Peanuts are one of the most relevant foods implicated in IgE-mediated adverse reactions in pediatric population. This study aimed to evaluate the pattern of sensitization towards five peanut allergenic components (rAra h 1, 2, 3, 8 and 9) in a population of Italian children and adolescents with specific IgE (sIgE) to peanut. rAra h 9 was the main allergen implicated in peanut sensitization (58%), followed by rAra h 8 (35%), rAra h 2 (27%), rAra h 3 (23%) and rAra h 1 (12.5%). rAra h 1, 2, and 3 were the main allergenic components in young children: 8/13 (62%) between 2 and 5 years, 8/23 (35%) between 6 and 11 years, and 3/12 (25%) between 1 and 16 years. No differences were found among the levels of sIgE towards rAra h 1, 2, 3, and 9 in the three groups; in contrast, the levels of sIgE against rAra h 8 showed an increasing trend according to age. In conclusion rAra h 1, 2, and 3 were the prevalent sensitizing allergens during the first years of life in Italian patients with sIgE to peanuts (“genuine” allergy); in contrast rAra h 9 and 8 were mainly involved in school-age children and adolescents with pollen allergy (“secondary” sensitization).
Peanuts (
The study involved 48 children (30 males, 62%, and 18 females, 38%) with a median age of 8 years (range 2–16 years) referred to the Pediatric Allergology Unit of Bologna University from November 2011 until December 2012. Inclusion criteria were a clinical history of suspected peanut and/or tree nuts allergy and a level of sIgE against peanut ≥ 1 kUA/L (ImmunoCAP 1000 Thermo Fisher Scientific, Uppsala, Sweden). Symptoms suggestive of atopic dermatitis and food and or respiratory allergy (asthma and rhino-conjunctivitis) were investigated in all enrolled patients. Parental history of atopy and the age of onset of allergic diseases were asked for all patients and/or to their parents. Of the forty-eight patients recruited for this study, 24 (50%) followed an elimination diet for peanuts or had never eaten them and were classified as “avoiders.” The rest of them, who used to eat peanuts without adverse reactions were defined to be “tolerant.” This research was performed in accordance with the principles of the Declaration of Helsinki.
Serum sIgE was detected by the means of the CAP system (ImmunoCAP 1000 Thermo Fisher Scientific, Uppsala, Sweden). The determination of sIgE against a panel of inhalant [pollen from grass (
Data were stored by means of customized databases. Statistical analyses were carried out by means of MedCalc statistical software (Version 12.5.0, MedCalc Software, Ostend, Belgium). The Chi-square test and nonparametrical tests were applied when appropriate. In particular, proportions were compared by Chi-square test; geometric mean levels of sIgE were compared by Mann-Whitney
The clinical and serological characteristics of the study population are resumed in Table
Clinical and laboratory features of the 48 children and adolescents with documented peanut sensitization (sIgE > 1 kUA/L). The patients have been categorized by the tolerance status against peanuts.
Study population ( |
Tolerant patients ( |
Avoiders ( |
|
|
---|---|---|---|---|
Sex, male, |
30 (62) | 12 (50) | 18 (75) | NS |
Age, median years (range) | 8 (2–16) | 9.5 (2–16) | 8 (2–16) | NS |
Parental history of atopy, |
21 (44) | 8 (33) | 13 (54) | NS |
Allergic respiratory disease, |
26 (54) | 13 (54) | 13 (54) | NS |
Age onset respiratory disease years, median (range) | 6 (2–13) | 6.5 (4–10) | 4.5 (2–13) | NS |
Atopic Dermatitis, |
27 (56) | 11 (46) | 16 (67) | NS |
Age onset atopic dermatitis years, median (range) | 0.5 (0.5–5) | 0.8 (0.5–4) | 0.5 (0.5–5) | NS |
Food allergy, |
40 (83) | 16 (67) | 24 (100) | <0.005 |
Age onset food allergy years, median (range) | 1 (0.5–11) | 1 (0.5–6) | 1.5 (0.5–11) | NS |
Peanut avoiders, |
24 (50) | 0 | 24 (100) | NA |
Never eaten, |
20 (42) | 0 | 20 (83) | NA |
Clinical reactions, |
4 (8) | 0 | 4 (17) | NA |
Inhalant allergen sensitization, |
40 (83) | 20 (83) | 20 (83) | NS |
Grass (Phleum p. and/or Cynodon d.), |
39 (81) | 19 (79) | 20 (83) | NS |
Birch, |
36 (75) | 17 (71) | 19 (79) | NS |
Bet v 1, |
