tuber, extract of bee pharyngeal glands, honey bee venom and bee whole body extract. The results show that 3/4 of honey-allergics are sensitive to dandelion honey and 13 of 22 also to compositae pollen. Nine of the honey allergic patients were sensitized to honey bee venom, 3 also to bee pharyngeal glands and to bee whole body extract. Analysis of diagnostic tests and RAST inhibition studies suggest that besides compositae pollen other allergens, most likely of bee origin are important. In honey allergics primary sensitization may be due either to the honey itself, to airborne compositae pollen or even to cross-reacting bee venom components.

↩

[50] - Aalberse RC, Koshte V, Clemens JG. Immunoglobulin E antibodies that crossreact with vegetable foods, pollen, and Hymenoptera venom. J Allergy Clin Immunol 1981;68:356-364

IgE in some human sera reacted with an antigen present in a large number of unrelated foods: potato, spinach, wheat, buckwheat, peanut, honey and others. The antigen, which was periodate-sensitive and heat-stable, was also found in pollen. Even more surprisingly, these antibodies often reacted in vitro with bee and vespid venom and were sometimes apparently induced by Hymenoptera stings

↩

[51] - Bauer L, Kohlich A, Hirschwehr R, Siemann U, Ebner H, Scheiner O, et al. Food allergy to honey: pollen or bee products ? J Allergy Clin Immunol 1996;97:65-73

To characterize the allergenic components of honey, 23 patients allergic to honey were investigated. All displayed allergic symptoms after ingestion of honey or honey-containing products, ranging from itching in the oral mucosa to severe systemic symptoms to anaphylactic shock. METHODS AND RESULTS: Immunoblot analyses of the patients' sera revealed IgE binding to proteins at a molecular mass of 54 kd, 60 kd, 72 kd, or to a 30 kd/33 kd double band, or to both in sunflower honey extracts. The three bands corresponding to higher molecular mass proteins could also be detected in the three other kinds of honey (locust tree, European chestnut and forest honey) that were tested and represented bee products because IgE binding to these proteins was inhibited by extracts of honeybee heads and extracts of isolated bee venom sacs. The 30 kd/33 kd bands could be identified as sunflower honey-specific. When testing sera from patients allergic to bee venom with honey extracts, in seven of 10 cases IgE binding to bee-specific components could be observed. CONCLUSION: Both proteins derived from secretions of pharyngeal and salivary glands of honeybee heads and pollen proteins contained in the honey cause allergic reactions to honey.

↩

[52] - Bousquet J, Campos J, Michel FB. Food intolerance to honey. Allergy 1984;39:73-75

A 42 year-old beekeeper who had an inhalant allergy to Compositeae pollen presented an adverse reaction while eating a honey which contained large numbers of Compositeae pollens. As she was not intolerant to honey of own production, which contained no Compositeae pollen, the adverse reaction seems to be attributed to these pollens.

↩

[53] - Sánchez Palacios A, Schamann F, Garcia Marreo JA, Figueroa J, Gallego M. Anaphylaxis induced by Matricaria chamomilla and honey in two asthmatic patients sensitized to Artemisia vulgaris pollen. Allergy 2007;62(suppl. 83):358

Introduction We describe 2 cases of severe anaphylaxis in 2 patients with allergic rhinitis and bronchial asthma sensitized to Artemisia vuglaris. These patients experienced the reactions after an eye wash with a chamomile solution and after the ingestion of honey. Material and Methods First case: 24 years old woman.Rhinitis and asthma seasonal allergy several minutes after an eye wash with a chamomile solution.Angioedema, shortness of breath. Lost of consciousness which required admission and treatment at the emergency. SPT: - Skin prick test aeroallergens and extract of M. chamomilla 5% w/v - Conjuntival provocation test (CPT) 0.001 - 100 UB/ml - IgE specific. - In vitro cross-reactivity between Artemisa vulgaris and chamomile ELISA inhibition. Second case: 36 years old male.Rhinitis and asthma seasonal allergy after ingestion of honey and fermented aqueous honey solution (hidromiel).Facial angioedema, bronchospasm and luss of consciousness. SPT acroallergens and extrac honey solution specificise. SDS - Page and inmunoblots RESULTS SPT positive: - L. peronne.A. vulgaris.Taraxacum officinali.M. chamomilla Specific IgE - ELISA inhibition - Chamomilla inhibited > 80%.Specific IgE binding to A. vulgaris Conclusions: 1.-The first case is severe anaphylaxis inouced by matricaria chamomilla wich show cross Reactivity to Artemisia vulgaris. 2.-The second case is severe anaphylaxis after the ingestion of honey and hidromiel. 3.-The microscopic exam of the honey and hidromiel revealed the presence of pollens of Composital and of eucalyptus spp. 4.-The patient had positive skin test to artemisa vulgaris,celery and honey. 5.-Pollen extracts of several compositae plants were able to inhibit IgE binding to hidromiel, Where Eucalyptus spp.Pollen did not inhibit.

↩

[54] - Helbling A, Peter C, Berchtold E, Bogdanov S, Müller U. Allergy to honey: relation to pollen and honey bee allergy. Allergy 1992;47:41-49

To identify the allergenic components of honey we studied 22 patients with a history of systemic allergic symptoms following honey ingestion. The group of honey-allergic patients was compared with three control groups: 10 subjects sensitized to artemisia, 10 with honey bee venom allergy and 10 without a history of atopy or bee sting reactions. The allergological tests included skin tests and RAST with three different kinds of Swiss honey (dandelion, forest and rape), pollen of compositae species, celery tuber, extract of bee pharyngeal glands, honey bee venom and bee whole body extract. The results show that 3/4 of honey-allergics are sensitive to dandelion honey and 13 of 22 also to compositae pollen. Nine of the honey allergic patients were sensitized to honey bee venom, 3 also to bee pharyngeal glands and to bee whole body extract. Analysis of diagnostic tests and RAST inhibition studies suggest that besides compositae pollen other allergens, most likely of bee origin are important. In honey allergics primary sensitization may be due either to the honey itself, to airborne compositae pollen or even to cross-reacting bee venom components.

↩

[55] - Fuiano N, Incorvaia C, Riario-Sforza GG, Casino G. Anaphylaxis to honey in pollinosis to mugwort: a case report. Eur Ann Allergy Clin Immunol 2006;38:364-365

A case of anaphylaxis to honey in a 19 year old female sensitized to Compositae pollen is described. The patient suffered from summer rhinoconjunctivitis since seven years; in January 2006, ten minutes after eating bread and honey she developed angioedema of the lips and tongue, runny nose, cough, dyspnoea, and collapse, requiring hospitalization and treatment with high dose corticosteroids and anti-histamines. After two weeks, skin prick tests (SPT) with a standard panel of inhalant allergens and prick + prick with a number of kinds of honey were performed. SPTs were positive to mugwort, ragweed, dandelion, and goldenrod. Concerning honey, the prick + prick was positive to "Millefiori" (obtained from bees foraging on Compositae) and also to sunflower, limetree, and gum tree honey, while was negative for other kinds of honey, including the frequently used chestnut honey and acacia honey. The allergenic component responsible of anaphylaxis in this case seems to be a molecule occurring in Compositae pollens, as previously reported for other three reports, but also in pollen from plants of different families.Honey contains a large number of components derived from bees, such as gland secretions and wax, as well as from substances related to their foraging activity, such flower nectar and pollens (1, 2). Honey as a food has been associated to allergic reactions and particularly to anaphylaxis (3-6). Among the pollens, the role of Compositae is somewhat controversial, since its responsibility is clear in some studies (3, 5, 6) but considered negligible in others (7). Here we present the case of a patient sensitized to Compositae pollen who had an anaphylactic reaction to the ingestion of honey obtained from bees foraging on Compositae flowers and was tested with a number of different varieties of honey.

