Allergen Data Collection: Peanut (Arachis hypogaea)
Internet Symposium on Food Allergens 2(2): 87-122 (2000) [
1 Prevalence of Peanut Allergy

1.1 General Population

Prevalences within the author's selected populations are listed. Those that are assigned randomly selected ("unselected") with numbers more than 500 may be regarded as representative of the "general population". Inclusion criteria may involve circumstances not related to atopic predisposition according to current knowledge.
Country / Subjects Allergy / Sensitivity to References
Sweden (Göteborg, Uppsala, Västerbotten)
1397 unselected adults, age of 20-44 years (study period 1991-92)
peanut 3% (RAST) Björnsson et al. 1996
a) 16420 randomly selected adults (age of >15 years)
b) based on 124 interview confirmed peanut allergic individuals (all ages) (questionniare)
a) peanut 0.4%
b) peanut 0.5%
Emmett et al. 1999
UK, Isle of Wight
1218 unselected children (birth cohort study: born in 1989-1990, reviewed at 1, 2, and 4 years of age)
peanut 1.1% (SPT, RAST)
peanut 0.5% (allergic reactions)
Tariq et al. 1996
12032 randomly selected individuals (questionnaire):
a) children (age of <18 years)
b) adults (age of >18years)
c) children and adults
a) peanut 0.4% (self-reported)
b) peanut 0.7% (self-reported)
c) peanut or tree nut 1.1% (corrected for typical IgE-mediated symptoms)
Sicherer et al. 1999b

1.2 Subjects with Atopic or Other Diseases
Country / Subjects Sensitivity / Allergy to References
Australia, Parkville
42 children with cow's milk allergy (followed for 2 years)
peanut 55% (SPT) Hill et al. 1994
Australia, Victoria
100 cow's milk allergic children
peanut 34% (parents reported) Bishop et al. 1990
81 cases of anaphylactic shock to food (from 1991-92)
peanut and other legumes 3% Moneret-Vautrin & Kanny 1995
80 cases of food- related anaphylaxis (from 1993-97)
peanut 11% (reported to CICBAA databank) European Commission 1998
France, Pierre Benite
a) 580 patients with adverse reactions to food
b) 60 cases of anaphylaxis (study period 1984-92)
a) peanut 37% (RAST)
b) peanut 12%
Andre et al. 1994
France, Toulouse
a) 142 food allergic children
b) 378 food allergic children
a) peanut 42% (labial food challenge)
b) peanut 34% (food challenge)
a) Rance & Dutau 1997
b) Rance et al. 1999a
Germany, Bonn
150 children allergic to egg white, milk, cod fish, wheat, peanut and/or soybean
peanut 59% (RAST) Liappis & Starke 1999
Italy, Florence
102 children with grass pollen allergy
peanut 22.5% (epicutaneous skin test) de Martino et al. 1988
Italy, Florence
54 episodes of food-dependent anaphylaxis in 44 children (age of 1 month to 16 years) (from 1994-1996)
peanut 1.9% Novembre et al. 1998
Italy, Genua
132 pollen and food sensitive patients
peanut 6.6% (self-reported) Troise et al. 1992
Italy, Milan
262 fruit and/or vegetable allergic patients
peanut 36% (clinical history, SPT, RAST) Ortolani et al. 1988
131 cases of food- induced anaphylaxis
(from 1993-1997)
peanut 23% (survey, reported to the TNO Nutrition and Food Research Institute) European Commission 1998
Netherlands, Rotterdam
91 patients with atopic dermatitis (<5 years of age)
peanut 34%  (SAFT) Oranje et al. 1992
163 food allergic infants
peanut 29% (RAST) Hofman 1994
124 children with food- induced anaphylaxis (study period 1992-96)
no severe reactions to peanut (clinical history) Goh et al. 1999
Spain, Barcelona
102 patients allergic to dried fruits
peanut 80%, 73%, and 68%
(SPT, HR, and RAST)
Amat Par et al. 1990
Spain, Madrid
355 food allergic children
legumes 19% (of patients, SPT, RAST)
peanut 3.9% (of 608 positiv results, SPT, RAST)
Crespo et al. 1995
Spain, Madrid
29 plant-derived food allergic patients
peanut 10% (SPT, RAST) Diez-Gomez et al. 1999
Spain, Salamanca
84 mugwort sensitive patients without other pollen sensitizations
peanut 1.2% (RAST) Garcia-Ortiz et al. 1996
South Africa, Cape Town
112 children with atopic dermatitis (age of 5 months to 13 years)
peanut 14% (questionnaire) Steinman & Potter 1994
61 cases of food- induced anaphylaxis (from 1994-1996)
peanut 21% (reported to the National Food Administration) European Commission 1998
55 cases of food- induced anaphylaxis (from 1994-1996)
peanut 36% (Hospital Reports) European Commission 1998
Sweden, Halmstad / Malmö
a) 380 birch pollen allergic patients
b) 103 patients without birch pollen allergy
a) peanut 14%
b) peanut 4%
Eriksson et al. 1982
Switzerland, Zurich
a) 402 food allergic adults (study period 1978-87)
b) 383 food allergic patients (study period 1990-94)
a) peanut 1.5%
b) peanut 13%
(anamnesis, clinical relevance, diagnostic tests)
a) Wüthrich 1993
b) Etesamifar & Wüthrich 1998
UK, London
100 patients with food intolerance
nuts/peanut 22% (repeated challenge) Lessof et al. 1980
UK, Manchester
90 patients experienced anaphylactic reactions to foods (from 1994-1996)
peanut 47%
legumes (excluding peanut) 4.6%
(suspected cause of patients' worst reaction)
Pumphrey & Stanworth 1996
USA, Baltimore, MD
196 food-allergic  patients with atopic dermatitis
peanut 49% (DBPCFC, n=41) Sampson & Ho 1997
USA, Denver, CO
a) 74 food allergic children (age of <3 years)
b) 111 food allergic children (age of 3-19 years)
a) peanut 18% (DBPCFC)
b) peanut 41% (DBPCFC)
Bock & Atkins 1990
USA, Little Rock, AR
165 patients with atopic dermatitis
peanut 33% (SPT) from which 27/44 were DBPCFC-positive Burks et al. 1998a
USA, Memphis, TN
266 patients with anaphylaxis (age of 12-75 years, study period 1978-92)
peanut 22% (from 89 food induced cases) Kemp et al. 1995
USA, Providence, RI
248 atopic patients evaluated for allergy
peanut 3.2% (skin scratch test), from which 5/8 presented clinical relevance Kalliel et al. 1989
USA, Rochester, MN
18 patients with food- related anaphylaxis 
peanut in 4 cases Yocum & Khan 1994

