Bargman et al. (1992) [734] describe the following symptoms in 8 patients: 3/8 angioedema, 4/8 hives, 2/8 nausea, 5/8 swelling, itching 5/8, 6/8 shortness of breath or difficulty breathing and swallowing and 1/8 anaphylaxis.
Roux et al. (1999) [731] describe 14 patients with life threatening symptoms and 11 with oral hives, itching or mild angioedema.
Pasini et al. (2000) [728] describe 2 patients with life-threatening laryngeal edema.
Poltronieri et al. (2002) [725] describe 4 patients with anaphylaxis and 1 with oral allergy syndrome.
Skin Prick Test
Number of Studies:
1-5
Food/Type of allergen:
Commercial almond extract (Pasini et al. 2000 [728]; Poltronieri et al. 2002 [725]; Clark and Ewan (2003) [615])
Protocol:
(controls, definition of positive etc)
Clark and Ewan (2003) [615] used a positive (histamine 10 mg/mL) and negative control (saline). SPT wheal diameters were listed as <3 mm, 3-7 mm and >8 mm.
Bargman et al. (1992) [734] reported positive SPT from 8 patients
Pasini et al. (2000) [728] found positive SPT for all 5 atopic patients although only 2 had clinical symptoms with almond.
Poltronieri et al. (2002) [725] report the 5 patients had positive SPT to almond.
Clark and Ewan (2003) [615] found that only 3% of 210 patients who tolerated almond had SPT ≥8 mm. However, there was only a slight correlation between wheal diameter and the severity of the symptoms for the almond allergic patients.
Bargman et al. (1992) [734] used sera from 8 patients
Poltronieri et al. (2002) [725] used Sera from 5 SPT and challenge positive patients and from 1 other with a high RAST who was not tested further.
Sathe et al. (2001) [730] used sera from 5 patients.
Pasini et al. (2000) [728] used sera from 5 atopic patients.
Summary of Results:
Bargman et al. (1992) [734] report RAST against almond for 7/8 sera. Ratios were 2.1-59.8 times controls.
Pasini et al. (2000) [728] found that 3 patients were CAP positive but asymptomatic while 2 were CAP negative and suffered allergy.
Immunoblotting
Immunoblotting separation:
Bargman et al. (1992) [734] used 10% acrylamide 1D gels for separation. Samples were reduced with beta-mercaptoethanol and heated for 5 minutes at 100 degrees C.
Poltronieri et al. (2002) [725] used 10-12% acrylamide (or 16% to resolve low molecular mass proteins) 1D gels for separation.
Sathe et al. (2001) [730] used 13% acrylamide 1D gels for separation. Samples were reduced with beta-mercaptoethanol and heated.
Pasini et al. (2000) [728] found that the 2 allergic patients reacted to a 37 kDa protein while the tolerant patients reacted to 50 and 62 kDa glycosylated proteins.
Immunoblotting detection method:
Bargman et al. (1992) [734] electrophoretically transferred proteins onto nitrocellulose membranes. These were cut into strips and incubated with individual sera (diluted 1:10). Almond proteins bound by serum IgE were detected using rabbit 125I-anti-human IgE.
Poltronieri et al. (2002) [725] transferred proteins onto nitrocellulose membranes and detected almond proteins bound by serum IgE by chemiluminescence.
Sathe et al. (2001) [730] transferred proteins onto nitrocellulose membranes which were incubated with pooled sera from five patients (diluted 1:5). Almond proteins bound by serum IgE were detected using equine polyclonal 125I-anti-human IgE (Sanofi Diagnostics Pasteur, Chaska, MN).
Pasini et al. (2000) [728] transferred proteins onto nitrocellulose membranes by semidry electroblotting. Almond proteins bound by serum IgE were detected by chemiluminescence.
Immunoblotting results:
Bargman et al. (1992) [734] report found that 7/8 patients showed diverse IgE specificity and one (RAST ratio 2.1) did not bind the extract. Binding to a 45-50 kDa protein or group of proteins was frequent and binding to 70 kDa fell after blanching.
Roux et al. (1999) [731] report binding to 66, 55, 50, 39-44, 37, 28, 17 and 10 kDa with different patterns for severe and mild symptoms. 12/14 subjects with life-threatening reactions to almonds showed IgE binding to almond extract and 11/14 to almond major protein (AMP). Sera from 6/11 patients with milder symptoms gave IgE binding to the 66 or 50 kDa allergens. 2/11 did not show IgE binding.
Poltronieri et al. (2002) [725] found that the 6 sera bound proteins from 12 to 66 kDa. Major bands were at 12 and 45 kDa.
Sathe et al. (2001) [730] found that the combined sera bound to proteins in the 39-66 kDa range and to a protein at about 16 kDa.
Pasini et al. (2000) [728] found that the 2 allergic patients reacted to a 37 kDa protein while the tolerant patients reacted to 50 and 62 kDa glycosylated proteins.
4 patients gave symptoms described as an anaphylactic reaction and 1 showed oral allergy syndrome (Poltronieri et al. 2002 [725]). It is not clear if the "anaphylactic reaction" was severe as suggested by Johansson et al. (2001) [946].