↩

[56] - Drouet M, Menehould C. Les composants mammifères dans les médicaments. Colloque SAICO, Angers, 29 juin 2006

↩

[57] - Petit N. Réactions allergiques aux vaccins: prévalence, rôle des additifs, substances des excipients et contaminants. Alim'Inter 2006;11:91-99

↩

[58] - Weber P, Steinhart H, Paschke A. Investigation of the Allergenic Potential of Wines Fined with Various Proteinogenic Fining Agents by ELISA. J Agric Food Chem 2007;55:3127-3133

Hidden allergens are a common problem in food safety that has been known for many years. This is why the European Parliament adopted Directive 2003/89/EC amending 2000/13/EC. In addition to specific ingredients, Directive 2003/89/EC also requests the declaration of specific products that were used in the production and could be a risk for allergic individuals. This also includes the declaration of fining agents and lysozyme used in wines. In fact, it could be assumed that fining agents would be almost completely removed during the manufacturing process; however, until now there has been no necessity to analyze wine for these fining agents. By applying enzyme-linked immunosorbent assay (ELISA), residuals of fining agent proteins and the stabilizer lysozyme were investigated in various German wines. The results showed no detectable amounts of fining agents in wines, except for dried egg white and lysozyme, both derived from hen's egg white. For those products, adverse reactions against treated wines could not be excluded. Keywords: Wine; fining agent; allergen; allergy; isinglass; lysozyme; food allergy; hidden allergens; immunoassay; fish gelatin; hen's egg protein; ovalbumin; casein.

↩

[59] - Lifrani A, Dos Santos J, Dubarry M, Rautureau M, Blachier F, Tome D. Development of Animal Models and Sandwich-ELISA Tests to Detect the Allergenicity and Antigenicity of Fining Agent Residues in Wines. J Agric Food Chem 2009;57:525-534

Food allergy can cause food-related anaphylaxis. Food allergen labeling is the principal means of protecting sensitized individuals. This motivated European Directive 2003/89 on the labeling of ingredients or additives that could trigger adverse reactions, which has been in effect since 2005. During this study, we developed animal models with allergy to ovalbumin, caseinate, and isinglass in order to be able to detect fining agent residues that could induce anaphylactic reactions in sensitized mice. The second aim of the study was to design sandwich ELISA tests specific to each fining agent in order to detect their residue antigenicity, both during wine processing and in commercially available bottled wines. Sensitized mice and sandwich ELISA methods were established to test a vast panel of wines. The results showed that although they were positive to our highly sensitive sandwich-ELISA tests, some commercially available wines are not allergenic in sensitized mice. Commercially available bottled wines made using standardized processes, fining, maturation, and filtration, do not therefore represent any risk of anaphylactic reactions in sensitized mice.

↩

[60] - Rolland JM, Apostolou E, Deckert K, de Leon MP, Douglass JA, Glaspole IN, et al. Potential food allergens in wine: Double-blind, placebo-controlled trial and basophil activation analysis. Nutrition 2006;22:882-888

OBJECTIVE: Recent Australian and international legislation requires labeling of wines made by using the potentially allergenic food proteins casein, milk, egg white, or isinglass (fish-derived) where "there is a detectable residual processing aid." We investigated whether wines fined using these proteins or non-grape-derived tannins (tree-nut derived) can provoke significant clinical allergic reactions (anaphylaxis) in patients with confirmed immunoglobulin E-mediated relevant food allergy. METHODS: A double-blind, placebo-controlled trial was performed to determine whether allergic reactions followed consumption of Australian commercial wines fined using one or more of the legislation-targeted food proteins. In addition, allergenicity of a larger panel of these wines was evaluated by blood basophil activation. RESULTS: No anaphylaxis was induced by wine consumption. Three mild clinical reactions to protein-fined wine and two mild reactions to unfined wine occurred, but there was no statistically significant difference in reaction parameters between subject groups or between processing aids. No pattern of basophil activation correlated with wine type, processing aid, or subject group. CONCLUSION: Wines fined with egg white, isinglass, or non-grape-derived tannins present an extremely low risk of anaphylaxis to fish-, egg-, or peanut-allergic consumers. Although consumption of milk protein-fined wine did not induce anaphylaxis, there were insufficient subjects to determine statistically whether wines fined with milk proteins present a risk to the very rare milk-allergic consumers. In summary, the observed lack of anaphylaxis and basophil activation induced by wines made using the legislation-targeted food proteins according to good manufacturing practice suggests negligible residual food allergens in these wines.

↩

[61] - Kirschner S, Belloni B, Kugler C, Ring J, Brockow K. Allergenicity of Wine Containing Processing Aids: A Double-Blind, Placebo-Controlled Food Challenge. J Investig Allergol Clin Immunol 2009;19:210-217

BACKGROUND: The European Union requires allergenic food ingredients to appear on labels in order to protect allergic consumers . OBJECTIVE: To determine whether traces of egg-, milk-, and fish-derived processing aids used in winemaking might elicit clinical reactions in food-allergic patients . METHODS: Five German wines were fined with a high dose of egg albumin, lysozyme, milk casein, fish gelatin, or isinglass, and filtered. Fourteen adults with allergy to egg (n = 5), milk (n = 5), or fish (n = 4) were included. Skin prick tests were performed with fining agents, and fined and unfined wines. All patients underwent double-blind placebo-controlled food challenges with fined and unfined wines . RESULTS: Skin prick tests were positive to hen's egg (n = 5), ovalbumin (n = 5), lysozyme (n = 4), cow's milk (n = 5), casein (n = 4), and cod (n = 3), but not to isinglass or fish gelatin (n = 0). Positive skin prick test results were observed for wines fined with albumin (n = 3), lysozyme (n = 2), casein (n = 1), gelatin (n = 0), and isinglass (n = 3), and for unfined wines (n = 1-2 in each patient group), with no significant differences between groups. Seventy-five percent of skin test-positive patients had specific immunoglobulin E to other allergens present in wine (eg, carbohydrates). The provocation test revealed no reactions to fined or unfined wines . CONCLUSIONS: Although concentrated fining agents containing ovalbumin, lysozyme, and casein were allergenic in the skin prick test, no patient reacted adversely in the provocation test to fined wine. Wines treated with fining agents at commercial concentrations appear not to present a risk to allergic individuals when filtered,

↩

[62] - Moneret-Vautrin DA. Allergie médicamenteuse et alimentaire à la gélatine. Alim'Inter 2003;8:241-243

↩

[63] - Pool V, Braun MM, Kelso JM, Mootrey G, Chen RT, Yunginger JW, et al. Prevalence of anti-gelatin IgE antibodies in people with anaphylaxis after measles-mumps rubella vaccine in the United States. Pediatrics 2002;110(6):e71

