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La moutarde
mercredi 12 mai 2010, par
La moutarde est un condiment (souvent inclus dans les épices) contenant entre autres des graines de différentes espèces de Brassicacées :
- Sinapis alba, la moutarde jaune (ou blanche)
- Brassica nigra, la moutarde noire
- Brassica juncea, la moutarde de Chine (ou brune), qui est un hybride de B.nigra et de B.napa oleifera (navette).
La moutarde est la cause d’un certain nombre de cas d’allergie alimentaire chez l’enfant 
.
Les statistiques établies par le CICBAA (mai 2007, Moneret-Vautrin DA, communication personnelle) placent la moutarde au 13ème rang parmi les allergies alimentaires de l’enfant, soit 1,15% des allergies relevées avant l’âge de 15 ans. Au-delà de cet âge, la moutarde ne fait pas partie des 20 premières causes d’allergie alimentaire.
La prévalence de l’allergie à la moutarde varie beaucoup d’une étude à une autre en raison des habitudes locales de consommation et de l’âge des patients.
Des taux allant jusqu’à 7 à 16 % ont été avancés, mais ils doivent être tempérés car la preuve d’une allergie à l’aide d’un TPODA n’a été que rarement obtenue . Le goût de la moutarde étant difficile à masquer, le diagnostic d’allergie a été souvent basé sur un TPO en simple aveugle et même, parfois, sur une histoire clinique confortée par un test cutané positif.
En mai 2010 le Réseau d’Allergo-Vigilance avait rapporté 3 cas d’allergie sévère à la moutarde (sur 900 déclarations).
Les allergènes de la moutarde
Bra j 1 (B. juncea) et Sin a 1 (S. alba) sont des 2S albumines proches des napines trouvées dans les graines de colza. Sin a 1 croise avec Bra n 1 du colza et avec Bra j 1 .
Ces allergènes sont, à priori, les allergènes principaux des graines de moutarde.
En plus des 2S albumines, ont été montrées IgE-réactives :
- une 11S globuline (Sin a 2) , qui est faiblement homologue d’Ara h 3 (arachide) et d’Ana o 2 (noix de cajou).
- Une LTP (Sin a 3) et une profiline (Sin a 4) dans la moutarde jaune, positives respectivement chez 9/15 et 4/15 patients Espagnols allergiques à la moutarde (et à la pêche) .
Un syndrome armoise-moutarde ?
Plusieurs études espagnoles semblent accréditer l’existence d’un syndrome armoise-moutarde, comme l’a suggéré Figueroa chez les sujets adultes .
Plus généralement, il pourrait s’agir d’une association Composées-Brassicacées :
- 37 TC positifs armoise parmi 38 allergiques à la moutarde, parmi lesquels une histoire clinique d’allergie au chou, chou-fleur et/ou brocoli est notée 9 fois .
- dans cette étude, moutarde et armoise croisent et les deux se montrent capables d’inhiber l’IgE-réactivité pour les différents choux
- 16 TC positifs armoise parmi 17 allergiques au chou, avec aussi 12 histoires cliniques positives pour la moutarde et 11 pour la pêche. Ici la moutarde croise avec la LTP du chou Bra o 3 .
- Dans une autre étude 90 % des sujets allergiques à la moutarde sont polliniques et de nombreux patients rapportent des réactions alimentaires pour les fruits des Rosacées . La pêche était montrée capable d’inhiber la LTP de moutarde Sin a 3.
Ces études espagnoles pointent bien vers un lien possible entre pollen (armoise) et aliments (moutarde, choux, Rosacées) par le truchement de LTP. La survenue fréquente de réactions ne se limitant pas à un syndrome oral (13 cas/15 <biblio11032), voire anaphylactiques , accrédite d’autant un rôle pour les LTP.
Mais la pollinose n’est pas systématique , ni l’allergie aux Rosacées . Et, ailleurs qu’en Espagne, une histoire clinique d’allergie à la moutarde semble ressortir d’un autre mécanisme, n’étant relevée que chez 2 patients sur 49 mono-réactifs aux LTP .
L’allergie à la moutarde chez l’enfant
L’allergie à la moutarde se manifeste parfois très tôt dans l’enfance et des contacts ignorés (petits pots, allaitement ?) ont été évoqués pour expliquer cette précocité .
Par exemple, une étude a montré que sur 15 cas pédiatriques d’allergie à la moutarde il n’y avait eu aucun contact connu pour 8 enfants .
Les études portant sur une population pédiatrique contrastent fortement avec celles menées chez l’adulte :
- pas de cas d’anaphylaxie en France
- et un rôle plus restreint ou absent pour une pollinose concomitante.
- Par exemple, un tableau en demi-teinte est vu dans un travail espagnol (8 TC positifs armoise parmi 42 enfants).
En France, les travaux de Rancé ont porté sur une population pédiatrique très souvent atteinte d’eczéma atopique (52 % , 86 % ).
- Ces enfants avaient également une allergie à des aliments classiques dans ce cadre : œuf, arachide, etc… et il est difficile de savoir si l’allergie à la moutarde est alors une entité bien spécifique ou une manifestation clinique à un aliment parmi une constellation de réactivités à des aliments en tous genres.
Quoi qu’il en soit, l’allergie à la moutarde chez l’enfant, hors d’un environnement méditerranéen, est bien réelle , même si elle ne met pas en jeu des pollens et/ou des LTP.
Le régime d’éviction de la moutarde concerne de multiples aliments manufacturés et l’alimentation de type fast-food .
Allergie à la moutarde : diagnostic
Des seuils de réactivité in vitro ont été proposés, mais ils restent insuffisants, la VPP culminant au mieux à 80 % , voire à 65 % . Il en est de même en suivi, pour déterminer une éventuelle acquisition de tolérance .
Le diagnostic de cette allergie gagnerait beaucoup à pouvoir être conforté par la mesure de l’IgE-réactivité vis à vis de Sin a 1 ou Bra j 1.
Accessoirement, il pourra être testé rPru p 3 comme témoin d’une réactivité à la LTP de moutarde. En effet, même si l’identité entre Pru p 3 (pêche) et Sin a 3 (moutarde) n’est globalement que de 54%, elle s’élève à environ 70% au niveau de 2 des 3 zones porteuses d’épitopes sur Pru p 3 .