1.3 Prevalence of Associated Allergies
Country / Subjects Sensitivity / Allergy to References
Spain, Barcelona
65 patients sensitive to peanuts 
tree pollen 49%
weed pollen 32%
grass pollen 23%
(2 out of 3 tests positive: SPT, HR, RAST)
Amat Par et al. 1990
South Africa, Cape Town
25 peanut-sensitized children (age of 0-3 years)
egg 64%
milk 64%
soybean 52%
wheat 28%
codfish 24% (RAST)
Frank et al. 1999
UK, Birmingham
96 children with peanut and/or nut allergy (age of 18 months to 18 years)
a) history of peanut allergy
b) history of tree nut allergy
a) tree nuts 18% (direct challenge)
a) tree nuts 47% (RAST)
b) peanut 21% (direct challenge)
Armstrong & Rylance 1999
UK, Cambridge
62 patients with peanut and/or nut allergy (age of 11 months to 53 years)
peanut 65%
brazil nut 29%
almond 23%
hazelnut 21%
walnut 13%
cashew nut 4.8%
(clinical history, SPT)
Ewan 1996
UK, Cambridge
55 patients with peanut and/or nut allergy (age of 11 months to 53 years)
house dust mites 69%
grass pollen 36%
tree pollen 3.6%
cat 35%
dog 15%
egg 18%
milk 7.3%
other legumes 7.3%
sesame 7.3%
Ewan 1996
UK, Manchester
731 patients with at least one positive RAST result to peanut, brazil nut or hazelnut (age 7 months to 65 years, median 6.6 years) (study period 1994-98)
one nut 39%
two nuts 18%
all three nuts 44%
similar pattern in all age groups (RAST >0.35 kU/L)
Pumphrey et al. 1999
UK, Southampton
60 adults with proven peanut allergy
(reported) (SPT)
soybean 5% 53%
tree nuts 56% 83%
milk 3% 20%
egg 13% 16%
grass pollen 81%
house dust mites 70%
cat (n=44) 77%
Hourihane et al. 1997a
USA, New York, NY
68 peanut-, 20 tree nut-, and 34 peanut and tree nut reactive children (age of 6 months to 9 years), (tested sera from 111 children of these)
Correlation of peanut specific IgE to:
hazelnut 0.60
almond 0.58
brazil nut 0.56
sesame 0.50
pine nut 0.37
pistachio 0.26
walnut 0.24
pecan nut 0.23
Sicherer et al. 1998

2 Outgrowing / Persistence of Peanut Allergy
Country / Subjects Sensitivity / Allergy References
France, Nancy and Toulouse
192 children with peanut allergy
Sensitivity to peanut according to age groups:
0-1 year in 11%
1-3 years in 44%
3-6 years in 26%
6-15 years in 19%
(SPT and/or RAST, food challenge)
Rance et al. 1999b
UK, Manchester, Southampton
120 children evaluated of suspected peanut allergy (median age of resolvers 5 years, range 2-9 years)
18% resolved peanut allergy 
(criteria: clear history of peanut allergy and negative oral challenge with peanut or peanut butter)
Hourihane et al. 1998b
Food allergic patients 
soy, egg, milk, wheat, and peanut:
26% loss (after 1 year of onset, DBPCFC)
Sampson & Scanlon 1989
USA, Denver, CO
32 children with peanut allergy (DBPCFC positive)
2 to 14 years after first positive DBPCFC none of the patients lost clinical sensitivity to peanut Bock & Atkins 1989

3 Symptoms of Peanut Allergy
Symptoms & Case Reports References
systemic reactions
anaphylaxis (4, 6, 10, 14, 15, 16), excercise induced anaphylaxis (12), fatal reactions (5, 7, 9, 10, 15)

cutaneous symptoms
angioedema (2, 3, 7, 11, 14), atopic dermatitis (6, 14, 16), contact urticaria (2, 13, 14), eczema (1), erythema (11), pruritus (14), urticaria (1, 3, 16)

gastrointestinal symptoms
abdominal pain (1), burning mouth (8), diarrhea (1), nausea (1), oral allergy syndrome (14), vomiting (1, 3), general (14)

respiratory symptoms
allergic rhinitis (1, 14), asthma (7), choking (3, 11), conjunctivitis (1), dyspnea (14), laryngeal oedema (11), rhinorrhoea (3), sneezing (1), wheeze (1, 3, 16)

other symptoms
collapse (14), loss of consciousness (11)