OBJECTIVE: Anaphylaxis after immunization, although rare, is serious and potentially life-threatening. Understanding risk factors for this reaction is therefore important. Gelatin is added to many vaccines as a heat stabilizer. Japanese researchers have demonstrated a strong association between immediate hypersensitivity reactions to measles, mumps, rubella, varicella, and Japanese encephalitis immunizations and subsequent detection of anti-gelatin immunoglobulin E (IgE) antibodies. They suggested that previous receipt by these patients of diphtheria-tetanus-acellular pertussis vaccines with trace amounts of gelatin was responsible for the sensitization. We aimed to assess whether a similar association exists for vaccinees in the United States who reported anaphylaxis after receipt of measles-mumps-rubella (MMR) or measles vaccines and to review recent trends in reporting of hypersensitivity reactions. METHODS: We conducted a retrospective case-control study. Cases of anaphylaxis that met a predefined case definition were identified from the US Vaccine Adverse Event Reporting System (VAERS). Mayo Clinic patients who received MMR vaccine uneventfully served as controls. The study subjects were interviewed to obtain the history of allergies. Sera from study subjects and their matched controls were tested for IgE antibodies to gelatin, whole egg, and vaccine viral antigens using solid-phase radioimmunoassay. Data from the Biologics Surveillance System on annual numbers of doses of MMR and varicella vaccines distributed in the United States were used to evaluate possible changes in reporting of selected allergic adverse events. RESULTS: Fifty-seven study subjects were recruited into the study and interviewed. Of these, 22 provided serum samples for IgE testing. Twenty-seven subjects served as a comparison group and provided a sample for IgE testing; 21 of these completed an allergy history questionnaire. Self-reported history of food allergies was present more frequently in the interviewed study subjects than in the controls, whereas the proportions of people with other characteristics were similar in both groups. None of the interviewed people had a history of food allergy to gelatin. The level of anti-gelatin IgE antibodies was significantly higher among study subjects than among controls, whereas the levels of IgE antibodies against egg and all 3 viral antigens did not differ significantly. Of 22 study subjects, 6 (27%) tested positive for anti-gelatin IgE, whereas none of the 27 controls did. The rate of anaphylactic reactions reported to VAERS after measles virus-containing immunization in the United States between 1991 and 1997 is 1.8 per 1 million doses distributed. No substantial increase in the number of reported allergic events after frequently used gelatin containing MMR and varicella vaccines could be observed during the first 4 years (1997-2000) since the introduction of diphtheria-tetanus-acellular pertussis vaccines for use in infancy. CONCLUSION: Anaphylactic reactions to MMR in the United States are rare. The reporting rate has the same order of magnitude as estimates from other countries. Almost one fourth of patients with reported anaphylaxis after MMR seem to have hypersensitivity to gelatin in the vaccine. They may be at higher risk of developing anaphylaxis to subsequent doses of other gelatin-containing vaccines. These people should seek an allergy evaluation before such immunization.

↩

[64] - Petit N. Réactions allergiques aux vaccins: prévalence, rôle des additifs, substances des excipients et contaminants. Alim'Inter 2006;11:91-99

↩

[65] - Ponvert C. Vaccinations et allergie. Rev Fr Allergol Immunol Clin 2007;47:9-15

Chez les atopiques, les vaccinations posent les problèmes d'une possible réaction allergique à un constituant des vaccins et le risque de réaction liée à des allergènes environnementaux, favorisée par l'injection de vaccin. On se demande aussi si les vaccinations de l'enfant sont susceptibles d'influencer le risque atopique. La valeur diagnostique et/ou prédictive des tests cutanés aux vaccins et des dosages des anticorps sériques varie selon le type de réaction et les substances responsables. En cas d'allergie prouvée ou hautement probable, le rappel doit être repoussé si le taux des anticorps protecteurs est élevé. Lorsque les taux d'anticorps protecteurs sont faibles, les injections de rappel doivent être effectuées en milieu hospitalier, selon une méthode d'accoutumance, chez les patients rapportant des réactions préoccupantes, immédiates ou accélérées. Le phénomène du « flash » correspond à des exacerbations de la maladie allergique, qui résultent d'une diminution du seuil de réactivité des patients aux allergènes, suite à l'injection de vaccin. Lorsqu'elle est effectuée chez des patients dont l'asthme est bien équilibré, la vaccination anti-grippale ne modifie pas, ou que peu, les paramètres fonctionnels respiratoires de base, non plus que l'hyperréactivité bronchique non spécifique, et est bien tolérée. D'une façon générale, la vaccination des allergiques doit être effectuée dans des conditions optimales de contrôle de la maladie allergique. Enfin, en ce qui concerne le troisième problème, la majorité des études et méta-analyses actuellement publiées suggère que les vaccinations n'ont pas d'influence significative sur le risque atopique, quel que soit l'âge auquel elles sont effectuées.

↩

[66] - Sakaguchi M, Nakayama T, Fujita H, Toda M, Inouye S. Estimated incidence in Japan of anaphylaxis to gelatin in vaccines. Vaccine 2000;19:431-436

In this study the authors tried to estimate the incidence in Japan of allergic reactions to the gelatin in vaccines before the gelatin elimination was started. There were 44 children with life-threatening severe anaphylaxis (airway obstruction or anaphylactic shock) during the 3-year period, 41 of whom had anti-gelatin IgE. There were 64 children with mild anaphylaxis (without airway obstruction); 62 had anti-gelatin IgE. There were 100 children with only systemic cutaneous signs; 81 had anti-gelatin IgE. The estimates for the incidence of the severe anaphylaxis in 1994-1996 are: 6.84, 7.31, 4. 36, and 10.3 cases per million doses of gelatin-containing measles, rubella, mumps, and varicella vaccines, respectively. Minimum estimated incidence in Japan of anaphylaxis to live virus vaccines including gelatin.

↩

[67] - Sakaguchi M, Inouye S. Systemic allergic reactions to gelatin included in vaccines as a stabilizer. Jpn J Infect Dis 2000;53:189-195

Most of the children who showed systemic immediate-type reactions, including anaphylactic shock, to measles, mumps, rubella, and varicella vaccines had IgE antibodies to gelatin; thus we suspected that the allergic symptoms are caused by gelatin antigen, which is usually included in these live-virus vaccines as a stabilizer. We hypothesized that the anti-gelatin IgE is elicited by immunization with DTaP (diphtheria-tetanus-acellular pertussis) vaccines, which contained a small amount of gelatin as a spillover protein after purification of pertussis toxin. To test this hypothesis, we conducted a case-control study to determine whether children with anti-gelatin IgE had received gelatin-containing DTaP vaccines, and it was indeed found that all such children in the study had immunization histories that included the gelatin-containing DTaP vaccines. Based on these findings, the vaccine manufacturers had removed gelatin from all the DTaP and live-virus vaccines produced in Japan by 2000. [References: 51]

↩

[68] - Sakaguchi M, Inouye S. Anaphylaxis to gelatin-containing rectal suppositories. J Allergy Clin Immunol 2001;108:1033-1034

Background: Some children˜though the number is few˜have been sensitized with gelatin. Objective: To investigate the relationship between the presence of antigelatin IgE and anaphylaxis to gelatin-containing rectal suppository, we measured antigelatin IgE in the sera of the children with anaphylaxis. Methods: Ten children showed systemic allergic reactions, including anaphylaxis, to a chloral hydrate rectal suppository containing gelatin (231 mg/dose) that had been used as a sedative. These children's clinical histories and serum samples were submitted from physicians to the National Institute of Infectious Diseases during a 2-year period from 1996 to 1997. Results: Of the 10 children, 5 showed apparent anaphylaxis, including hypotension and/or cyanosis, along with urticaria or wheezing; 2 showed both urticaria and wheezing without hypotension or cyanosis; the other 3 showed only urticaria. All of the children had antigelatin IgE (mean value ± SD, 7.9 ± 8.4 Ua/mL). As a control, samples from 250 randomly selected children had no antigelatin IgE. These findings suggest that the 10 children's systemic allergic reactions to this suppository were caused by the gelatin component. Conclusion: Gelatin-containing suppositories must be used with the same caution as gelatin-containing vaccines and other medications

↩

[69] - Scurlock AM, Althage KA, Christie L, Burks AW, Jones SM. Anaphylaxis after ingestion of gummy bears. J Allergy Clin Immunol 2002;110:936