[1] - Rancé F, Kanny G, Dutau G, Moneret-Vautrin DA. Food hypersensitivity in children: clinical aspects and distribution of allergens. Pediatr Allergy Immunol 1999;10:33-38
The aims of this work were to investigate, in children and adolescents, the clinical aspects of food hypersensitivity and the distribution of allergens, in a prospective and descriptive study. Five hundred and forty-four pediatric cases from a series of 703 patients with food allergies, confirmed by food challenge, were studied. Their clinical characteristics and the distribution according to allergen were investigated. There was a family history of atopic disease in 70.5% of patients. Atopic dermatitis was the main symptom (275/544; 50.5% of patients), followed by urticaria and angio-edema (165/544; 30%). There was asthma in 8.6% of patients (47 children) and anaphylaxis in 4.5% (27 patients). The rarest signs were rhinitis (n=2; 0.3%), oral allergy syndrome (n=8; 1.4%), and gastrointestinal signs (n=11; 2%). Five allergens accounted for 78% of food hypersensitivity. These allergens were: eggs (36%), peanuts (24%), cow's milk (8%), mustard (6%), and cod (4%). Peanut was the most common allergen for children over the age of 3 yr. In this selected population, sensitivity of individuals to more than three foods was unusual (5%). Atopic dermatitis was the main symptom of food allergy in children. The symptoms changed over time, with respiratory disorders, oral allergy syndrome and ocular problems occuring later. Anaphylaxis also occured mostly in older children. Five allergens were responsible for more than three-quarters of food allergies in children. However, the number of allergens implicated was higher for the group of children over the age of 6 yr than for younger children.
↩[2] - Le Manach G, Breinig S, Rancé F. Allergie alimentaire associée à la moutarde et au colza. Rev Fr Allergol Immunol Clin 2007;47:284 ↩
[3] - Morisset M, Moneret-Vautrin DA, Maadi F, Frémont S, Guénard L, Croizier A, et al. Prospective study of mustard allergy: first study with double-blind placebo-controlled food challenge trials (24 cases). Allergy 2003;58:295-299
BACKGROUND: Mustard allergy accounts for 1.1% of food allergies in children. However, double-blind placebo-controlled food challenge trials (DB PCFCs) have not yet been proposed .
OBJECTIVE: To carry out DB PCFCs to determine the real frequency of mustard allergy in patients sensitized to mustard .
METHODS: A prospective study was conducted in 30 subjects aged 3-20 years presenting positive prick tests to ground mustard seeds (Brassica nigra), mustard flour (B. juncea), metabisulfite-free strong mustard seasoning (B. juncea) and a commercialized allergenic extract (B. nigra). Twenty-seven subjects were screened for mustard-specific immunoglobulin E (IgE). PCFCs were carried out either DB or single blind (SB) with up to 1340 mg of metabisulfite-free seasoning .
RESULTS: The mean diameter of the wheal induced by prick tests with the allergenic extract was lower (n.s.) than that induced by the native mustard products: 5.8 mm (1.5-15) vs 6.9 mm (0.5-18) for B. nigra ground seeds, 7.8 mm (1-20) for B. juncea flour and 9.7 mm (3-20) for the strong mustard seasoning. The diameter of the wheal induced by the allergenic extract was significantly different from that induced by the mustard seasoning (P < 0.005). The mean of mustard specific-IgE values was 8.7 KU/l (0.35-72.4). Seven of 30 food challenges were considered positive. Mean prick test results in the positive and negative PCFC subgroups were 5.5 mm vs 5.9 mm for the commercialized extract, 10.9 mm vs 5.8 mm for B. nigra ground seeds (P < 0.01), 9.9 mm vs 7.1 mm for B. juncea flour (n.s. P > 0.25) and 11.5 mm vs 9.1 mm for the metabisulfite-free mustard seasoning (n.s. P > 0.1). Mean specific IgE values determined by CAP system radioallergosorbent test (Phadebas Pharmacia) were higher but not significantly so (P > 0.25) in the subgroup with mustard allergy (12.3 K/l vs 7.6 KU/l) .
CONCLUSIONS: About 23.3% of the sensitized subjects were allergic to a routine dose of mustard. Positive prick tests and the presence of specific IgE were not predictive. SB PCFC or DB PCFC is required before recommending avoidance diets.
↩[4] - Gonzales de la Pena MA, Menendez-Arias L, Monsalve RI, Rodriguez R. Isolation and characterization of a major allergen from oriental mustard seeds, Bra j I. Int Arch Allergy Appl Immunol 1991;96:263-270
A 2 S albumin from oriental mustard (Brassica juncea) seeds has been isolated and characterized as an allergen. This protein, BrajI, was recognized by human IgE from mustard-sensitive individuals, as proved by using two different enzyme immunoassays. BrajI was found to be closely related to Sin a I, the major allergen from yellow mustard seeds. Many fractions with molecular weights ranging from 16,000 to 16,400 and with differences in charge were separated by ion-exchange chromatography. They exhibited small but significant amino acid composition differences for Glx, Val, Ile, Lys, and Arg contents. The heterogeneity of BrajI can be explained by size and charge differences of its heavy and light chains. All of the isoallergenic forms of BrajI gave a single precipitation band in double diffusion immunoassays when using a Sin a-I-specific rabbit polyclonal serum
↩[5] - Dominguez J, Cuevas M, Urena V, Munoz T, Moneo I. Purification and characterization of an allergen of mustard seed. Ann Allergy 1990;64:352-357
A protein allergen has been isolated from mustard seed extracts by gel filtration. In RAST-inhibition experiments the allergen inhibited more than 60% of the binding of mustard-specific IgE from a pool of seven patients' sera. The allergenic activity was also demonstrated by histamine release from whole blood from two sensitive patients. The allergen had an isoelectric point close to 10.5 and an apparent molecular weight of 14,000. It was stable in alkaline and acid solutions and showed resistance to heating and to degradation by proteolytic enzymes
↩[6] - Monsalve RI, Delapena MAG, Lopezotiin C, Fiandor A, Fernandez C, Villalba M, et al. Detection, isolation and complete amino acid sequence of an aeroallergenic protein from rapeseed flour. Clin Exp Allergy 1997;27:833-841
Seed proteins have been found to cause hypersensitivity by ingestion or inhalation. Rapeseed flour was responsible for allergic symptoms in a patient, who develops into allergy to mustard spice.
Objective To determine the presence of allergenic proteins in rapeseed flour, and analyse the structure of the main component and its crossreactivity with the mustard allergen.