(1) Bock et al. 1978b
(2) Mathias 1983
(3) Kemp et al. 1985
(4) Ortolani et al. 1988
(5) Yunginger et al. 1988
(6) Burks et al. 1989
(7) Settipane 1989
(8) Whitley et al. 1991
(9) Sampson et al. 1992
(10) Malmheden Yman et al. 1994
(11) Ewan 1996
(12) Guinnepain et al. 1996
(13) Cantani 1997
(14) de Jong et al. 1998
(15) Foucard & Malmheden Yman 1999
(16) Szabo & Eigenmann 2000
Percentage of Reactions
Symptoms / Ref. (1)  (2)  (3)  (4) (5) (6) 
Anaphylaxis     6%   6% 4.7%
Collapse / fainting 7%          
Cyanosis 14%          
Cutaneous   95%   94%    
Angio-oedema     37%      
Atopic dermatitis     40%   43% 46%
Facial swelling 72%          
Itch 55%          
Rash 65%          
Urticaria / Angio-oedema           32%
Gastrointestinal   65% 1.4% 34% 1.5% 2%
Abdominal pain / cramp 21%          
Oral allergy syndrome         0.7% 0.5%
Vomiting 38%          
Respiratory   35%   42%    
Asthma     14%   14% 15%
Breathing difficulty 37%          
Wheeze 38%          
Hoarseness         35%  
No. of patients 406 20 142 102 132 192
(1) first reaction (questionnaire)
(2) children, symptoms after DBPCFC
(3) age of 6 months to 27 years
(4) median age of 7.4 years (questionnaire)
(5) age of 6 months to 15 years
(6) age of 0-15 years
(1) Hourihane et al. 1997b
(2) Sampson & Ho 1997
(3) Moneret-Vautrin et al. 1998
(4) Sicherer et al. 1998
(5) Rance & Dutau 1999
(6) Rance et al. 1999b
Onset of Symptoms
52% of patients reported immediate type reactions, onset of symptoms after exposure to peanut within 5 min in 76% and within 30 min in 93% of 622 self- reported peanut allergic subjects (questionnaire) (1)
Onset of symptoms after ingestion of peanut proteins within 3 min (median, range 0.3 to 45 min) in 102 peanut allergic children (2)
(1) Hourihane et al. 1997b
(2) Sicherer et al. 1998
Age at Onset of Peanut Allergy
Onset of peanut allergy in 55 children with peanut and/or nut allergy at age of:
<1 year in 20%, <2 years in 42%, <3 years in 49%, <5 years in 71%, and <7 years in 75% (cumulative percentage) (1)
Onset of peanut allergy in 142 children with peanut allergy at age of:
<1 year in 46%, <3 years in 80%, and <15 years in 93% (cumulative percentage) (2)
Median age at first reaction 24 months (range 6 to 108 months) in 102 peanut allergic children (3)
(1) Ewan 1996
(2) Moneret-Vautrin et al. 1998
(3) Sicherer et al. 1998
Threshold for Elicitation of Symptoms
Amounts of peanut inducing symptoms: 100 mg - 8 g dry weight (DBPCFC, 14 peanut allergic children) (1)
Amounts of peanut protein inducing objective symptoms: 5 mg (systemic reaction), 2 and 50 mg (mild reactions); subjective symptoms: 1-5 mg and 4-50 mg; short- lived subjective symptoms to preceeding doses of 100 µg in 2 cases (DBPCFC with peanut flour, 14 peanut allergic patients) (2)
Amounts of peanut inducing symptoms: <100 mg in 25%, 100-1000 mg in 62.5%, and 1-7 g in 12.5%  (DBPCFC, 50 peanut allergic patients) (3)
Amounts of peanut inducing symptoms: </= 500 mg in 26%, 500 mg to 2.7 g in 43.5%, 2.7 to 4.3 g in 13%, 4.3 to 8 g in 8.7%, and >8 g in 8.7% (DBPCFC, 24 peanut allergic children with atopic dermatitis) (4)
(1) Bock et al. 1978b
(2) Hourihane et al. 1997c
(3) Moneret-Vautrin et al. 1998
(4) Sicherer et al. 2000b
Allergen Contact Route
90% of patients reported reactions after ingestion of less than 1 peanut and 50% reported reactions after skin contact (622 patients with self- reported peanut allergy, questionnaire) (1)
Symptoms occurred in 40% after ingestion, in 20% after skin contact, and in 40% after inhalation of peanut allergens (35 individuals experiencing self- reported allergic reactions to peanut on airliners, questionnaire) (2)
(1) Hourihane et al. 1997b
(2) Sicherer et al. 1999a

4 Diagnostic Features of Peanut Allergy
Family History References
Family History
Relatives Reported Peanut Allergy Ref.
monozygotic twins (n=14) in 64% (concordance) (2)
dizygotic twins (n=44) in 7% (concordance) (2)
Siblings (n=610) in 7% (1)
Mothers (n=609) in 2.3% (1)
Fathers (n=609) in 0.8% (1)
Aunts / uncles (n=1213) in 0.6% (1)
Grandparents (n=2409) in 0.1% (1)

(1) Questionnaire: 622 adults and children with reported, suspected, or known peanut allergy: Atopy significantly more common in successive generations and more common in maternal than paternal relatives
(2) Questionnaire: 58 twin pairs with at least one member with convincing history of peanut allergy