18 (37) | 7 (29) | 9 (37) | NS |
Hazel tree, |
36 (75) | 18 (75) | 18 (75) | NS |
Olive tree, |
37 (77) | 18 (75) | 19 (79) | NS |
Food allergen sensitization, |
48 (100) | 24 (100) | 24 (100) | NA |
Peanut, |
48 (100) | 24 (100) | 24 (100) | NA |
Ara h 1, |
6 (12.5) | 0 (0) | 6 (25) | <0.05 |
Ara h 2, |
13 (27) | 3 (12) | 10 (42) | <0.05 |
Ara h 3, |
11 (23) | 4 (17) | 7 (29) | NS |
Ara h 8, |
17 (35) | 8 (33) | 9 (37) | NS |
Ara h 9, |
28 (58) | 17 (71) | 11 (46) | NS |
Hazelnut, |
43 (90) | 21 (87) | 22 (92) | NS |
Walnut, |
34 (71) | 15 (62) | 19 (79) | NS |
Rice, |
28 (58) | 13 (54) | 15 (62) | NS |
Wheat, |
35 (73) | 16 (67) | 9 (37) | <0.05 |
Soy, |
33 (69) | 13 (54) | 20 (83) | <0.05 |
Apple, |
31 (65) | 14 (58) | 17 (71) | NS |
Probability (
Rates of sensitization against one of the five peanuts’ molecular components (rAra h 1, 2, 3, 8, and 9) in a population of 48 children and adolescents (median age: 8 years; range: 2–16) with documented peanut sensitization (sIgE > 1 kUA/L). Patients sensitized against one allergenic component were defined as “monosensitized,” whereas those sensitized to more than one of the five peanuts’ allergens were defined as “polysensitized.” Patients were categorized according to the tolerance status against peanuts.
Study population |
Tolerant patients ( |
Avoiders ( |
|
|
---|---|---|---|---|
Monosensitized patients, |
26 (54) | 15 (62) | 11 (46) | NS |
Polysensitized patients, |
20 (42) | 8 (33) | 12 (50) | NS |
Two allergens, |
14 (29) | 7 (29) | 7 (29) | NS |
Three allergens, |
4 (8) | 1 (4) | 3 (12) | NS |
Four allergens, |
1 (2) | 0 | 1 (4) | NS |
Five allergens, |
1 (2) | 0 | 1 (4) | NS |
None of the 5 allergens, |
2 (4) | 1 (4) | 1 (4) | NS |
Probability (
We grouped patients in three age categories (2–5 years old (
Peanut specific IgE profiles of the 48 children and adolescents (median age: 8 years; range: 2–16) with documented peanut sensitization (sIgE > 1 kUA/L). Patients have been grouped in three age categories (2–5 years old (
Our results confirm the relevance of the LTP Ara h 9 (positive in 58% of our study population) as a major allergen in peanut sensitized subjects living in a country of the Mediterranean area [
Interestingly, our data showed an age-dependent sensitization pattern in patients with sIgE against peanut extract. Pre-school children were mostly sensitized (62%) to one of the SSPs peanuts allergens. In contrast, the Bet v 1 homologue Ara h 8 and the LTP Ara h 9 were prevalent in school children and adolescents, with levels of sIgE against Ara h 8 increasing with age. Since the sensitization to one of the peanuts’ SSPs (in particular Ara h 2) has been proved to be a marker of positive oral provocation test in patients with suspected peanut allergy, our findings show a possible more relevant risk of clinical reactions in patients with early onset of peanut sensitization [
The methodological limitations of this research need to be mentioned. Indeed, although the component-resolved diagnosis approach showed a detailed picture of the molecules implicated in the mechanism of peanut sensitization, the lack of complementary diagnostic tests (e.g., skin prick test, oral provocation test, and metabolite evaluation) is a bias of this study [
Despite these limitations, our data highlight the need for further research focusing on this phenomenon.
In conclusion, in our study the LTP rAra h 9 was the main implicated allergen in Italian patients with sIgE to peanuts, with similar prevalence in tolerant patients and patients avoiding peanuts. Moreover, both rAra h 9 and rAra h 8 were mainly involved in peanut sensitization in school age children and adolescents, with sIgE levels increasing with age, probably due to mechanism of cross-reactivity (secondary sensitization) in patients with pollen allergy. In contrast, the SSPs, in particular Ara h 1 and Ara h 2, were the prevalent sensitizing allergenic components in peanut avoiders, and their rates of sensitization were higher in preschool children, showing a phenomenon of genuine IgE-specific sensitization. Further research is needed to prove the clinical implications of these data.