Methods SDS-PAGE (sodium dodecyl sulfate-polyacrylamide gel electrophoresis) and subsequent immunoblotting with a serum from a rapeseed allergic patient were performed to detect IgE-binding proteins. Proteolytic digestions and high performance liquid chromatography were used to obtain the peptides from the allergenic BnIII napin from rapeseed flour. Automatic Edman degradations were carried out to determine their amino acid sequences, which were compared with other sequences in nucleotide and amino acid sequence databases. Crossreactivity assays were carried out by ELISA inhibition using sera from a rapeseed allergic patient and from patients allergic to mustard.
Results The 2S albumins of rapeseed were recognized by the serum from a patient allergic to this seed. The most abundant isoform of the allergenic napins, BnIII, was used for structural and immunological analysis. The protein consists of two different chains of 9.5 and 4.5 kDa. Their complete amino acid sequences were determined. The protein exhibited structural relationships with other napin-like storage proteins from seeds. IgE and IgG crossreactivity between rapeseed and mustard allergens was also demonstrated. Considering the structural and immunological data, certain polypeptide regions are suggested to be involved in the allergenicity of these proteins.
Conclusions Rapeseed contains 2S storage proteins which may cause allergy in hypersensitive individuals. These proteins exhibit great sequence similarity with 2S albumins from different seeds. Crossreactivity between mustard and rapeseed flours can be explained by sequence homology
↩[7] - Monsalve RI, Gonzalez de la Pena MA, Menendez-Arias L, Lopez-Otin C, Villalba M, Rodriguez R. Characterization of a new oriental-mustard (Brassica juncea) allergen, Bra j IE: detection of an allergenic epitope. Biochem J 1993;293 :625-632
Bra j IE, a major allergen from oriental-mustard (Brassica juncea) seeds, has been isolated and characterized. Its primary structure has been elucidated. This protein is composed of two chains (37 and 92 amino acids) linked by disulphide bridges. The amino acid sequence obtained is closely related to that previously determined for Sin a I, an allergen isolated from yellow mustard (Sinapis alba). A common epitope has been detected in the large chain of both Bra j IE and Sin a I by means of electroblotting and immunodetection with 2B3, which is a monoclonal antibody raised against the yellow-mustard allergen. A histidine residue of the large chain of both mustard allergens has been found to be essential for the recognition by 2B3 antibody. A synthetic multiantigenic peptide containing this His was recognized by 2B3 as well as by sera of mustard-hypersensitive individuals. Therefore this antigenic determinant must be involved in the allergenicity of these proteins.
↩[8] - Palomares O, Vereda A, Cuesta-Herranz J, Villalba M, Rodríguez R. Cloning, sequencing, and recombinant production of Sin a 2, an allergenic 11S globulin from yellow mustard seeds. J Allergy Clin Immunol 2007;119:1189-1196
BACKGROUND: Among allergenic spices, mustard represents 1 of the most important in terms of allergenic potency and widespread use. An 11S globulin (Sin a 2) has been isolated from yellow mustard seeds and identified as a new major allergen .
OBJECTIVE: Cloning and sequencing a cDNA encoding a Sin a 2 subunit and producing the allergen as a recombinant protein .
METHODS: Sin a 2 subunit-encoding cDNA was amplified by polymerase chain reaction, cloned, and sequenced. The allergen was produced as a recombinant protein in Escherichia coli and used for enzyme-linked immunosorbent assay, immunoblotting, and inhibition experiments. Sera from patients with mustard allergy and an anti-polyhistidine monoclonal antibody were used .
RESULTS: Sin a 2-specific cDNA comprises an open reading frame that encodes a protein of 510 amino acids, in which the first 23 residues correspond to the signal peptide. Sequence alignment with other allergenic 11S globulins showed levels of sequence identity ranging between 27% and 38%. Three peptides described as epitopes in Ara h 3 were moderately conserved in Sin a 2. Approximately 87% of the IgE binding to natural Sin a 2 was inhibited by the recombinant allergen using sera from patients with mustard allergy .
CONCLUSION: The recombinant 11S globulin from yellow mustard seeds produced in E coli retained the IgE-binding capability of the natural allergen. CLINICAL IMPLICATIONS: The availability of Sin a 2 sequence and its recombinant production could help to develop future therapeutic approaches and might well open new investigation lines to resolve whether 11S globulins are proteins implicated in cross-reactivity processes involving mustard seeds.
↩[9] - Sirvent S, Palomares O, Vereda A, Villalba M, Cuesta-Herranz J, Rodríguez R. nsLTP and profilin are allergens in mustard seeds: cloning, sequencing and recombinant production of Sin a 3 and Sin a 4. Clin Exp Allergy 2009;39:1929-1936 ↩
[10] - Figueroa J, Blanco C, Dumpiérrez AG, Almeida L, Ortega N, Castillo R, et al. Mustard allergy confirmed by double-blind placebo-controlled food challenges: clinical features and cross-reactivity with mugwort pollen and plant-derived foods. Allergy 2005;60:48-55
BACKGROUND: Mustard IgE-mediated allergy is supposed to be a rare cause of food allergy, and its clinical features and cross-reactivities have not been fully elucidated .
METHODS: A prospective study was carried out, recruiting mustard allergic patients, and paired control subjects. A clinical questionnaire was administered, and skin-prick tests (SPT) with panels of aeroallergens and foods, serum extraction for in vitro tests and double-blind placebo-controlled food challenges (DBPCFC) were performed .
RESULTS: Thirty-eight mainly adult patients, with 10.5% reporting systemic anaphylaxis, were included in the study [age (mean +/- SD): 21.9 +/- 8.6 years]. DBPCFC were performed in 24 patients, being positive in 14 cases (58.3%). Patients with positive outcome showed significantly greater mustard SPT than those with negative outcome (8.2 +/- 3.7 vs 5.3 +/- 2.4 mm, P <0.05), and the receiver-operating characteristic (ROC) curve analysis yielded a cut-off value for mustard commercial SPT of 8 mm, with a specificity of 90% (95% CI, 55.5-98.3), and a sensitivity of 50% (95% CI, 23.1-76.9). A significant association between mustard hypersensitivity and mugwort pollen sensitization was found (97.4% of patients), with partial cross-reactivity demonstrated by UniCAP System inhibition assays. All patients showed sensitization to other members of Brassicaceae family, and cross-reactivity among them was also confirmed. Moreover, significant associations with nut (97.4%), leguminous (94.7%), corn (78.9%), and Rosaceae fruit (89.5%) sensitizations were also shown. Around 40% of these food sensitizations were symptomatic, including food-dependent exercise-induced anaphylaxis in six patients .