(1) Hourihane et al. 1996
(2) Sicherer et al. 2000a

Parameters / Subjects Outcome References
Predictors of Peanut Allergy
1218 unselected children (birth cohort study: born in 1989-1990, reviewed at 1, 2, and 4 years of age)
Family history (92% in peanut allergic vs. 58% in non- peanut allergic children), allergy to egg (23% vs. 2.2% in SPT), and eczema (at age of 4 years) were important predictors for peanut allergy (all predictors have poor positive predictive values) Tariq et al. 1996
Maternal Peanut Consumption
15 nut-sensitized children including 13 peanut- sensitized children (SPT, RAST)
Maternal peanut and/or tree nut ingestion during pregnancy and/or lactation did not increase sensitization to nuts in children Tariq et al. 1996
Maternal Peanut Consumption
a) 25 peanut-sensitized children (age of 0-3 years)
b) 18 controls (milk and/or egg sensitive, not to peanut)
Consumption of peanuts during pregnancy (and lactation): a) 48% of mothers consumed peanuts more than once a week (during lactation: 30%), b) 19% of mothers consumed peanuts more than once a week (during lactation: 17%) (p=0.063 and p=0.47) Frank et al. 1999
Reactions to First Exposure
(1) 8 infants with immediate hypersensitivity reactions to foods (milk, egg, or peanut)
(2) 622 adults and children with reported, suspected, or known peanut allergy (questionnaire)
(3) 102 peanut allergic children (questionnaire)
Symptoms occurring at the first- known exposure: irritability, erythematous rash, urticaria, angio- oedema, vomiting, rhinorrhoea, and cough
(positive SPT in every case) (1)
Reactions to first obvious exposure reported in 81% (2) and 72% (3) of patients
(1) van Asperen et al. 1983
(2) Hourihane et al. 1997b
(3) Sicherer et al. 1998
Resolved, Persistent Allergy
a) 15 children with persistent peanut allergy
b) 15 children with resolved peanut allergy
(both age of 5-38 months)
Allergy to other foods:
a) in 60%, b) 13% (p=0.02)
Wheal size of <6 mm (SPT):
a) in 21%, b) in 100% (p<0.0001)
No difference in total and peanut- specific serum IgE; some children will be tolerant to peanut despite a history of reactions and positive SPT (open challenge, SPT, PRIST, RAST)
Hourihane et al. 1998b
Puncture Skin Test, DBPCFC
26 peanut sensitive children (5 months to 15 years of age)
46% of skin test positive patients were positive in DBPCFC Bock et al. 1978a
SPT, Extracts
104 children tested for evaluation of allergic disease
Raw, roasted (145°C, 1 h) and commercial peanut extracts tested: roasted extract had best specificity in SPT (8 children with peanut allergy after ingestion of peanut or peanut products) Kemp et al. 1985
SPT, Extracts
peanut allergic patients
Comparison of 6 commercial SPT extracts: Differences in contents of major allergens Ara h 1 and Ara h 2, protein pattern was the same in extracts from roasted peanuts but varied in extracts from raw peanuts, all extracts reactive in SPT (RAST inhibition, SDS-PAGE immunoblot) Hefle et al. 1995
SPT, Extracts
peanut allergic patients
SPT results with a) commercial extracts and b) fresh peanuts as compared to labial food challenge:
Positive SPT a) 50%, b) 80%
Sensitivity a) 66%, b) 90%
Specificity a) 69%, b) 30%
Rance et al. 1997
a) RAST and Clinical Relevance
b) SPT and Clinical Relevance
24 patients with clinical history of peanut allergy (oral allergy syndrome)
a)  RAST (specific IgE > 0.7 kU/L):
positive results in 42%
positive preditive value 48% 
negative preditive value 55%
b) SPT with commercial extracts and fresh food:
positive results in 67% and 13%
positive preditive value 51% and 59%
negative preditive value 62% and 55%
Ortolani et al. 1989
peanut allergic patients
a)  <3 years, b) 3-19 years of age
SPT ( > 3 mm)
positive predictive value a) 72%, b) 45%
negative predictive value a) and b) 100%
Bock & Atkins 1990
Children suspected of IgE- mediated symptoms of peanut allergy
Significant differences in SPT (wheal sizes) between peanut allergic or tolerant individuals (DBPCFC) (P < 0.05); SPT cut-off values mean diameter 6 mm / surface area of wheal 40 mm2 Eigenmann & Sampson 1998
food-allergic children with atopic dermatitis
a) predictive values Phadebas RAST score >/= 3
positive preditive value 44%
negative preditive value 100%
b) predictive values of SPT ( > 3 mm)
positive preditive value 44%
negative preditive value 100%
Sampson & Albergo 1984
60 children with positive prick test to peanuts
52% true positive, 48% false positive as compared to DBPCFC; wheal diameter significantly greater in DBPCFC positive children (median 25 mm vs. 5 mm, p<0.001) Bernhisel-Broadbent & Sampson 1989
food-allergic children with atopic dermatitis
a) predictive values of specific IgE > 0.35 kU/L
positive predictive value 78% 
(>95% at IgE 15 kU/L)
negative predictive value 85%
b) predictive values of SPT ( > 3 mm)
positive predictive value 55%
negative predictive value 75%
Sampson & Ho 1997
Negative Tests, Open Challenge
17 children with negative SPT or RAST perceived to be peanut or nut sensitive
Simple open challenge procedure:
2 positive challenges with peanuts; clinical sensitivity persisted in 2 children despite negative SPT and RAST tests
Baker et al. 1999
Clinical Severity, Immunoblot
89 peanut allergic patients
Sensitivity to 15 kDa allergen significantly associated with severe symptoms (wheeze, cyanosis) but not to skin or gut symptoms; patients with specific IgE to 15 kDa allergen presented with mild 30%, moderate 36%, and severe reactions 72% (p<0.005); no significant differences for 17 and 63 kDa allergens (SDS-PAGE immunoblot) Clarke et al. 1998
Specific IgE, IgG, IgG4
10 peanut allergic patients (age of 3 months to 20 years)
Positivity of serum immunoglobulins in patients:
Specific IgE IgG IgG4
Ara h 1* 60% 80% 50%
Ara h 2* 80% 90% 80%
Ara h 3* 70% 90% 80%
* presumed according to Mr of appr. 60, 16, and 14 kDa (SDS-PAGE immunoblot)
Similar IgE and IgG binding patterns
Szabo & Eigenmann 2000
Levels of Specific IgE
a) 70 peanut allergic children (age of 1-16 years)
b) 21 peanut allergic adults (age of 17-38 years)
Peanut specific IgE levels (RAST):
a) 49 kU/L (median) 
b) 20 kU/L (median)
Clarke et al. 1998
Levels of Specific IgE
a) 91 peanut reactive children
b) 13 non-reactive children
Peanut specific IgE levels (RAST):
a) 52 (mean), 46 (median) kU/L
b) 2.8 (mean), 0.5 (median) kU/L
Sicherer et al. 1998
Spontaneous Histamine Release
Children sensitive to peanut or other foods (3-16 years)
High spontaneous histamine release of basophils in vitro only in sensitized persons (predominantly to food antigens) May & Remigio 1981
Heavy Chain Variable Region of IgE
2 patients with peanut allergy
Heavy chain variable region (VH) sequences of IgE from blood lymphocytes: predominantly VH1 family use; IgE VH sequences highly somatically mutated; in only 6/17 cases clear evidence for clustering of amino acids indicative of antigen selection  (PCR amplification) Janezic et al. 1998