↩

[70] - Kuehn A, Hilger C, Hentges F. Anaphylaxis to fish gelatin. Allergy 2008;63(suppl. 88):124

Background: Fish gelatin represents a useful alternative to porcine or bovine gelatins. The risk of allergic reactions to gelatin in general and fish gelatin in particular is considered to be low. We report a 12-year-old boy with known fish allergy, who suffered from a severe anaphylactic reaction with angioedema, urticaria and severe asthma after eating from a barbecue composed of animal meat, but no fish, and marshmallows. Methods: The patient‚s history was examined. Skin prick tests with commercial meat and fish extracts including cod, salmon and tuna were performed. Specific IgE were determined by ImmunoCap method. Fish muscle proteins and gelatins were separated using SDS-PAGE and tested by IgE-immunoblotting. From 8 commonly consumed fish species, 12 recombinant parvalbumins and 8 native parvalbumins as naturally occurring isoform mixtures were chromatographically purified to homogeneity. The patient‚s IgE-binding to these parvalbumin preparations and to different gelatins was analyzed for IgE-titer in ELISA experiments. Results: The patient had strongly positive skin tests to house dust mites, grass pollen, cod, salmon and tuna. Total IgE was 700 kU/L. Specific IgE was 63 kU/L for dermatophagoi¨ des pteronyssinus, 64 kU/L for meadow grass pollen, 65 kU/L for tuna, 32 kU/L for salmon and 16 kU/L for cod. IgE-immunoblotting showed IgE-binding to several fish parvalbumins at ca. 10 kDa and to gelatin proteins of different molecular size. The quantitative ELISA with recombinant parvalbumins gave IgE-binding values below those found in the commercial CAP system for the specific fish extracts. The difference was mostly significant for tuna where about half of the IgE-reactivity was not directed to tuna parvalbumin. This was consistent with the finding that the patient had specific IgE to fish gelatin as shown in ELISA assay. Conclusion: For some fish allergic patients, the ingestion of fish gelatin-containing products, as for instance marshmallows, harbors a risk for severe anaphylaxis. A primary source of fish gelatin is skin from tuna, a fish species considered less allergenic because of low parvalbumin content. As shown in this clinical case, it is highly recommended to detail the IgE reactivity of fish allergic patients and distinguish between IgE binding to recombinant, purified parvalbumins and gelatin.

↩

[71] - Sakaguchi M, Nakayama T, Inouye S. Food allergy to gelatin in children with systemic immediate-type reactions, including anaphylaxis, to vaccines. J Allergy Clin Immunol 1996;98:1058-1061

BACKGROUND: Anaphylaxis to measles-mumps-rubella vaccines has been reported. We have suspected that most such reactions are caused by gelatin contained in the vaccines. OBJECTIVE: To confirm the relation between systemic allergic reactions to vaccines and the presence of anti-gelatin IgE, we measured anti-gelatin IgE in children who demonstrated allergy to gelatin-containing vaccines. Furthermore, to clarify the relation between allergic reactions to gelatin in vaccines and foods, we surveyed the occurrence of allergic reactions to gelatin-containing foods in the same children. METHODS: Serum samples were taken from 26 children who had systemic immediate-type reactions, including anaphylactic shock, to vaccines and the same number of children without allergic reactions. Specific IgE to gelatin in these samples was measured. We then surveyed whether these children had allergic reactions to gelatin-containing foods before and after vaccination. RESULTS: Twenty-four of the 26 children with allergic reactions to vaccines had anti-gelatin IgE ranging from 1.2 to 250 Ua/ml. Seven had allergic reactions on ingestion of gelatin-containing foods. Of these, two had reactions before vaccination, and five had reactions after vaccination. All the control children without allergic reactions to vaccines had no anti-gelatin IgE. CONCLUSION: We reconfirmed a strong relationship between systemic immediate-type allergic reactions, including anaphylaxis, to vaccines and the presence of specific IgE to gelatin. Moreover, some of the children also had allergic reactions to food gelatin before or after vaccination.

↩

[72] - Kelso JM. The gelatin story. J Allergy Clin Immunol 1999;103:200-202

↩

[73] - Codreanu F. L'activité du réseau Allergo-Vigilance: allergies alimentaires. Alim'Inter 2007;12:239-242

↩

[74] - Hori H, Hattori S, Inouye S, Kimura A, Irie S, Miyazawa H, et al. Analysis of the major epitope of the alpha 2 chain of bovine type I collagen in children with bovine gelatin allergy. J Allergy Clin Immunol 2002;110:652-657

BACKGROUND: Anaphylaxis to measles, mumps, and rubella vaccines has been reported. It has been found that most of these reactions to live vaccines are caused by type I allergy with the bovine gelatin present in the vaccines as an allergen. Gelatin mainly includes denatured type I collagen, which consists of alpha1 and alpha2 chains. We previously reported that allergic reactions to gelatin are caused by the type I collagen alpha2 (alpha2[I]) chain . OBJECTIVE: To aid in the development of gelatin that has little or no allergenicity in human subjects, we investigated epitopes of bovine alpha2(I) chain with use of IgE in gelatin-sensitive children . METHODS: Serum samples were collected from 15 patients who had systemic allergic reactions to vaccines and high levels of specific IgE to bovine gelatin. Eleven overlapping recombinant proteins that cover bovine alpha2(I) were prepared with a bacterial expression vector. We examined IgE reactivity to these recombinant proteins by means of ELISA. Fifteen peptides covering a major reactive recombinant protein were synthesized. The IgE-reacting epitope was identified by means of IgE-ELISA inhibition with these synthetic peptides and pooled serum from the patients . RESULTS: We found that of the 15 patients, 13 showed IgE reactivity to a recombinant protein (no. 3) spanning the central region of the collagenous domain ((418)Gly-(662)Pro). Furthermore, all 13 patients showed IgE reactivity to the 4-kd recombinant protein (no. 3a) spanning the region from (461)Pro to (500)Glu. In IgE-ELISA inhibition we found that a minimum IgE epitope of gelatin allergen was composed of the 10-amino-acid sequence (485)Ile-Pro-Gly-Glu-Phe-Gly-Leu-Pro-Gly-Pro(494). This sequence is not observed in the human type I collagen alpha1 and alpha2 chains, nor is it found in the bovine type I collagen alpha1 chain . CONCLUSIONS: We found that Ile-Pro-Gly-Glu-Phe-Gly-Leu-Pro-Gly-Pro is a major IgE epitope of the alpha2 chain of bovine type I collagen in patients with gelatin allergy. The degree of anaphylaxis to gelatin in vaccines might be reduced by digestion of this IgE-binding site in gelatin.

↩

[75] - Sakaguchi M, Nakayama T, Inouye S. Food allergy to gelatin in children with systemic immediate-type reactions, including anaphylaxis, to vaccines. J Allergy Clin Immunol 1996;98:1058-1061

BACKGROUND: Anaphylaxis to measles-mumps-rubella vaccines has been reported. We have suspected that most such reactions are caused by gelatin contained in the vaccines. OBJECTIVE: To confirm the relation between systemic allergic reactions to vaccines and the presence of anti-gelatin IgE, we measured anti-gelatin IgE in children who demonstrated allergy to gelatin-containing vaccines. Furthermore, to clarify the relation between allergic reactions to gelatin in vaccines and foods, we surveyed the occurrence of allergic reactions to gelatin-containing foods in the same children. METHODS: Serum samples were taken from 26 children who had systemic immediate-type reactions, including anaphylactic shock, to vaccines and the same number of children without allergic reactions. Specific IgE to gelatin in these samples was measured. We then surveyed whether these children had allergic reactions to gelatin-containing foods before and after vaccination. RESULTS: Twenty-four of the 26 children with allergic reactions to vaccines had anti-gelatin IgE ranging from 1.2 to 250 Ua/ml. Seven had allergic reactions on ingestion of gelatin-containing foods. Of these, two had reactions before vaccination, and five had reactions after vaccination. All the control children without allergic reactions to vaccines had no anti-gelatin IgE. CONCLUSION: We reconfirmed a strong relationship between systemic immediate-type allergic reactions, including anaphylaxis, to vaccines and the presence of specific IgE to gelatin. Moreover, some of the children also had allergic reactions to food gelatin before or after vaccination.