CONCLUSIONS: Mustard allergy is a not-uncommon disorder that can induce severe reactions. Significant associations with mugwort pollinosis and several plant-derived food allergies are demonstrated, suggesting a new mustard-mugwort allergy syndrome. A relationship between this syndrome and food-dependent exercise-induced anaphylaxis is also reported.
↩[11] - Figueroa J, Blanco C, Dumpiérrez AG, Almeida L, Ortega N, Castillo R, et al. Mustard allergy confirmed by double-blind placebo-controlled food challenges: clinical features and cross-reactivity with mugwort pollen and plant-derived foods. Allergy 2005;60:48-55
BACKGROUND: Mustard IgE-mediated allergy is supposed to be a rare cause of food allergy, and its clinical features and cross-reactivities have not been fully elucidated .
METHODS: A prospective study was carried out, recruiting mustard allergic patients, and paired control subjects. A clinical questionnaire was administered, and skin-prick tests (SPT) with panels of aeroallergens and foods, serum extraction for in vitro tests and double-blind placebo-controlled food challenges (DBPCFC) were performed .
RESULTS: Thirty-eight mainly adult patients, with 10.5% reporting systemic anaphylaxis, were included in the study [age (mean +/- SD): 21.9 +/- 8.6 years]. DBPCFC were performed in 24 patients, being positive in 14 cases (58.3%). Patients with positive outcome showed significantly greater mustard SPT than those with negative outcome (8.2 +/- 3.7 vs 5.3 +/- 2.4 mm, P <0.05), and the receiver-operating characteristic (ROC) curve analysis yielded a cut-off value for mustard commercial SPT of 8 mm, with a specificity of 90% (95% CI, 55.5-98.3), and a sensitivity of 50% (95% CI, 23.1-76.9). A significant association between mustard hypersensitivity and mugwort pollen sensitization was found (97.4% of patients), with partial cross-reactivity demonstrated by UniCAP System inhibition assays. All patients showed sensitization to other members of Brassicaceae family, and cross-reactivity among them was also confirmed. Moreover, significant associations with nut (97.4%), leguminous (94.7%), corn (78.9%), and Rosaceae fruit (89.5%) sensitizations were also shown. Around 40% of these food sensitizations were symptomatic, including food-dependent exercise-induced anaphylaxis in six patients .
CONCLUSIONS: Mustard allergy is a not-uncommon disorder that can induce severe reactions. Significant associations with mugwort pollinosis and several plant-derived food allergies are demonstrated, suggesting a new mustard-mugwort allergy syndrome. A relationship between this syndrome and food-dependent exercise-induced anaphylaxis is also reported.
↩[12] - Palacin A, Cumplido J, Figueroa J, Ahrazem O, Sanchez-Monge R, Carrillo T, et al. Cabbage lipid transfer protein Bra o 3 is a major allergen responsible for cross-reactivity between plant foods and pollens. J Allergy Clin Immunol 2006;117:1423-1429
BACKGROUND: Food IgE-mediated allergy to members of the Brassicaceae family has been increasingly reported .
OBJECTIVE: To characterize cabbage-Brassica oleracea var capitata-allergy and its major allergens .
METHODS: A prospective study was performed, recruiting 17 patients allergic to cabbage, and control subjects. Skin prick tests and double-blind placebo-controlled food challenges were performed. A major allergen was isolated from cabbage by RP-HPLC and characterized by N-terminal amino acid sequencing and matrix-assisted laser desorption/ionization mass spectrometry analysis. Specific IgE determinations, IgE immunoblots, and CAP-inhibition assays were also performed .
RESULTS: Skin prick test and specific IgE were positive to cabbage in all patients. Five of them referred anaphylactic reactions when eating cabbage, and in another 5 patients, cabbage allergy was further confirmed by double-blind placebo-controlled food challenge. Most of them showed associated sensitizations to mugwort pollen, mustard, and peach. A 9-kd cabbage IgE-binding protein, Bra o 3, was identified as a lipid transfer protein (LTP) with 50% of identity to peach LTP Pru p 3. Skin prick test with Bra o 3 showed positive results in 12 of 14 cases (86%). On CAP inhibition assays, Bra o 3 managed to inhibit significantly the IgE binding to cabbage, mugwort pollen, and peach. Both Bra o 3 and Pru p 3 were recognized by IgE from the patients' sera .
CONCLUSION: Bra o 3, a cabbage LTP, is a major allergen in this food, cross-reacting with mugwort pollen and with other plant foods, such as peach. CLINICAL IMPLICATIONS: Cabbage IgE-mediated allergy is a potentially severe condition that can present with other plant food and pollen allergies.
↩[13] - Sirvent S, Palomares O, Vereda A, Villalba M, Cuesta-Herranz J, Rodríguez R. nsLTP and profilin are allergens in mustard seeds: cloning, sequencing and recombinant production of Sin a 3 and Sin a 4. Clin Exp Allergy 2009;39:1929-1936 ↩
[14] - Caballero T, Sanmartin MS, Padial MA, Contreras J, Cabanas R, Barranco P, et al. Clinical characteristics of patients with mustard hypersensitivity. Ann Allergy Asthma Immunol 2002;89:166-171
Background: Although mustard is frequently consumed in Spain and elsewhere, only isolated case reports of mustard allergy have been reported. No large series of case studies have been published.
Objectives: We sought to describe demographic, clinical, and immunologic characteristics of patients with mustard hypersensitivity and to determine whether any significant differences exist in age, sex, atopic family history, total immunoglobulin E (IgE) level, and specific IgE to mustard ratio among patients with differing characteristics.
Methods: Twenty-nine patients with a history of mustard allergy underwent skin prick tests with mustard, determination of total IgE, and evaluation of specific IgE to mustard. Skin prick tests with Lolium perenne, Olea europaea, and Artemisia vulgaris were done in patients with symptoms of pollinosis. The aforementioned variables were compared between various subgroups of patients for systemic versus local reactions to mustard, association versus no association with allergies to other vegetable foods, and association versus no association with pollinosis.