IgE cross-reactivity and Polysensitisation
Although almond is taxonomically close to cherry, polysensisitzation has been reported with tree nuts and with peanut. This is probably because the almond nut is eaten and expresses seed storage proteins. However, Clark and Ewan (2003) [615] found in a study of 1000 peanut and tree nut allergic patients that 55% of patients allergic to another nut could tolerate almond. Only 3% (34 patients) reacted most strongly to almond.
Other Clinical information
Teuber et al. (1997) [729] report that almond oils varied widely in their allergen content depending on their processing. Guillet and Guillet (2000) [733] report that a five month old child with atopic dermatitis developed contact dermatitis to almond from the oil (no almond had been ingested).
Many studies report allergy to "tree nuts". Allergy to almond was the third most common of the tree nuts reported by Sicherer et al. (2001) [826] with 15% of the 1667 self-reported nut allergic registrants reporting almond allergy. In a later self-reported survey, Sicherer et al. (2003) [736] report that almond is the third most common tree nut to cause allergy in the USA after walnut and cashew with 32/82 responders reporting allergy.
Sicherer et al. (1998) [517] report 13/54 nut allergic patients as almond allergic. However, the symptoms, described as 89% involved the skin (urticaria, angioedema), 52% the respiratorytract (wheezing, throat tightness, repetitive coughing, dyspnea),and 32% the gastrointestinal tract (vomiting, diarrhea) were not associated with specific nuts. Similarly, Ewan (1996) [323] report 14 almond allergic patients and symptoms for 62 peanut and nut allergics. Clark and Ewan (2003) [615] report 34/1000 peanut or nut allergic patients showed their strongest reaction to almond. Considering only patients with a clear history of allergy or tolerance to almond, 210 patients (55%), who were allergic to peanut or another nut, tolerated almond.
Reviews (1)
Roux KH, Teuber SS, Sathe SK.
Tree nut allergens. Int Arch Allergy Immunol. 131(4):234-244. 2003
PUBMED ID:
12915766
Bargman TJ, Rupnow JH, Taylor SL.
IgE-binding proteins in almonds (Prunus amygdalus); identification and immunoblotting with sera from almond-allergic adults J Food Sci 57:717-720. 1992
PUBMED ID:
unknown
[734]
Clark AT, Ewan PW.
Interpretation of tests for nut allergy in one thousand patients, in relation to allergy or tolerance. Clin Exp Allergy 33(8):1041-1045. 2003
PUBMED ID:
12911776
Ewan PW
Clinical study of peanut and nut allergy in 62 consecutive patients: new features and associations. Brit Med J. 312:1074-1078. 1996
PUBMED ID:
8616415
Guillet G, Guillet MH.
[Percutaneous sensitization to almond oil in infancy and study of ointments in 27 children with food allergy] Allerg Immunol (Paris). 32(8): 309-311. 2000
PUBMED ID:
11244925
Johansson SG, Hourihane JO, Bousquet J, Bruijnzeel-Koomen C, Dreborg S, Haahtela T, Kowalski ML, Mygind N, Ring J, van Cauwenberge P, van Hage-Hamsten M, Wuthrich B; EAACI (the European Academy of Allergology and Cinical Immunology) nomenclature task force.
A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force. Allergy 56(9):813-824. 2001
PUBMED ID:
11551246
Pasini G, Simonato B, Giannattasio M, Gemignani C, Curioni A.
IgE binding to almond proteins in two CAP-FEIA-negative patients with allergic symptoms to almond as compared to three CAP-FEIA-false-positive subjects. Allergy. 55(10): 955-958. 2000
PUBMED ID:
11030377
Poltronieri P, Cappello MS, Dohmae N, Conti A, Fortunato D, Pastorello EA, Ortolani C, Zacheo G.
Identification and characterisation of the IgE-binding proteins 2S albumin and conglutin gamma in almond (Prunus dulcis) seeds. Int Arch Allergy Immunol. 128(2): 97-104 2002
PUBMED ID:
12065909
Roux, K. H.; Sathe, S. K.; Peterson, W. R.; Teuber, S. S.
The major seed storage protein of almond (Almond Major Protein) is an allergen. J. Allergy Clin. Immunol. 103, S66, abstract 255 1999
PUBMED ID:
unknown
[731]
Sathe SK, Teuber SS, Gradziel TM, Roux KH.
Electrophoretic and immunological analyses of almond (Prunusdulcis l.) genotypes and hybrids. J Agric Food Chem. 49(4): 2043-2052. 2001
PUBMED ID:
11308365
Sicherer SH, Burkes AW, Sampson HA.
Clinical features of acute allergic reactions to peanut and tree nuts in children Pediatrics 102 1-6 1998
PUBMED ID:
9651458
Sicherer SH, Furlong TJ, Munoz-Furlong A, Burks AW, Sampson HA.
A voluntary registry for peanut and tree nut allergy: characteristics of the first 5149 registrants. J Allergy Clin Immunol. 108(1):128-32. 2001
PUBMED ID:
11447394
Sicherer SH, Munoz-Furlong A, Sampson HA.
Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol. 112(6): 1203-7. 2003
PUBMED ID:
14657884
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