↩

[76] - Sakaguchi M, Hori H, Ebihara T, Irie S, Yanagida M, Inouye S. Reactivity of the immunoglobulin E in bovine gelatin-sensitive children to gelatins from various animals. Immunology 1999;96:286-290

It has been reported that most children who showed anaphylaxis to measles, mumps and rubella vaccines containing bovine gelatin as a stabilizer have anti-bovine gelatin IgE. The present study was designed to investigate the reactivity of IgE in bovine gelatin-sensitive children to gelatins from various animals, and the antigenic cross-reactivity between the gelatins. Serum samples taken from 10 children who showed anaphylaxis to vaccines containing bovine gelatin were used in this study. The level of anti-bovine gelatin IgE in these serum samples ranged from 11.0 to 251 Ua/ml. The IgE in most of the children reacted to kangaroo and mouse gelatins, to which they had had little or no exposure as a food or a vaccine stabilizer. The IgE binding to kangaroo and mouse gelatins was completely inhibited by bovine gelatin, whereas reciprocal inhibition was not complete, indicating that antigenic cross-reactivity is present between the mammalian gelatins. Only one child had strong IgE reactivity to fish gelatins, and this reactivity was not inhibited by bovine gelatin, indicating that no antigenic cross-reactivity exists between bovine and fish gelatins. Most of the children who displayed sensitivity to bovine gelatin showed IgE reactivity to other mammalian gelatins. This reactivity may be due primarily to the antigenic cross-reactivity between mammalian gelatins.

↩

[77] - Hamada Y, Nagashima Y, Shiomi K. Identification of collagen as a new fish allergen. Biosci Biotechnol Biochem 2001;65:285-291

This study was intended to identify a high molecular weight allergen that had been detected in fish. Analyses by ELISA of five protein fractions prepared from bigeye tuna muscle showed that the high molecular weight allergen was contained in the myostromal protein fraction. Based on the results of SDS-PAGE, immunoblotting and amino acid analysis of the myostromal protein fraction, the high molecular weight allergen was judged to be collagen. Five of the eight patient sera used were found to react to the bigeye tuna collagen. In competitive ELISA inhibition experiments, the bigeye tuna collagen almost completely inhibited the IgE reactivity to the heated extracts from five species of fish, suggesting that collagen is commonly allergic regardless of fish species. However, no antigenic cross-reactivity was observed between collagens from fish and other animals.

↩

[78] - André F, Cavagna S, André C. Gelatin Prepared from Tuna Skin: A Risk Factor for Fish Allergy or Sensitization ? Int Arch Allergy Immunol 2003;130:17-24

Background: Although fish gelatin may represent a useful alternative to bovine or porcine gelatins, the clearly recognized high prevalence of fish allergy could increase the risk of anaphylaxis to gelatin. The rationale for investigating tuna gelatin rather than gelatins from more allergenic fishes is the availability of an industrial gelatin under development. The infrequent occurrence of tuna allergy should influence the safety of a derived product. The present study investigated IgE antibodies to tuna-skin-derived gelatin in adults and children with documented fish allergy or sensitization. Methods: Serum samples were taken from 100 consecutive patients with fish allergy or sensitization and tested for IgE antibodies against hydrolyzed or nonhydrolyzed gelatin extracted from tuna skin as compared to extracts from tuna flesh, tuna skin as well as bovine or porcine gelatins. Patients with tuna allergies or sensitization were sensitive to the same tuna species (yellowfin) as that from which the gelatin was obtained. IgE antibodies to these various extracts were analyzed using SDS-PAGE and immunoblotting. Results: Only 3 of the 100 serum samples tested gave evidence of reactivity to gelatin extracted from tuna skin. Cross-reactivity between bovine/porcine and fish gelatins was not observed. Conclusion: The risk of adverse reactions to tuna skin gelatin seems to be significantly lower than the risk of fish allergy. Fish gelatin may represent a valuable alternative to bovine or porcine gelatins.

↩

[79] - Hamada Y, Nagashima Y, Shiomi K, Shimojo N, Kohno Y, Shibata R, et al. Reactivity of IgE in fish-allergic patients to fish muscle collagen. Allergol Int 2003;52:139-148

In addition to parvalbumin, the well-known major allergen in fish, collagen was recently identified as a new allergen in the muscle of bigeye tuna and in the skin of several species of fish. Collagen was purified from the white muscle of five species of fish (Japanese eel, alfonsin, mackerel, skipjack and bigeye tuna). The IgE reactivities to collagen and parvalbumin were examined by ELISA, whereas antigenic cross-reactivity among fish muscle collagens was investigated by ELISA inhibition experiments. When 15 sera from fish-allergic patients were subjected to ELISA using bigeye tuna collagen and parvalbumin, 10 sera reacted only to parvalbumin, two reacted only to collagen, two reacted to both collagen and parvalbumin and one reacted to neither collagen nor parvalbumin. The sera containing specific IgE to bigeye tuna collagen also reacted to collagens from the other four species of fish. In the ELISA inhibition experiments, cross-reactivity among the collagens from five species of fish was suggested.

↩

[80] - Sakaguchi M, Toda M, Ebihara T, Irie S, Hori H, Imai A, et al. IgE antibody to fish gelatin (type I collagen) in patients with fish allergy. J Allergy Clin Immunol 2000;106:579-584

BACKGROUND: Most children with anaphylaxis to measles, mumps, and rubella vaccines had shown sensitivity to bovine gelatin that was included in the vaccines. Recently, it was found that bovine type I collagen, which is the main content in the gelatin, is a major allergen in bovine gelatin allergy. Fish meat and skin also contain type I collagen. OBJECTIVE: The present study was designed to investigate IgE antibody to fish gelatin in children with fish allergy. METHODS: Serum samples were taken from patients in 3 groups: (1) 10 patients with fish allergy and specific IgE to fish meat; (2) two patients with allergies to both fish meat and bovine gelatin and specific IgE to fish meat and bovine gelatin; and (3) 15 patients with atopic dermatitis and specific IgE to fish meat. Various fish gelatins (type I collagen) were prepared from fish skin. IgE antibody to fish gelatin was analyzed by using ELISA and immunoblotting. RESULTS: Of 10 patients with fish allergy, 3 had specific IgE to fish gelatin. Of two patients with fish allergy and bovine gelatin allergy, all had specific IgE to fish gelatin. Of 15 patients with atopic dermatitis and specific IgE to fish meat, 5 had specific IgE to fish gelatin. Furthermore, IgE from pooled serum of the patients reacted with both the alpha1 and alpha2 chains of fish type I collagen in immunoblots. There is cross-reactivity among gelatins from various fishes, but there is little cross-reactivity between fish and bovine gelatins. CONCLUSION: Some fish-sensitive patients possessed IgE antibody to fish gelatin. Fish gelatin (type I collagen) might be an allergen in subjects with fish allergy.