Results: The male:female ratio was 10: 19. Skin prick tests to mustard were positive in all patients. The total IgE geometric mean was 189.3 kU/L. The specific IgE to mustard was positive in all patients (0.7 to > 100 kU/L). Of the 29 patients, 19 (66%) had a systemic reaction after consumption of mustard, and 10 (34%) had a local reaction; 14 (48%) had anaphylaxis. Fifteen patients (52%) had symptoms after ingestion of other vegetable foods, and 15 also had typical symptoms of pollinosis. No significant differences were found in age, sex, atopic family history, total IgE, and specific IgE to mustard between the various subgroups studied.
Conclusions: Most study patients with mustard hypersensitivity had a systemic reaction and had associated pollinosis or allergy to other vegetable foods. Mustard sensitivity should be routinely tested in patients with idiopathic anaphylaxis.
↩[15] - Figueroa J, Blanco C, Dumpiérrez AG, Almeida L, Ortega N, Castillo R, et al. Mustard allergy confirmed by double-blind placebo-controlled food challenges: clinical features and cross-reactivity with mugwort pollen and plant-derived foods. Allergy 2005;60:48-55
BACKGROUND: Mustard IgE-mediated allergy is supposed to be a rare cause of food allergy, and its clinical features and cross-reactivities have not been fully elucidated .
METHODS: A prospective study was carried out, recruiting mustard allergic patients, and paired control subjects. A clinical questionnaire was administered, and skin-prick tests (SPT) with panels of aeroallergens and foods, serum extraction for in vitro tests and double-blind placebo-controlled food challenges (DBPCFC) were performed .
RESULTS: Thirty-eight mainly adult patients, with 10.5% reporting systemic anaphylaxis, were included in the study [age (mean +/- SD): 21.9 +/- 8.6 years]. DBPCFC were performed in 24 patients, being positive in 14 cases (58.3%). Patients with positive outcome showed significantly greater mustard SPT than those with negative outcome (8.2 +/- 3.7 vs 5.3 +/- 2.4 mm, P <0.05), and the receiver-operating characteristic (ROC) curve analysis yielded a cut-off value for mustard commercial SPT of 8 mm, with a specificity of 90% (95% CI, 55.5-98.3), and a sensitivity of 50% (95% CI, 23.1-76.9). A significant association between mustard hypersensitivity and mugwort pollen sensitization was found (97.4% of patients), with partial cross-reactivity demonstrated by UniCAP System inhibition assays. All patients showed sensitization to other members of Brassicaceae family, and cross-reactivity among them was also confirmed. Moreover, significant associations with nut (97.4%), leguminous (94.7%), corn (78.9%), and Rosaceae fruit (89.5%) sensitizations were also shown. Around 40% of these food sensitizations were symptomatic, including food-dependent exercise-induced anaphylaxis in six patients .
CONCLUSIONS: Mustard allergy is a not-uncommon disorder that can induce severe reactions. Significant associations with mugwort pollinosis and several plant-derived food allergies are demonstrated, suggesting a new mustard-mugwort allergy syndrome. A relationship between this syndrome and food-dependent exercise-induced anaphylaxis is also reported.
↩[16] - Palomares O, Cuesta-Herranz J, Vereda A, Sirvent S, Villalba M, Rodriguez R. Isolation and identification of an 11S globulin as a new major allergen in mustard seeds. Ann Allergy Asthma Immunol 2005;94:586-592
BACKGROUND: Although mustard seed allergy has been largely reported during the preceding 20 years, currently only 2 allergens, Sin a 1 and Bra j 1, have been identified. OBJECTIVE: To improve the characterization of the allergenic profile of yellow mustard seeds by reporting the identification and biochemical characterization of an 11S globulin as a new major allergen.
METHODS: Mustard seed proteins were separated using size exclusion and ion-exchange chromatographic columns, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and 2-dimensional polyacrylamide gel electrophoresis. Separation of different polypeptide chains was achieved by reverse-phase high-performance liquid chromatography. Mass spectrometry after tryptic digestion and Edman degradation were used to determine amino acid sequences of peptides. IgE binding assays were performed with 13 serum samples from mustard allergic patients in immunoblotting and enzyme-linked immunosorbent inhibition assays.
RESULTS: A protein of 51 kDa was recognized as a major allergen by patients allergic to mustard and called Sin a 2. The allergen was dissociated in 2 chains of 36 and 23 kDa, which also bound IgE. N-terminal end and internal amino acid sequences allowed identification of the new allergen as a seed storage 11S globulin belonging to the Cupin super family. Purified allergen was able to inhibit the IgE binding of sera from allergic patients to mustard seeds extract in up to 55% of the responses.
CONCLUSIONS: An 11S globulin storage protein has been isolated and identified as a novel major allergen of mustard seeds.
↩[17] - Caballero T, Sanmartin MS, Padial MA, Contreras J, Cabanas R, Barranco P, et al. Clinical characteristics of patients with mustard hypersensitivity. Ann Allergy Asthma Immunol 2002;89:166-171
Background: Although mustard is frequently consumed in Spain and elsewhere, only isolated case reports of mustard allergy have been reported. No large series of case studies have been published.
Objectives: We sought to describe demographic, clinical, and immunologic characteristics of patients with mustard hypersensitivity and to determine whether any significant differences exist in age, sex, atopic family history, total immunoglobulin E (IgE) level, and specific IgE to mustard ratio among patients with differing characteristics.
Methods: Twenty-nine patients with a history of mustard allergy underwent skin prick tests with mustard, determination of total IgE, and evaluation of specific IgE to mustard. Skin prick tests with Lolium perenne, Olea europaea, and Artemisia vulgaris were done in patients with symptoms of pollinosis. The aforementioned variables were compared between various subgroups of patients for systemic versus local reactions to mustard, association versus no association with allergies to other vegetable foods, and association versus no association with pollinosis.
Results: The male:female ratio was 10: 19. Skin prick tests to mustard were positive in all patients. The total IgE geometric mean was 189.3 kU/L. The specific IgE to mustard was positive in all patients (0.7 to > 100 kU/L). Of the 29 patients, 19 (66%) had a systemic reaction after consumption of mustard, and 10 (34%) had a local reaction; 14 (48%) had anaphylaxis. Fifteen patients (52%) had symptoms after ingestion of other vegetable foods, and 15 also had typical symptoms of pollinosis. No significant differences were found in age, sex, atopic family history, total IgE, and specific IgE to mustard between the various subgroups studied.
Conclusions: Most study patients with mustard hypersensitivity had a systemic reaction and had associated pollinosis or allergy to other vegetable foods. Mustard sensitivity should be routinely tested in patients with idiopathic anaphylaxis.