Cellular Parameters References
HLA Class II Genotypes
HLA Class II Frequency Ref.
DRB1*08 a vs. b (NS), b > c * (1)
DRB1*08 a > c *, b > c * (2)
DRB1*08/12 tyr 16 a > c *, b > c * (2)
DQB1*04 a > c *, b > c * (2)
DPB1*0101 a < c * (2)
DPB1*0201 a < c * (2)
DPB1*0301 a > c * (2)
* significant, (NS) no significant difference
(1) a) grass pollen allergic, b) peanut allergic individuals, c) controls (80 patients with pollen- associated food allergy and 120 patients with pollinosis)
(2) a) 152 individuals from families containing at least 1 peanut allergic member and 9 unrelated patients, b) individuals from a) with peanut allergy, c) 293 unrelated controls
(1) Boehncke et al. 1998
(2) Howell et al. 1998
PBMC Proliferation, IFN-gamma, IL-4 (Ara h 2)
Stimulation of PBMC from peanut allergic patients, patients with asthma and nonatopic controls with Ara h 2 and Candida albicans allergens induced significantly higher levels of PBMC proliferation than ovalbumin, casein, and soy. Significantly lower IFN-gamma levels produced by PBMC from peanut allergic group after stimulation with Ara h 2. Inverse correlation between Ara h 2- specific serum IgE and IFN-gamma production in peanut allergic group. IL-4 expression in Ara h 2- stimulated PBMCs from peanut allergic group and control group (detection by PCR).
Dorion et al. 1994
PBMC Proliferation, IFN-gamma, IL-4, IL-5 (Peanut Extract)
Stimulation of PBMC from peanut allergic patients with crude peanut extract: significantly higher dose- dependent proliferation as compared to controls, peanut-specific T-cell clones from 1 selected patient were all CD4+/CD8- T helper cells with Th2 cytokine profile (high levels of IL-4 and IL-5, low or no IFN-gamma secretion)
de Jong et al. 1996
PBMC Proliferation, IFN-gamma, IL-4 (Peanut Extract)
Significantly higher proliferation of PBMCs in peanut allergic patients with atopic dermatits as compared to controls with and without atopic dermatitis. 80-100% of cells were CD4+, proliferative responses correlated significantly with increased IL-4 mRNA expression after peanut- specific stimulation. Polyclonal stimulation was preferentially associated with CD8+ cell proliferation. 
Laan et al. 1998
PBMC Proliferation, Clinical Relevance, SPT, RAST (Peanut Extract)
Proliferation of PBMCs from peanut allergic patients stimulated with crude peanut extract was allergen-specific and dose- dependent, no correlation between PBMC proliferation and clinical severity, SPT reactions or peanut specific IgE levels (44 peanut allergic individuals, 13 non-peanut allergic controls)
Hourihane et al. 1998a
T-Cell Clones, HLA-Restriction
Peanut-reactive T-cell clones raised from a peanut- and Brazil nut-allergic individual without hazelnut allergy: T-cell clones were not cross- reactive to Brazil nut or hazelnut extracts (with the exception of 1 clone); peanut antigen recognition was associated with HLA-DR and HLA-DP but not with HLA-DQ MHC class II molecules; Th2-like profile of peanut specific clones (high levels of IL-4, low levels of IFN-gamma)
Higgins et al. 1995
T-Cell Receptor
Stimulation of T-cells from peanut allergic patients resulted in selective expansion of V beta 2+ T-cells (T-cell receptor variable beta regions)
Dorion & Leung 1995
T-Cells Preceeding Humoral IgE
Detection of peanut (Ara h 1) specific T-cell reactivity 3 months before peanut- specific IgE was detectable (1 child with initial cow's milk allergy and atopic dermatitis)
van Reijsen et al. 1998

5 Therapy of Peanut Allergy
Treatment* Outcome References
Rush Immunotherapy
3 peanut allergic patients completed therapy
Subcutaneous injection therapy with increasing doses of peanut extract (4 per day for 5 days), 67-100% decrease in symptoms (DBPCPC), reduction in end point SPT reactivity to peanut extract, all peanut- treated subjects were able to reach maintenance dose, incidence of systemic reactions during immunotherapy was 13% in a total of 120 injections (no anaphylactic reaction occurred) Oppenheimer et al. 1992
6 peanut allergic patients underwent therapy, 6 peanut allergic controls
Rush protocol with injections of increasing doses of aqueous peanut extracts maintained with weekly injections > 1 year.  All treated patients experienced increased dose tolerance in DBPCFC. 3 patients remained tolerant of the full maintenance dose of injections and maintained increased oral tolerance.  Partial or complete loss of protection in 2 and 1 patient who required dose reduction because of systemic reactions. Systemic reactions common in treated group both during rush immunotherapy and maintenance injections. Unmodified peanut extracts not suitable for immunotherapy. Nelson et al. 1997
Gene Immunization in Mice
Immunization of different mice strains with plasmid DNA encoding peanut allergen Ara h 2
After pDNA immunization mice were challenged with Ara h 2 or peanut protein injections: immunized C3H mice strain expierienced anaphylactic reactions, while AKR/J and BALB/c mice had no reactions Li et al. 1999
Oral Gene Immunization in Mice
Immunization of mice by oral administration of nanoparticles (plasmid DNA encoding peanut allergen Ara h 2 complexed with chitosan)
Transduced gene expression in the intestinal epithelium in mice (strain AKR/J). Mice receiving nanoparticles produced secretory IgA and serum IgG2a (with low levels of IgE) and showed substantial reduction in allergen- induced anaphylaxis as compared with non- immunized mice or mice treated with 'naked' DNA Roy et al. 1999
* Studies may be experimental, unproved, or controversial. Please notice the disclaimer !

6 Composition of Peanut

7 Allergens of Peanut
Proteins / Glycoproteins Allergen Nomenclature References
Vicilin [63.5 kDa] Ara h 1 Burks et al. 1991, Burks et al. 1995c
Conglutin [17 kDa] Ara h 2 Burks et al. 1992a, Stanley et al. 1997
Glycinin [14, 36, 57 kDa] Ara h 3 / Ara h 4 Eigenmann et al. 1996, Kleber-Janke et al. 1999, Rabjohn et al. 1999
Profilin [14 kDa] Ara h 5 Kleber-Janke et al. 1999
Conglutin-homologous protein [14.5 kDa] Ara h 6 Kleber-Janke et al. 1999
Conglutin-homologous protein [16 kDa] Ara h 7 Kleber-Janke et al. 1999
Peanut agglutinin [31 kDa]   Burks et al. 1994a
Peanut I: 20 and 30 kDa allergens   Sachs et al. 1981
65 kDa Allergen   Barnett & Howden 1986