↩

[81] - André F, Cavagna S, André C. Gelatin Prepared from Tuna Skin: A Risk Factor for Fish Allergy or Sensitization ? Int Arch Allergy Immunol 2003;130:17-24

Background: Although fish gelatin may represent a useful alternative to bovine or porcine gelatins, the clearly recognized high prevalence of fish allergy could increase the risk of anaphylaxis to gelatin. The rationale for investigating tuna gelatin rather than gelatins from more allergenic fishes is the availability of an industrial gelatin under development. The infrequent occurrence of tuna allergy should influence the safety of a derived product. The present study investigated IgE antibodies to tuna-skin-derived gelatin in adults and children with documented fish allergy or sensitization. Methods: Serum samples were taken from 100 consecutive patients with fish allergy or sensitization and tested for IgE antibodies against hydrolyzed or nonhydrolyzed gelatin extracted from tuna skin as compared to extracts from tuna flesh, tuna skin as well as bovine or porcine gelatins. Patients with tuna allergies or sensitization were sensitive to the same tuna species (yellowfin) as that from which the gelatin was obtained. IgE antibodies to these various extracts were analyzed using SDS-PAGE and immunoblotting. Results: Only 3 of the 100 serum samples tested gave evidence of reactivity to gelatin extracted from tuna skin. Cross-reactivity between bovine/porcine and fish gelatins was not observed. Conclusion: The risk of adverse reactions to tuna skin gelatin seems to be significantly lower than the risk of fish allergy. Fish gelatin may represent a valuable alternative to bovine or porcine gelatins.

↩

[82] - Sakaguchi M, Hori H, Ebihara T, Irie S, Yanagida M, Inouye S. Reactivity of the immunoglobulin E in bovine gelatin-sensitive children to gelatins from various animals. Immunology 1999;96:286-290

It has been reported that most children who showed anaphylaxis to measles, mumps and rubella vaccines containing bovine gelatin as a stabilizer have anti-bovine gelatin IgE. The present study was designed to investigate the reactivity of IgE in bovine gelatin-sensitive children to gelatins from various animals, and the antigenic cross-reactivity between the gelatins. Serum samples taken from 10 children who showed anaphylaxis to vaccines containing bovine gelatin were used in this study. The level of anti-bovine gelatin IgE in these serum samples ranged from 11.0 to 251 Ua/ml. The IgE in most of the children reacted to kangaroo and mouse gelatins, to which they had had little or no exposure as a food or a vaccine stabilizer. The IgE binding to kangaroo and mouse gelatins was completely inhibited by bovine gelatin, whereas reciprocal inhibition was not complete, indicating that antigenic cross-reactivity is present between the mammalian gelatins. Only one child had strong IgE reactivity to fish gelatins, and this reactivity was not inhibited by bovine gelatin, indicating that no antigenic cross-reactivity exists between bovine and fish gelatins. Most of the children who displayed sensitivity to bovine gelatin showed IgE reactivity to other mammalian gelatins. This reactivity may be due primarily to the antigenic cross-reactivity between mammalian gelatins.

↩

[83] - Hamada Y, Nagashima Y, Shiomi K. Identification of collagen as a new fish allergen. Biosci Biotechnol Biochem 2001;65:285-291

This study was intended to identify a high molecular weight allergen that had been detected in fish. Analyses by ELISA of five protein fractions prepared from bigeye tuna muscle showed that the high molecular weight allergen was contained in the myostromal protein fraction. Based on the results of SDS-PAGE, immunoblotting and amino acid analysis of the myostromal protein fraction, the high molecular weight allergen was judged to be collagen. Five of the eight patient sera used were found to react to the bigeye tuna collagen. In competitive ELISA inhibition experiments, the bigeye tuna collagen almost completely inhibited the IgE reactivity to the heated extracts from five species of fish, suggesting that collagen is commonly allergic regardless of fish species. However, no antigenic cross-reactivity was observed between collagens from fish and other animals.

↩

[84] - Sakaguchi M, Toda M, Ebihara T, Irie S, Hori H, Imai A, et al. IgE antibody to fish gelatin (type I collagen) in patients with fish allergy. J Allergy Clin Immunol 2000;106:579-584

BACKGROUND: Most children with anaphylaxis to measles, mumps, and rubella vaccines had shown sensitivity to bovine gelatin that was included in the vaccines. Recently, it was found that bovine type I collagen, which is the main content in the gelatin, is a major allergen in bovine gelatin allergy. Fish meat and skin also contain type I collagen. OBJECTIVE: The present study was designed to investigate IgE antibody to fish gelatin in children with fish allergy. METHODS: Serum samples were taken from patients in 3 groups: (1) 10 patients with fish allergy and specific IgE to fish meat; (2) two patients with allergies to both fish meat and bovine gelatin and specific IgE to fish meat and bovine gelatin; and (3) 15 patients with atopic dermatitis and specific IgE to fish meat. Various fish gelatins (type I collagen) were prepared from fish skin. IgE antibody to fish gelatin was analyzed by using ELISA and immunoblotting. RESULTS: Of 10 patients with fish allergy, 3 had specific IgE to fish gelatin. Of two patients with fish allergy and bovine gelatin allergy, all had specific IgE to fish gelatin. Of 15 patients with atopic dermatitis and specific IgE to fish meat, 5 had specific IgE to fish gelatin. Furthermore, IgE from pooled serum of the patients reacted with both the alpha1 and alpha2 chains of fish type I collagen in immunoblots. There is cross-reactivity among gelatins from various fishes, but there is little cross-reactivity between fish and bovine gelatins. CONCLUSION: Some fish-sensitive patients possessed IgE antibody to fish gelatin. Fish gelatin (type I collagen) might be an allergen in subjects with fish allergy.

↩

[85] - Sakaguchi M, Toda M, Ebihara T, Irie S, Hori H, Imai A, et al. IgE antibody to fish gelatin (type I collagen) in patients with fish allergy. J Allergy Clin Immunol 2000;106:579-584

BACKGROUND: Most children with anaphylaxis to measles, mumps, and rubella vaccines had shown sensitivity to bovine gelatin that was included in the vaccines. Recently, it was found that bovine type I collagen, which is the main content in the gelatin, is a major allergen in bovine gelatin allergy. Fish meat and skin also contain type I collagen. OBJECTIVE: The present study was designed to investigate IgE antibody to fish gelatin in children with fish allergy. METHODS: Serum samples were taken from patients in 3 groups: (1) 10 patients with fish allergy and specific IgE to fish meat; (2) two patients with allergies to both fish meat and bovine gelatin and specific IgE to fish meat and bovine gelatin; and (3) 15 patients with atopic dermatitis and specific IgE to fish meat. Various fish gelatins (type I collagen) were prepared from fish skin. IgE antibody to fish gelatin was analyzed by using ELISA and immunoblotting. RESULTS: Of 10 patients with fish allergy, 3 had specific IgE to fish gelatin. Of two patients with fish allergy and bovine gelatin allergy, all had specific IgE to fish gelatin. Of 15 patients with atopic dermatitis and specific IgE to fish meat, 5 had specific IgE to fish gelatin. Furthermore, IgE from pooled serum of the patients reacted with both the alpha1 and alpha2 chains of fish type I collagen in immunoblots. There is cross-reactivity among gelatins from various fishes, but there is little cross-reactivity between fish and bovine gelatins. CONCLUSION: Some fish-sensitive patients possessed IgE antibody to fish gelatin. Fish gelatin (type I collagen) might be an allergen in subjects with fish allergy.