↩[18] - Jorro G, Morales C, Braso JV, Pelaez A. Mustard allergy: three cases of systemic reaction to ingestion of mustard sauce. J Investig Allergol Clin Immunol 1995;5:54-56
Very few cases of hypersensitivity due to ingestion of mustard have been described in the literature, although this spice enjoys widespread use. We present three cases of anaphylactic reactions to ingestion of a small amount of mustard sauce. In our patients we performed skin prick tests with mustard and with the rest of the vegetables belonging to the Cruciferae family. We also performed skin prick tests with common pneumoallergens. We measured specific serum IgE to mustard using the CAP System (Pharmacia). Oral challenges with the other vegetables of the Cruciferae family were performed in the patients with no evidence of previous tolerance. Skin prick tests and specific serum IgE determinations to mustard were positive in all three patients. The tests with the rest of the vegetables belonging to the same family were negative. In conclusion, we consider that skin prick tests and the measurement of specific serum IgE to mustard are good methods for the diagnosis of mustard hypersensitivity. We did not detect cross-sensitivity with other vegetables of the same family or with pneumoallergens.
↩[19] - Caballero T, Sanmartin MS, Padial MA, Contreras J, Cabanas R, Barranco P, et al. Clinical characteristics of patients with mustard hypersensitivity. Ann Allergy Asthma Immunol 2002;89:166-171
Background: Although mustard is frequently consumed in Spain and elsewhere, only isolated case reports of mustard allergy have been reported. No large series of case studies have been published.
Objectives: We sought to describe demographic, clinical, and immunologic characteristics of patients with mustard hypersensitivity and to determine whether any significant differences exist in age, sex, atopic family history, total immunoglobulin E (IgE) level, and specific IgE to mustard ratio among patients with differing characteristics.
Methods: Twenty-nine patients with a history of mustard allergy underwent skin prick tests with mustard, determination of total IgE, and evaluation of specific IgE to mustard. Skin prick tests with Lolium perenne, Olea europaea, and Artemisia vulgaris were done in patients with symptoms of pollinosis. The aforementioned variables were compared between various subgroups of patients for systemic versus local reactions to mustard, association versus no association with allergies to other vegetable foods, and association versus no association with pollinosis.
Results: The male:female ratio was 10: 19. Skin prick tests to mustard were positive in all patients. The total IgE geometric mean was 189.3 kU/L. The specific IgE to mustard was positive in all patients (0.7 to > 100 kU/L). Of the 29 patients, 19 (66%) had a systemic reaction after consumption of mustard, and 10 (34%) had a local reaction; 14 (48%) had anaphylaxis. Fifteen patients (52%) had symptoms after ingestion of other vegetable foods, and 15 also had typical symptoms of pollinosis. No significant differences were found in age, sex, atopic family history, total IgE, and specific IgE to mustard between the various subgroups studied.
Conclusions: Most study patients with mustard hypersensitivity had a systemic reaction and had associated pollinosis or allergy to other vegetable foods. Mustard sensitivity should be routinely tested in patients with idiopathic anaphylaxis.
↩[20] - Asero R, Mistrello G, Roncarolo D, Amato S. Detection of Some Safe Plant-Derived Foods for LTP-Allergic Patients. Int Arch Allergy Immunol 2007;144:57-63
BACKGROUND: Lipid transfer protein (LTP) is a widely cross-reacting plant pan-allergen. Adverse reactions to Rosaceae, tree nuts, peanut, beer, maize, mustard, asparagus, grapes, mulberry, cabbage, dates, orange, fig, kiwi, lupine, fennel, celery, tomato, eggplant, lettuce, chestnut and pineapple have been recorded .
OBJECTIVE: To detect vegetable foods to be regarded as safe for LTP-allergic patients .
METHODS: Tolerance/intolerance to a large spectrum of vegetable foods other than Rosaceae, tree nuts and peanut was assessed by interview in 49 subjects monosensitized to LTP and in three distinct groups of controls monosensitized to Bet v 1 (n = 24) or Bet v 2 (n = 18), or sensitized to both LTP and birch pollen (n = 16), all with a history of vegetable food allergy. Patients and controls underwent skin prick test (SPT) with a large spectrum of vegetable foods. The absence of IgE reactivity to foods that were negative in both clinical history and SPT was confirmed by immunoblot analysis and their clinical tolerance was finally assessed by open oral challenge (50 g per food) .
RESULTS: All patients reported tolerance and showed negative SPT to carrot, potato, banana and melon; these foods scored positive in SPT and elicited clinical symptoms in a significant proportion of patients from all three control groups. All patients tolerated these four foods on oral challenge. Immunoblot analysis confirmed the lack of IgE reactivity to these foods by LTP-allergic patients .
CONCLUSION: Carrot, potato, banana and melon seem safe for LTP-allergic patients. This finding may be helpful for a better management of allergy to LTP.
↩[21] - Niinimäki A, Björkstén F, Puukka M, Tolonen K, Hannuksela M. Spice allergy: results of skin prick tests and RAST with spice extracts. Allergy 1989;44:60-65
Skin prick tests (SPT) with freeze-dried spices and 5% (w/v) spice extracts were performed on 50 patients with 2+ or stronger SPT reactions to spices per se, and RAST were performed on 10 of them. Freeze-dried extracts produced mostly equal or stronger SPT reactions than corresponding whole spices, but 5% (w/v) extracts produced weaker reactions and also remained totally negative in some patients. Positive RAST results were seen in all 10 patients tested. The correlation between the RAST and SPT results was good for mustard and paprika, but poor for cayenne, coriander, caraway and white pepper. Five patients with positive SPT and RAST for spices contracted rhinitis from powdered spices in their working environments, and one patient suffered from gastrointestinal pains caused by spiced food. The others had noticed no clinical symptoms caused by spices. The present results thus indicate that both SPT and RAST should include purified spice extracts.
↩[23] - Rancé F, Dutau G. L'allergie à la moutarde chez l'enfant. Rev Fr Allergol Immunol Clin 1993;33:292-294 ↩
[24] - Rancé F, Dutau G. L'allergie à la moutarde chez l'enfant. Rev Fr Allergol Immunol Clin 1993;33:292-294 ↩
[25] - Rancé F, Dutau G, Abbal M. Mustard allergy in children. Allergy 2000;55:496-500
Mustard allergy is not well known. This study aimed to assess its clinical features and other associated allergies, and to define skin prick tests (SPT), specific IgE, and dose response by oral food challenge.