7.1 Sensitization to Peanut Allergens
Country / Subjects Sensitivity References
Australia, North Ryde
a) 10 patients with peanut allergy
b) 8 peanut with peanut allergy
a) alpha-arachin, conarachin I, and concanavalin A-reactive glycoprotein gave significant  RAST results; peanut lectin and phospholipase D gave poor RAST responses
b) peanut lectin: agglutinin (30 kDa)  in all patients (RAST)
a) Barnett et al. 1983
b) Barnett & Howden 1987
France, Nancy
2 peanut allergic patients
a) Allergens from peanut kernels:
15, 18, 28, 41, and 67 kDa
b) Allergens from peanut shells:
18 and 41 kDa
Moutete et al. 1995
Germany, Borstel
9 peanut allergic patients
>50% to 17, 30, 48-66, and 116 kDa allergens
(SDS-PAGE immunoblot)
Uhlemann et al. 1993
Germany, Borstel
40 peanut allergic patients
6 Recombinant Allergens  
Ara h 1 65%
Ara h 2 85%
Ara h 4 (Ara h 3) 53%
Ara h 5 13%
Ara h 6 38%
Ara h 7 43%
(SDS-PAGE immunoblot)
Kleber-Janke et al. 1999
Netherlands, Zeist
14 peanut allergic patients
13 Allergens from raw peanuts  
18 kDa (Ara h 2) 80%
20 and 21 kDa 70%
40 kDa 60%
33 and 44 kDa 50%
14, 60, and 71 kDa 35%
36 kDa 30%
16, 28, 29 kDa </= 20%
(SDS-PAGE immunoblot)
de Jong et al. 1998
UK, Southampton
91 peanut allergic patients
19 Allergens from peanut powder  
63 kDa (Ara h 1) 73%
17 kDa (Ara h 2) 71%
15 kDa 54%
10, 18, 27, 28, 30, and 51  kDa 30-45%
7, 20, 21, 25, 33, 38, 44, 71, 96 and kDa <30%
(SDS-PAGE immunoblot)
Clarke et al. 1998
USA, Little Rock, AR
6 (a, b), 12 (c), and 18 (d) peanut allergic patients with atopic dermatitis
a) Ara h 1 in 100%
b) Ara h 2 in 100%
c) Agglutinin in 50%
d) Ara h 3 in 44%
 (IgE specific ELISA)
Weak IgE- binding inhibition by agglutinin
a) Burks et al. 1991
b) Burks et al. 1992a
c) Burks et al. 1994a
c) Rabjohn et al. 1999
USA, Madison, WI
peanut allergic patients
38, 44, and 65 kDa allergens (SDS-PAGE immunoblot) Hefle et al. 1990

7.2 Properties of Vicilin (Ara h 1)
7.3 Properties of Conglutin-like Protein (Ara h 2)
7.4 Properties of Glycinin (Ara h 3 / Ara h 4)
7.5 Properties of Profilin (Ara h 5)
7.6 Properties of Conglutin-homologue Protein (Ara h 6)
7.7 Properties of Conglutin-homologue Protein (Ara h 7)

8 Isolation & Preparation
Extract / Purified Allergens Methods References
Peanut I: 20 and 30 kDa allergens Extraction of dry defatted peanut powder with 0.1-M NH4HCO3 (pH 8.75), centrifugation, supernatant lyophilized, dissolved in phosphate buffer, centrifugation and dialysis followed by two steps of IEC-chromatography (DEAE column), purification by preparative PAGE Sachs et al. 1981
65 kDa Allergen Extraction of ground defatted peanut meal with Tris-HCl / NaCl (pH 8.0), isolation with affinity chromatography (ConA-Sepharose) and purification by SEC and IEC Barnett & Howden 1986
a) Ara h 1
b) Ara h 2
Extraction of defatted, powdered peanuts with phosphate / NaCl buffer (pH 7.0), centrifugation, dialysis, anion exchange chromatography (a: Mono Q column, b: PL-SAX column), fractions dialyzed and lyophilized a) Burks et al. 1991
b) Burks et al. 1992a
Ara h 1 Immunoaffinity chromatography: Ara h 1 specific mAb bound to cynogen bromide- activated Sepharose beads; isolation of Ara h 1 from crude peanut extract Burks et al. 1994b
a) Ara h 1
b) Ara h 2
Lyophilized crude peanut extract dissolved in TRIS- bis- propane buffer (pH 7.2), centrifugation, anion exchange chromatography (Source Q column); Ara h 2 containing fractions were dialyzed and further purified by IEC (Source S column) de Jong et al. 1998
Agglutinin Isolation by IEC and further purification by SDS-PAGE electroelution Burks et al. 1994a

9 Cross-Reactivities
Cross-Reacting Allergens Subjects / Methods References
Peanut: (Nuts)
almond, brazil nut, black walnut, pecan
Positiv inhibition of IgE-binding:
to peanut by brazil nut and pecan (1 patient each), by peanut to almond, brazil nut, and pecan (1 patient each) (5 patients, RAST inhibition)
Gillespie et al. 1976
Peanut: (Nuts)
coconut and walnut
Almost complete inhibition of IgE binding to 35, 36.5, and 55 kDa allergens from coconut and 35, 36, and 50 kDa allergens from walnut by peanut extract (2 tree nut allergic patients, SDS-PAGE immunoblot inhibition) (1)
Minimal or no cross- reactivity between walnut and peanut proteins (4 walnut sensitive patients, immunoblot inhibition) (2)
(1) Teuber & Peterson 1999
(2) Teuber et al. 1999
Peanut: (Legumes)
peanut (sensitivity in 90% of patients), soybean (90%), green pea (80%), lima bean (53%), string bean (43%)*
30 atopic children with suspected soybean allergy (Skin test) Fries 1971
Peanut: (Legumes)
soybean, garden pea, and chick pea
15 peanut-sensitive patients (RAST-inhibition) Barnett et al. 1987
Peanut: (Legumes)
peanut (sensitivity in 87% of patients), soybean (43%), green bean (22%), pea (26%), and lima bean (41%) (SPT)*
69 legume-sensitive patients (SPT) (1)
frequency of multiple sensitization: 4.9%;
43 patients DBPCFC positive: peanut 72%, soybean 23%, pea 5% (1)
In vitro cross-reactivity did not correlate with clinical hypersensitivity, most prominent 20 kDa allergen in all legumes except green beans (SDS-PAGE and dot / immunoblot) (2)
(1) Bernhisel-Broadbent & Sampson 1989
(2) Bernhisel-Broadbent et al. 1989
Peanut: (Legumes)
patient allergic to peanut and soy:
73% reduction of IgE-binding to peanut after adsorption of cross-reacting antibodies (ELISA)
Eigenmann et al. 1996
Peanut: (Legumes)
soybeans and peas
4 peanut allergic and 2 pea allergic adults (RAST-inhibition) Hagner et al. 1998
Peanut: (Legumes)
lupine flour *
Lupine allergens with 21 kDa and 35-55 kDa, positive SPT with extract from lupine-flour containing pasta in 5 patients (7 peanut allergic patients, RAST, SDS-PAGE immunoblot) Hefle et al. 1994
Peanut: (Legumes)
lupine flour and pollen
Positive SPT with lupine flour in 44% patients, positive DBPCFC with lupine flour in 7/8 patients, cross- reactivity between peanut and lupine flour / pollen extracts in RAST and immunoblot inhibition, major lupine flour allergen: 43 kDa (24 peanut allergic patients) Moneret-Vautrin et al. 1999
Peanut: (Legumes)
carob bean *
Carob allergens with 17.5, 48, and 66 kDa; positive SPT with raw carob bean in 50%, with carob pulp in 25%, and with cooked carob in none of 12 peanut sensitive patients; carob specific RAST positive in 25%; no clinical reactivity to raw and cooked carob (RAST, SDS-PAGE immunoblot) Fiocchi et al. 1999
Peanut: (Legumes)
A case of lupine- induced anaphylaxis with positive SPT and in vitro cross- reactivity with other legumes (peanut), positive open challenge with pea, but negative open challenge to peanut and green bean Matheu et al. 1999
Peanut: (Gramineae, Legumes)
corn, rice, and soybean
123 soybean, corn, rice, and/or peanut allergic patients: significant inhibition of IgE- binding to peanut by soybean, but not by corn and rice; significant inhibition to soybean, corn, and rice by peanut; significant correlation between soybean and peanut specific RAST (r=0.76) (RAST, RAST inhibition) Lehrer et al. 1999
Peanut: (Grass Pollen)
grass pollen and tomato
Inhibition of IgE-binding: peanut, grass pollen, and tomato (grass pollen allergic children, RAST inhibition) de Martino et al. 1988
Peanut: (Grass Pollen)
cross-reactive carbohydrate determinants (CCD) from grass pollen
a) 11 patients with grass pollen allergy and positive RAST to peanut without clinical relevant peanut sensitivity
b) 4 controls with clincal relevant peanut allergy
a) 94% inhibition of IgE-binding to peanut allergens by CCD, b) only partial inhibition (59%) in 1 patient
van der Veen et al. 1997
*  multiple sensitization (not proven by  inhibition-tests)
Unique Allergens Subjects / Methods References
Peanut / Soybean
46, 29, 25, 19, 17, 14, and 5 kDa allergens from peanut did not cross-react with soybean allergens;
46 and 21 kDa allergens from soybean did not cross-react with peanut allergens
3 patients allergic to peanut
2 patients allergic to peanut and soy
a) removal of cross-reacting antibodies from serum by soy- and peanut-affinity chromatography, respectively
b) detection of unique IgE-binding proteins in SDS-PAGE immunoblot
Eigenmann et al. 1996