↩

[86] - Hamada Y, Nagashima Y, Shiomi K. Identification of collagen as a new fish allergen. Biosci Biotechnol Biochem 2001;65:285-291

This study was intended to identify a high molecular weight allergen that had been detected in fish. Analyses by ELISA of five protein fractions prepared from bigeye tuna muscle showed that the high molecular weight allergen was contained in the myostromal protein fraction. Based on the results of SDS-PAGE, immunoblotting and amino acid analysis of the myostromal protein fraction, the high molecular weight allergen was judged to be collagen. Five of the eight patient sera used were found to react to the bigeye tuna collagen. In competitive ELISA inhibition experiments, the bigeye tuna collagen almost completely inhibited the IgE reactivity to the heated extracts from five species of fish, suggesting that collagen is commonly allergic regardless of fish species. However, no antigenic cross-reactivity was observed between collagens from fish and other animals.

↩

[87] - André F, Cavagna S, André C. Gelatin Prepared from Tuna Skin: A Risk Factor for Fish Allergy or Sensitization ? Int Arch Allergy Immunol 2003;130:17-24

Background: Although fish gelatin may represent a useful alternative to bovine or porcine gelatins, the clearly recognized high prevalence of fish allergy could increase the risk of anaphylaxis to gelatin. The rationale for investigating tuna gelatin rather than gelatins from more allergenic fishes is the availability of an industrial gelatin under development. The infrequent occurrence of tuna allergy should influence the safety of a derived product. The present study investigated IgE antibodies to tuna-skin-derived gelatin in adults and children with documented fish allergy or sensitization. Methods: Serum samples were taken from 100 consecutive patients with fish allergy or sensitization and tested for IgE antibodies against hydrolyzed or nonhydrolyzed gelatin extracted from tuna skin as compared to extracts from tuna flesh, tuna skin as well as bovine or porcine gelatins. Patients with tuna allergies or sensitization were sensitive to the same tuna species (yellowfin) as that from which the gelatin was obtained. IgE antibodies to these various extracts were analyzed using SDS-PAGE and immunoblotting. Results: Only 3 of the 100 serum samples tested gave evidence of reactivity to gelatin extracted from tuna skin. Cross-reactivity between bovine/porcine and fish gelatins was not observed. Conclusion: The risk of adverse reactions to tuna skin gelatin seems to be significantly lower than the risk of fish allergy. Fish gelatin may represent a valuable alternative to bovine or porcine gelatins.

↩

[88] - Hansen TK, PoulsenLK, Skov PS, Hefle SL, Hlywka JJ, Taylor SL, et al. A randomized, double-blind, placebo-controlled oral challenge study to evaluate the allergenic potential of commercial, food-grade fish gelatin. Food Chem Toxicol 2004;42:2037-2044

BACKGROUND: Recent interest in the labeling of foods and food proteins derived from allergenic sources necessitates determination of the potential allergenicity of such food ingredients. Fish gelatin is extracted from the skin of fish species known to elicit allergic reactions in sensitized individuals. OBJECTIVE: To determine the allergenicity of fish gelatin by double-blinded, placebo-controlled food challenges (DBPCFC) in clinically fish-allergic individuals. METHODS: Thirty fish-allergic patients diagnosed according to the EAACI Guidelines were included (age 9-50 years). Skin prick tests (SPT) and Histamine Release tests (HR) were performed with fish gelatin and codfish, and codfish-specific IgE was measured. All patients underwent DBPCFC with a cumulative dose of 14.61 g fish gelatin. RESULTS: In all 30 patients SPT, HR, and specific IgE to codfish were positive. SPT and HR with fish gelatin were positive in 3/30 and 7/30, respectively. One patient showed mild reaction to placebo and no reaction to the active challenge. Two patients reported mild subjective reactions to active challenge. Upon re-challenge one of them described subjective symptoms again to the active challenge (7.61 g cumulated dose of fish gelatin) with no reaction to placebo, while the other experienced very mild subjective symptoms to placebo and nothing to the active. The proportion of truly sensitive patients was estimated to 0.03 in the total study group. CONCLUSION: None of 30 fish allergic patients reacted adversely to the ingestion of 3.61 g cumulative dose of fish gelatin. In this study fish gelatin presents no risk to fish-allergic patients at the doses typically used. Statistically, these results indicate that there is 95% certainty that 90% of fish-allergic consumers will not react to ingestion of a 3.61 g cumulative dose of fish gelatin.

↩

[89] - Kuehn A, Hilger C, Hentges F. Anaphylaxis provoked by ingestion of marshmallows containing fish gelatin. J Allergy Clin Immunol 2009;123:708-709

↩

[90] - Mullins RJA, Apostolou E. Anaphylaxis to Beef, Gelatin and Haemaccel. AAAAI 60th Annual Meeting, San Francisco, 19-23 March 2004, Poster n°861

Rationale Meat-derived gelatin is commonly added to processed foods. 3 pts were seen initially, 1 allergic to topical & oral gelatin & 2 with anaphylaxis (Ax) to Haemaccel. All subsequently developed allergy to beef, suggesting that gelatin was a trigger. Method s : 14 patients with suspected beef/gelatin Ax, 62 controls & 31 with idiopathic Ax (IAx; 14 prospectively) were investigated for gelatin sensitivity by skin testing (ST) & RAST. Result s : 8/14 patients with beef allergy reacted clinically to gelatin on separate occasions; gelatin RAST/ST were positive in 7 & 8/8, respectively. Gelatin ST were positive in 3 additional patients (6-20mm weals). Overall, 3/14 beef allergics had positive beef ST. 3 with negative gelatin ST/RAST had positive RAST to other beef proteins - BSA, bovine gammaglobulin & betalipoprotein IV, betalactobulin. 1/18 recalled IAx patients 1995-2001 had positive gelatin ST. By contrast, ST were negative in RJM (45 occasions) & 62 controls. 10/10 control sera had negative RAST. 92 patients with Ax were evaluated prospectively 2002-3. Triggers were animals, exercise, medication, idiopathic, stings, food allergy, healthy controls (1, 5, 5, 13,18, 47, 2 cases, respectively). Ax occurred after beef in 2/2 with positive gelatin ST, but only 1 had positive beef ST. The beef ST negative subject nonetheless reacted to deliberate Haemaccel challenge (~1.1gm IVI gelatin). Conclusions : Gelatin is an important beef allergen and may account for some cases of IAx. A positive ST convey risk for gelatin, meat & Haemaccel Ax which may be missed if one relies only on commercial beef allergens.

↩

[91] - Bogdanovic J, Halsey NA, Wood RA, Hamilton RG. Prevalence of Bovine and Porcine Gelatin-Specific IgE in Food Allergic Children. J Allergy Clin Immunol 2008;121:S244

RATIONALE: We studied the prevalence of gelatin-specific IgE antibodies in the serum of children with sensitivity to relevant foods (beef, pork and cow‚s milk) to assess their potential risk for sensitization and allergic reactions following exposure to gelatin-containing products. METHODS: Sera from 100 selected children (ages 1-18 yrs, total IgE range 29-49,457 kIU/L) with detectable (>0.35 kUa/L) IgE to cow‚s milk (n 5 99), beef (n 5 80), and/or pork (n 5 68) were analyzed for IgE antibovine and porcine gelatin using the Phadia ImmunoCAP System. RESULTS: Of cow‚s milk-IgE positive sera (range:1.43-464 kUa/L), 79 (80%) had detectable beef-IgE (range:0.36-95 kUa/L). Bovine gelatin-IgE was detected in 13 (16.3%) of beef-IgE positive sera and none of sera containing only milk-IgE but not beef-IgE. Of 68 pork-IgE positive sera, 26 (38.2%) had detectable porcine gelatin-IgE (range 0.35-3.25 kUa/L). Three pork-IgE negative sera were weakly positive for porcine gelatin (0.36-0.74 kUa/L). Partial (20%-80%) cross-inhibition was seen by pre-incubating sera with soluble bovine/porcine gelatin in some but not all gelatin-IgE positive sera. The probability of gelatin-IgE positivity tended to increase with higher concentrations (especially at levels > 25 kUa/L) of beef-IgE or pork-IgE. CONCLUSIONS: The majority of beef- and pork-IgE positive sera do not contain detectable gelatin-IgE antibody, suggesting that these individuals may safely receive gelatin-containing biological products. While IgE antibody reactivity to beef and pork does not automatically mean sensitivity to bovine/porcine gelatin, the true risk of clinical reactivity to gelatin in individuals allergic to beef and pork deserves further study.