METHODS: Our study investigated 36 children with positive mustard SPT. The diagnosis of mustard allergy was based on open or single-blind, placebo-controlled food challenge (SBPCFC). We compared the subjects to 22 controls.
RESULTS: The initial clinical features were atopic dermatitis (51.8%), and urticaria and/or angioedema (37%). Fifteen children were allergic (positive SBPCFC) and 21 children were nonallergic (negative SBPCFC). Symptoms after mustard ingestion started under 3 years of age in 53.3% of the subjects. There was no significant difference in the food allergies and associated inhalant allergen sensitizations between the two groups. In the allergic group, the mean wheal diameter for mustard SPT was 8.8 mm and the median concentration of mustard serum (s) IgE 14.8 kU/l.
The mean cumulative reactive dose were 153 mg.
CONCLUSIONS: Allergic reactions to mustard started early in life. Clinical symptoms were not severe in children. Mustard should be included in screening tests of food allergy in children.
↩[26] - Morisset M, Moneret-Vautrin DA, Maadi F, Frémont S, Guénard L, Croizier A, et al. Prospective study of mustard allergy: first study with double-blind placebo-controlled food challenge trials (24 cases). Allergy 2003;58:295-299
BACKGROUND: Mustard allergy accounts for 1.1% of food allergies in children. However, double-blind placebo-controlled food challenge trials (DB PCFCs) have not yet been proposed .
OBJECTIVE: To carry out DB PCFCs to determine the real frequency of mustard allergy in patients sensitized to mustard .
METHODS: A prospective study was conducted in 30 subjects aged 3-20 years presenting positive prick tests to ground mustard seeds (Brassica nigra), mustard flour (B. juncea), metabisulfite-free strong mustard seasoning (B. juncea) and a commercialized allergenic extract (B. nigra). Twenty-seven subjects were screened for mustard-specific immunoglobulin E (IgE). PCFCs were carried out either DB or single blind (SB) with up to 1340 mg of metabisulfite-free seasoning .
RESULTS: The mean diameter of the wheal induced by prick tests with the allergenic extract was lower (n.s.) than that induced by the native mustard products: 5.8 mm (1.5-15) vs 6.9 mm (0.5-18) for B. nigra ground seeds, 7.8 mm (1-20) for B. juncea flour and 9.7 mm (3-20) for the strong mustard seasoning. The diameter of the wheal induced by the allergenic extract was significantly different from that induced by the mustard seasoning (P < 0.005). The mean of mustard specific-IgE values was 8.7 KU/l (0.35-72.4). Seven of 30 food challenges were considered positive. Mean prick test results in the positive and negative PCFC subgroups were 5.5 mm vs 5.9 mm for the commercialized extract, 10.9 mm vs 5.8 mm for B. nigra ground seeds (P < 0.01), 9.9 mm vs 7.1 mm for B. juncea flour (n.s. P > 0.25) and 11.5 mm vs 9.1 mm for the metabisulfite-free mustard seasoning (n.s. P > 0.1). Mean specific IgE values determined by CAP system radioallergosorbent test (Phadebas Pharmacia) were higher but not significantly so (P > 0.25) in the subgroup with mustard allergy (12.3 K/l vs 7.6 KU/l) .
CONCLUSIONS: About 23.3% of the sensitized subjects were allergic to a routine dose of mustard. Positive prick tests and the presence of specific IgE were not predictive. SB PCFC or DB PCFC is required before recommending avoidance diets.
↩[27] - Caballero T, Martin-Esteban M, Garcia-Ara C, Pascual C, Ojeda A. Relationship between pollinosis and fruit or vegetable sensitization. Pediatr Allergy Immunol 1994;5:218-222
The prevalence of vegetable sensitization in children with pollinosis (Group A; n = 48) and the prevalence of pollen sensitization in children with fruit or vegetable allergy (Group B; n = 42) were studied by means of prick-test and determination of serum specific IgE to several pollens, fruits and vegetables. Fifteen patients from Group A (31%) showed sensitivity to fruits and/or vegetables, but only three of them had any symptoms after ingestions. Twenty nine patients from Group B (69%) showed pollen sensitization, mainly to grass and Compositae pollen. An association was found between sensitivity to Compositae pollen and sensitivity to several fruits and vegetables (Compositae, Fagaceae, Brassica, Betulaceae and Leguminoseae).
↩[28] - Rancé F, Juchet-Gibon A, Fejji S, Brémont F, Dutau G. Sensibilisation aux épices chez l'enfant. Rev Fr Allergol Immunol Clin 1994;34:475-479 ↩
[29] - Le Manach G, Breinig S, Rancé F. Allergie alimentaire associée à la moutarde et au colza. Rev Fr Allergol Immunol Clin 2007;47:284 ↩
[30] - Rancé F, Dutau G, Abbal M. Mustard allergy in children. Allergy 2000;55:496-500
Mustard allergy is not well known. This study aimed to assess its clinical features and other associated allergies, and to define skin prick tests (SPT), specific IgE, and dose response by oral food challenge.
METHODS: Our study investigated 36 children with positive mustard SPT. The diagnosis of mustard allergy was based on open or single-blind, placebo-controlled food challenge (SBPCFC). We compared the subjects to 22 controls.
RESULTS: The initial clinical features were atopic dermatitis (51.8%), and urticaria and/or angioedema (37%). Fifteen children were allergic (positive SBPCFC) and 21 children were nonallergic (negative SBPCFC). Symptoms after mustard ingestion started under 3 years of age in 53.3% of the subjects. There was no significant difference in the food allergies and associated inhalant allergen sensitizations between the two groups. In the allergic group, the mean wheal diameter for mustard SPT was 8.8 mm and the median concentration of mustard serum (s) IgE 14.8 kU/l.
The mean cumulative reactive dose were 153 mg.
CONCLUSIONS: Allergic reactions to mustard started early in life. Clinical symptoms were not severe in children. Mustard should be included in screening tests of food allergy in children.
↩[31] - Rancé F, Dutau G. L'allergie à la moutarde chez l'enfant. Rev Fr Allergol Immunol Clin 1993;33:292-294 ↩
[32] - Morisset M, Moneret-Vautrin DA, Maadi F, Frémont S, Guénard L, Croizier A, et al. Prospective study of mustard allergy: first study with double-blind placebo-controlled food challenge trials (24 cases). Allergy 2003;58:295-299
BACKGROUND: Mustard allergy accounts for 1.1% of food allergies in children. However, double-blind placebo-controlled food challenge trials (DB PCFCs) have not yet been proposed .