10 Stability of Peanut Allergens
Treatment Effects References
Peanuts (Heat)
raw and roasted peanuts (140°C, 45 min)
IgE binding proteins were heat stable (SDS-PAGE immunoblot, pooled serum from 3 peanut allergic patients) Vieths et al. 1998
Crude Peanut Protein (Heat)
heat RT to 100°C, 5 to 60 min
No change in IgE and IgG binding (10 peanut allergic patients, EAST inhibition) Burks et al. 1992b
65 kDa Allergen (Heat, pH-Range)
heated in solution (20-100°C, 30 min), pH  2.8-10.0
Stable in-vitro allergenicity over the whole temperature and pH range (RAST inhibition) Barnett & Howden 1986
Ara h 1 (Heat)
heating of ground peanuts (20-140°C, 15 min)
No difference of IgE binding inhibition between purified Ara h 1 from raw and heated peanuts (EAST inhibition, 8 peanut allergic patients) Koppelman et al. 1999
Crude Peanut Protein (Chewing)
a) 10 min chewing of peanuts in the mouth
b) successive treatment with artificial gastric fluid (pH 1.3, 10-80 min)
a) No detectable degradation of peanut allergens
b) No detectable degradation of Ara h 1 (SDS-PAGE immunoblot, 10 patients with peanut allergy)
Becker 1997
Crude Peanut Protein (Hydrolysis)
2 step enzyme digestion a) pepsin and b) trypsin, chymotrypsin and intestinal mucosal peptidase digestion
50%-inhibition concentration: 100 fold increased  for digested peanut proteins (10 peanut allergic patients, EAST inhibition) Burks et al. 1992b
Peanuts (Hydrolysis)
Digestion of crude peanut extract with pepsin (immobilized to agarose) at pH 1.8 (24 or 48 h)
Complete loss of IgE binding from sera of 5 peanut allergic patients (SDS-PAGE immunoblot); Positive T-cell response after stimulation with pepsin- digested peanut extract in 7 peanut allergic patients (PBMC proliferation) Hong et al. 1999
Peanuts (Hydrolysis)
2 step digestion with a) pepsin (2 h) and b) pancreatic enzymes (45 min) (extract from roasted peanuts)
Various IgE binding fragments after peptic digestion, IgE binding decreased strongly after subsequent pancreatic digestion;
inhibition of IgE binding to peanut proteins persisted after both digestions at values of about 50% (SDS-PAGE immunoblot, peanut allergic patients)
Vieths et al. 1999
Ara h 1 (Hydrolysis)
Digestion with pepsin, trypsin, or chymotrypsin (up to 3 h)
After hydrolysis with each enzyme 5-8 IgE binding fragments of Ara h 1 detected in the range of 16-60 kDa (SDS-PAGE immunoblot, pooled serum from 12-15 peanut allergic patients) Maleki et al. 2000