↩

[92] - Drouet M, Menehould C. Les composants mammifères dans les médicaments. Colloque SAICO, Angers, 29 juin 2006

↩

[93] - Chung CH, Mirakhur B, Chan E, Le QT, Berlin J, Morse M, et al. Cetuximab-induced anaphylaxis and IgE specific for galactose-alpha-1,3-galactose. N Engl J Med 2008;358:1109-1117

BACKGROUND: Cetuximab, a chimeric mouse-human IgG1 monoclonal antibody against the epidermal growth factor receptor, is approved for use in colorectal cancer and squamous-cell carcinoma of the head and neck. A high prevalence of hypersensitivity reactions to cetuximab has been reported in some areas of the United States . METHODS: We analyzed serum samples from four groups of subjects for IgE antibodies against cetuximab: pretreatment samples from 76 case subjects who had been treated with cetuximab at multiple centers, predominantly in Tennessee, Arkansas, and North Carolina; samples from 72 control subjects in Tennessee; samples from 49 control subjects with cancer in northern California; and samples from 341 female control subjects in Boston . RESULTS: Among 76 cetuximab-treated subjects, 25 had a hypersensitivity reaction to the drug. IgE antibodies against cetuximab were found in pretreatment samples from 17 of these subjects; only 1 of 51 subjects who did not have a hypersensitivity reaction had such antibodies (P<0.001). IgE antibodies against cetuximab were found in 15 of 72 samples (20.8%) from control subjects in Tennessee, in 3 of 49 samples (6.1%) from northern California, and in 2 of 341 samples (0.6%) from Boston. The IgE antibodies were shown to be specific for an oligosaccharide, galactose-alpha-1,3-galactose, which is present on the Fab portion of the cetuximab heavy chain . CONCLUSIONS: In most subjects who had a hypersensitivity reaction to cetuximab, IgE antibodies against cetuximab were present in serum before therapy. The antibodies were specific for galactose-alpha-1,3-galactose

↩

[94] - Hosen J, Perzanowski M, Carter MC, Odhiambo J, Ng’ang’a L, Ngari P, et al. IgE Antibodies to Helminths and the Cross-Reactive Oligosaccharide Galactose-alpha-1,3-galactose (alphaGal) among Children in a Village in Africa. J Allergy Clin Immunol 2008;121:S140

RATIONALE: Recent reports have identified IgE antibodies to alphaGal as a cause of anaphylactic reactions to the mAb cetuximab. These IgE antibodies cross-react with proteins from cat, dog, beef and pork. Previous reports showed that children in Africa had IgE ab to cat allergens despite negative skin tests and no exposure to cats. We report here the connection between IgE ab to alphaGal, cat proteins and helminth parasites. METHODS: Sera from children (age 9-11) in rural (Kabati) and urban (Thika) Kenya and Atlanta, GA were assayed for IgE ab to alphaGal, cat, mite, Ascaris and Echinococcus, using ImmunoCAP or the modified assay with biotinylated antigens bound to Streptavidin CAP. RESULTS: Of 130 sera tested from Kabati 100 were positive for alphaGal IgE (GM: 3.96 IU/mL). In Thika 36 out of 123 were positive, in Atlanta 0 out of 52 were. In Kabati 95 of 130 sera were positive for Ascaris and 75 were positive for Echinococcus. The correlation with IgE to alphaGal was much stronger for Echinococcus (r = 0.84; p < 0.001) than for Ascaris (r = 0.19; p = 0.05). There was a close correlation between IgE ab to cat and IgE to alphaGal (r = 0.86; p < 0.001). CONCLUSIONS: IgE ab to alphaGal is widespread among children in an African village, less common in a small town and virtually non-existent among African American children in Atlanta. While the cause of sensitization is unclear, the correlation with Echinococcus suggests a tapeworm could be responsible. The correlation with IgE ab to alphaGal explains the previously enigmatic IgE ab to cat found in African sera.

↩

[95] - Roper JM, Berg A, Satinover SM, Ronmark E, Lundback B, Platts-Mills TAE. IgE Antibodies to Mammalian Antigens in a Population-based Cohort of 963 Teenagers Living in Northern Sweden. J Allergy Clin Immunol 2009;123:S22

RATIONALE: In this cold and dry climate, cat and dog sensitization strongly predict asthma risk. By contrast, sensitization to dust mite, cockroach, and fungi are not associated with respiratory symptoms. Using sera from teenagers participating in a prospective study, we evaluated IgE antibodies to mammalian allergens. METHODS: Sera from 963 18 year olds from Northern Sweden were assayed for IgE to cat, dog, and horse using ImmunoCAP. RESULTS: IgE to cat (e1) was present in 219 (23%) sera, and correlated closely with IgE to Fel d 1 (r = 0.91, p < 0.001). The assessment for dog sensitization was influenced by the choice of assay: there were 84 (9%) positive sera to epithelium (e2), compared with 190 (20%) positive sera to dander (e5). The correlation between dog epithelium and cat was higher (r =0.59, p < 0.01) than that of dog dander versus cat (r =0.24, p < 0.01). Additionally, 142 individuals (15%) were positive to horse (e3). While inter- species correlations were significant, 73 individuals (8%) had IgE to only one of the three allergens: 46 sera for cat, 18 for dog, and 9 were only positive for horse. Cross reactivity could be explained by IgE to the carbohydrate galactose-alpha-1,3-galactose, however assay of 150 sera with IgE to mammalian allergens identified only one positive (titer = 0.52 IU/mL). CONCLUSIONS: In this cohort where sensitization to mammalian proteins is strongly associated with asthma, there was extensive correlation between each of the allergens. However, 73 sera were positive to only one mammal.

↩

[96] - Commins SP, Satinover SM, Hosen J, Mozena J, Borish L, Lewis BD et al. Delayed anaphylaxis, angioedema, or urticaria after consumption of red meat in patients with IgE antibodies specific for galactose-alpha-1,3-galactose. J Allergy Clin Immunol 2009;123:426-433

Carbohydrate moieties are frequently encountered in food and can elicit IgE responses, the clinical significance of which has been unclear. Recent work, however, has shown that IgE antibodies to galactose-alpha-1,3-galactose (alpha-gal), a carbohydrate commonly expressed on nonprimate mammalian proteins, are capable of eliciting serious, even fatal, reactions. This study sought to determine whether IgE antibodies to alpha-gal are present in sera from patients who report anaphylaxis or urticaria after eating beef, pork, or lamb. Twenty-four patients with IgE antibodies to alpha-gal were identified. These patients described a similar history of anaphylaxis, angiodema or urticaria 3 to 6 hours after the ingestion of meat and reported fewer or no episodes when following an avoidance diet. SPTs to mammalian meat produced wheals of usually less than 4 mm, whereas intradermal or fresh-food SPTs provided larger and more consistent wheal responses. CAP-RAST testing revealed specific IgE antibodies to beef, pork, lamb, cow's milk, cat, and dog but not turkey, chicken, or fish. Absorption experiments indicated that this pattern of sensitivity was explained by an IgE antibody specific for alpha-gal.

↩

Le miel

Les gélatines

Rubriques