OBJECTIVE: To carry out DB PCFCs to determine the real frequency of mustard allergy in patients sensitized to mustard .
METHODS: A prospective study was conducted in 30 subjects aged 3-20 years presenting positive prick tests to ground mustard seeds (Brassica nigra), mustard flour (B. juncea), metabisulfite-free strong mustard seasoning (B. juncea) and a commercialized allergenic extract (B. nigra). Twenty-seven subjects were screened for mustard-specific immunoglobulin E (IgE). PCFCs were carried out either DB or single blind (SB) with up to 1340 mg of metabisulfite-free seasoning .
RESULTS: The mean diameter of the wheal induced by prick tests with the allergenic extract was lower (n.s.) than that induced by the native mustard products: 5.8 mm (1.5-15) vs 6.9 mm (0.5-18) for B. nigra ground seeds, 7.8 mm (1-20) for B. juncea flour and 9.7 mm (3-20) for the strong mustard seasoning. The diameter of the wheal induced by the allergenic extract was significantly different from that induced by the mustard seasoning (P < 0.005). The mean of mustard specific-IgE values was 8.7 KU/l (0.35-72.4). Seven of 30 food challenges were considered positive. Mean prick test results in the positive and negative PCFC subgroups were 5.5 mm vs 5.9 mm for the commercialized extract, 10.9 mm vs 5.8 mm for B. nigra ground seeds (P < 0.01), 9.9 mm vs 7.1 mm for B. juncea flour (n.s. P > 0.25) and 11.5 mm vs 9.1 mm for the metabisulfite-free mustard seasoning (n.s. P > 0.1). Mean specific IgE values determined by CAP system radioallergosorbent test (Phadebas Pharmacia) were higher but not significantly so (P > 0.25) in the subgroup with mustard allergy (12.3 K/l vs 7.6 KU/l) .
CONCLUSIONS: About 23.3% of the sensitized subjects were allergic to a routine dose of mustard. Positive prick tests and the presence of specific IgE were not predictive. SB PCFC or DB PCFC is required before recommending avoidance diets.
↩[33] - Sergeant P, Rancé F. Conseils pour un régime d'éviction de la moutarde. Alim'Inter 2009;14:29 ↩
[34] - Rancé F, Dutau G, Abbal M. Mustard allergy in children. Allergy 2000;55:496-500
Mustard allergy is not well known. This study aimed to assess its clinical features and other associated allergies, and to define skin prick tests (SPT), specific IgE, and dose response by oral food challenge.
METHODS: Our study investigated 36 children with positive mustard SPT. The diagnosis of mustard allergy was based on open or single-blind, placebo-controlled food challenge (SBPCFC). We compared the subjects to 22 controls.
RESULTS: The initial clinical features were atopic dermatitis (51.8%), and urticaria and/or angioedema (37%). Fifteen children were allergic (positive SBPCFC) and 21 children were nonallergic (negative SBPCFC). Symptoms after mustard ingestion started under 3 years of age in 53.3% of the subjects. There was no significant difference in the food allergies and associated inhalant allergen sensitizations between the two groups. In the allergic group, the mean wheal diameter for mustard SPT was 8.8 mm and the median concentration of mustard serum (s) IgE 14.8 kU/l.
The mean cumulative reactive dose were 153 mg.
CONCLUSIONS: Allergic reactions to mustard started early in life. Clinical symptoms were not severe in children. Mustard should be included in screening tests of food allergy in children.
↩[35] - Figueroa J, Blanco C, Dumpiérrez AG, Almeida L, Ortega N, Castillo R, et al. Mustard allergy confirmed by double-blind placebo-controlled food challenges: clinical features and cross-reactivity with mugwort pollen and plant-derived foods. Allergy 2005;60:48-55
BACKGROUND: Mustard IgE-mediated allergy is supposed to be a rare cause of food allergy, and its clinical features and cross-reactivities have not been fully elucidated .
METHODS: A prospective study was carried out, recruiting mustard allergic patients, and paired control subjects. A clinical questionnaire was administered, and skin-prick tests (SPT) with panels of aeroallergens and foods, serum extraction for in vitro tests and double-blind placebo-controlled food challenges (DBPCFC) were performed .
RESULTS: Thirty-eight mainly adult patients, with 10.5% reporting systemic anaphylaxis, were included in the study [age (mean +/- SD): 21.9 +/- 8.6 years]. DBPCFC were performed in 24 patients, being positive in 14 cases (58.3%). Patients with positive outcome showed significantly greater mustard SPT than those with negative outcome (8.2 +/- 3.7 vs 5.3 +/- 2.4 mm, P <0.05), and the receiver-operating characteristic (ROC) curve analysis yielded a cut-off value for mustard commercial SPT of 8 mm, with a specificity of 90% (95% CI, 55.5-98.3), and a sensitivity of 50% (95% CI, 23.1-76.9). A significant association between mustard hypersensitivity and mugwort pollen sensitization was found (97.4% of patients), with partial cross-reactivity demonstrated by UniCAP System inhibition assays. All patients showed sensitization to other members of Brassicaceae family, and cross-reactivity among them was also confirmed. Moreover, significant associations with nut (97.4%), leguminous (94.7%), corn (78.9%), and Rosaceae fruit (89.5%) sensitizations were also shown. Around 40% of these food sensitizations were symptomatic, including food-dependent exercise-induced anaphylaxis in six patients .
CONCLUSIONS: Mustard allergy is a not-uncommon disorder that can induce severe reactions. Significant associations with mugwort pollinosis and several plant-derived food allergies are demonstrated, suggesting a new mustard-mugwort allergy syndrome. A relationship between this syndrome and food-dependent exercise-induced anaphylaxis is also reported.
↩[36] - Rancé F, Micheau P, Morelle K, Abbal M, Söderström L. Evolution de l'allergie alimentaire à la moutarde chez l'enfant. Rev Fr Allergol Immunol Clin 2004;44:347 ↩
[37] - Sirvent S, Palomares O, Vereda A, Villalba M, Cuesta-Herranz J, Rodríguez R. nsLTP and profilin are allergens in mustard seeds: cloning, sequencing and recombinant production of Sin a 3 and Sin a 4. Clin Exp Allergy 2009;39:1929-1936 ↩
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