11 Allergen Sources
Reported Adverse Reactions References
Various Food Products
4 cases of fatal anaphylaxis after ingestion of cake and cookie containing peanuts, chili containing peanut butter, and a Vietnamese dish with slivered peanuts atop (1)
3 cases of fatal anaphylaxis after ingestion of candy, cake, and a sandwich containing peanuts in different forms; 1 case of severe anaphylaxis after ingestion cookies  (2)
Life-threatening allergic reactions after ingestion of peanut butter and peanut paste (3)
Recurrent anaphylactic reactions after ingestion of Asian food, chocolate products, and bakery products containing hidden peanut protein in 3 peanut allergic patients (4)
(1) Yunginger et al. 1988
(2) Sampson et al. 1992
(3) Foucard & Malmheden Yman 1999
(4) Borelli et al. 1999
Almond Icing
Fatal reaction to peanut antigen in almond icing (1)
(1) Evans et al. 1988
"Almond" Bun
Fatal reaction after ingestion of an "almond bun" with peanut flakes (substituted for almond flakes) in a 15 year old boy (presumed co-factor: cold beverage) (1)
(1) Foucard & Malmheden Yman 1999
Anaphylaxis after ingestion of cake containing undeclared peanut proteins (1)
(1) Malmheden Yman et al. 1994
Anaphylaxis after ingestion of gingersnap cookies containing undeclared peanut proteins (1)
(1) Kemp & Lockey 1996
Dry Soup Mixture
Systemic allergic reaction after ingestion of a soup in a 33 year old peanut sensitive woman; the dry soup preparation contained undeclared peanut flour as a component of flavouring ingredient; appr. 45 mg peanut protein were ingested (1)
(1) McKenna & Klontz 1997
Urticaria and angioedema after ingestion of spaghetti-like pasta fortified with sweet lupine seed flour in a 5-year old peanut sensitive girl (1)
(1) Hefle et al. 1994
Pizza Sauce
2 cases of severe anaphylaxis after ingestion of pizza sauce containing peanut proteins (1)
(1) Hogendijk et al. 1998
Milk Formulas, Peanut Oil
Adverse reactions in 4 children (4-13 months) with atopic dermatitis after ingestion of infant formula containing peanut oil; 2 children positive on labial challenge with peanut oil (1)
(1) Moneret-Vautrin et al. 1994
Crude Peanut Oil
DBPCFC with doses of 1 to 10 mL of unrefined peanut oil: 6 positiv reactions (oral and throat itching, swelling of lips, wheeze) in 60 peanut allergic patients (1)
(1) Hourihane et al. 1997a
Refined Peanut Oil
DBPCFC with doses of 5 - 15 mL refined peanut oil: 14 positiv reactions in 62 peanut allergic patients. Immediate reactions: facial erythema and pruritus (6 cases), bronchospasm ( 1 case). Delayed reactions: bronchospasm (1 case), labial oedema (1 case), abdominal pain with nausea (2 cases), eczema (3 cases), buccual itching and oral syndrome (2 cases) (1)
(1) Moneret-Vautrin et al. 1998
Peanut Oil
Labial food challenge with peanut oil positive in 4% of 50 tested and 30% of 63 peanut allergic children tested by oral food challenge (1)
(1) Rance & Dutau 1999

Allergens in Food Products Content / Products References
Roasted Peanuts
Dry and oil roasted peanuts  (serum pool from 5 peanut allergic patients)
Roasted peanuts had almost the same inhibition of IgE-binding to raw peanut extract as compared to standard peanut inhibitor (RAST inhibition) (1) Nordlee et al. 1981
Roasted Peanuts
Roasted peanuts  (serum pool from 10 peanut allergic patients)
No difference of raw and roasted peanuts in RAST inhibition; 16 IgE binding antigens in raw peanut and 7 in roasted peanut (CRIE) (1) Barnett et al. 1983
Peanut Flour
8 commercially available peanut flours and 1 peanut hull flour  (serum pool from 5 peanut allergic patients)
All peanut flour extracts showed high inhibition of IgE-binding to raw peanut extract, RAST slopes from 3 flours significantly different from raw peanut; the peanut hull flour was less allergenic  (RAST inhibition) (1) Nordlee et al. 1981
Hydrolyzed Peanut Protein
Commercially available acid hydrolyzed peanut protein (serum pool from 5 peanut allergic patients)
No inhibition of IgE-binding by hydrolyzed peanut protein to raw peanut extract (RAST inhibition) (1) Nordlee et al. 1981
Peanut Butter Products
a) Peanut butter, b) Peanut butter powder (peanut butter, dried whey), c) Peanut butter syrup (ingredients: corn syrup, peanut butter, water, dried whey, cellulose, and lecithin), d) Peanut butter flavoured chips
All peanut butter product extracts showed high inhibition of IgE-binding to raw peanut extract (serum pool from 5 peanut allergic patients, RAST inhibition) (1) Nordlee et al. 1981
Peanut Butter Products
3 allergens in peanut butter identified
Greatest reactivity to heat- stable, water- soluble, nonglycosylated protein >10 kDa (1 patient) (1) Whitley et al. 1991
Peanut Oil
Commercially available peanut oil (serum pool from 5 peanut allergic patients)
No inhibition of IgE-binding by peanut oil to raw peanut extract (RAST inhibition) (1) Nordlee et al. 1981
Peanut Oil
4 Commercially available peanut oils (serum pool from 17 peanut and/or nut allergic patients)
IgE-binding potencies:
unrefined oil (54°C max. processing temperature) > unrefined oil (65-93°C) >> refined, bleached, deodorized oils (230-260°C) (dot immunoblot)
Protein contents of unrefined oils: 10-11 µg/mL and 2 refined oils: 3 and 5.7 µg/mL
Teuber et al. 1997
Peanut Oil
Crude, neutralized and refined peanut oils
18-20 kDa allergen in protein extract of refined peanut oil (SDS-PAGE immunoblot, 2 peanut allergic patients),
9-52% inhibition of IgE-binding to peanut proteins by peanut oil protein extract in 7 of 11 peanut allergic patients (RAST inhibition)
Protein contents of unrefined oil: 3.4 µg/g, neutralized oil: 0.2 µg/g, and 5 refined oils: 0.1 to 0.2 µg/g
Olszewskiet al. 1998
Crude Peanut Oil
Protein extract from unrefined peanut oil (41 peanut sensitive children)
Positive SPT in 37% of peanut sensitive children Kull et al. 1999
Used Vegetable Oils
Vegetable oils used to roast peanuts (serum pool from 5 peanut allergic patients)
Detection of peanut allergens in used oils; 100-1000 fold reduction of peanut allergen contents after filtration and steam cleaning (RIA) (1) Keating et al. 1990

Reported Safe Products References
Refined Peanut Oil *
10 patients with clinical relevant peanut allergy: safe ingestion of 8 mL refined peanut oil (total dose)  in DBPCFC (1)
No reaction in 60 peanut allergic patients after ingestion of 16 mL of refined peanut oil (total dose) in DBPCFC (2)
No reaction in 41 peanut sensitive children in SPT with protein extract from refined peanut oil (3)
(1) Taylor et al. 1981
(2) Hourihane et al. 1997a
(3) Kull et al. 1999
* see also Reported Adverse Reactions

12 Food Allergen Labelling
Food Allergen  Labelling / Regulation Status References
International Regulations
Peanuts, soybeans and products of these
mandatory labelling of prepackaged food / advisary status (1) (1) Codex Alimentarius Commission 1999
European Regulations
Peanuts and peanut products
labelling appropriate / recommendation (1) (1) Bousquet et al. 1998

13 References

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