The Journal of Pediatrics
Volume 156, Issue 5 , Pages 777-781.e1, May 2010

Association Between Peanut Allergy and Asthma Morbidity

  • Alyson B. Simpson, MD

      Affiliations

    • Department of Pediatrics, Alfred I. duPont Hospital for Children, Wilmington, DE
    • Division of Allergy and Immunology, Thomas Jefferson University, Philadelphia, PA
    • ,
  • Ejaz Yousef, MD

      Affiliations

    • Department of Pediatrics, Alfred I. duPont Hospital for Children, Wilmington, DE
    • Division of Allergy and Immunology, Thomas Jefferson University, Philadelphia, PA
    • Corresponding Author InformationReprint requests: Ejaz Yousef, MD, Associate Professor of Pediatrics, Chief, Division of Allergy, Asthma, and Immunology, Alfred I. duPont Hospital for Children, 1600 Rockland Road, Wilmington, DE 19803.
    • ,
  • Jobayer Hossain, PhD

      Affiliations

    • Department of Pediatrics, Alfred I. duPont Hospital for Children, Wilmington, DE

Received 15 June 2009; received in revised form 12 October 2009; accepted 24 November 2009. published online 15 February 2010.

Article Outline

Objective

To evaluate the relationship between peanut allergy and asthma morbidity in school-age children.

Study design

The study involved a medical chart review to assess the association of peanut allergy with asthma morbidity in children beyond age 3 years. Peanut allergy was assessed by specific and validated criteria. A Poisson regression model was used to compare the frequency of systemic steroid use and of hospitalization for asthma beyond age 3 years in children with asthma with and without peanut allergy.

Results

Children with peanut allergy had a 2.32-times greater rate of hospitalization (P = .03) and a 1.59-times greater rate of systemic steroid use (P <.001) after controlling for covariates.

Conclusions

Peanut allergy serves as an early marker for asthma morbidity. Early prevention and intervention can improve quality of care.

CI, Confidence interval, ICAP RAST, ImmunoCAP radioallergosorbent test, NAEPP, National Asthma Education and Prevention Program, PPV, Positive predictive value, RR, Risk ratio, SPT, Skin prick test

 

Asthma is a highly prevalent disease, affecting approximately 9 million children under age 18.1, 2 Asthma exacerbations are the leading cause of childhood inpatient admissions, causing 2 million emergency department visits and 500 000 hospitalizations among all patients with asthma in 2005.3 Asthma also is a major risk factor for fatal and near-fatal food-induced anaphylaxis.4, 5, 6 More than one-third of children with food allergies are currently living with asthma.7, 8

Morbidity from asthma has been increasing in the United States. Reducing asthma morbidity is a key focus of research and public health initiatives. A better understanding of the underlying mechanisms of asthma and risk factors for poor asthma control is therefore essential to improve the outcomes of these patients.

Several risk factors for increased asthma morbidity have been identified, including the presence of food allergy.4, 9, 10, 11 In a previous study, we established a link between allergy to milk and peanut and asthma morbidity in children in the early childhood years.11 As more children are entering school with a dual diagnosis of peanut allergy and asthma,12, 13, 14 we now need to focus on the effect of peanut allergy on asthma symptoms beyond age 3 years. Because children often present with food allergy in early childhood, peanut allergy could serve as an early marker for asthma morbidity. In the present study, we assess the effect of peanut allergy on asthma morbidity beyond age 3 years.

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Methods 

The study population comprised 410 children age 5-18 years with asthma and a food allergy who received care at a large tertiary care children's hospital at any time between their third birthday up to September 2008. A central computerized patient database was used to identify potential subjects. Information in the database included hospitalizations, discharge summaries, outpatient and emergency department records, prescribed medications (including systemic steroids), laboratory tests, and medical imaging.

A list of patients with International Classification of Diseases, Ninth Revision codes 493.90 (asthma, unspecified), 493.91 (asthma with status asthmaticus), and/or 493.92 (asthma with acute exacerbation), was obtained. The medical records of 410 patients age 5-18 years with a diagnosis of asthma were reviewed. Study subjects were identified by collecting data on those patients age ≥5 years who had developed persistent asthma symptoms by age 3 years. The study protocol was approved by the hospital's Institutional Review Board.

Definition and Characteristics of Children With Asthma with and without Peanut Allergy 

Asthma was diagnosed based on the following criteria: (1) symptoms of recurrent (ie, more than 2) episodes of wheezing, cough, shortness of breath, or a combination of these; and (2) documented reversibility with bronchodilators.15 All of the patients were prescribed inhaled corticosteroids. Patients in the peanut allergy group were diagnosed based on the following criteria: (1) adverse reaction to food;16 (2) food-specific IgE level >95% positive predictive value (PPV) to peanut (IgE ≥15) (Table I; available at www.jpeds.com);17, 18 (3) and a skin prick test (SPT) 3 mm greater than negative control.19, 20, 21

Exclusion Criteria 

Patients were excluded from the study if: (1) their clinical history did not support the diagnosis of asthma; (2) were not being treated according to National Asthma Education and Prevention Program (NAEPP) guidelines;15 (3) did not attend >75% of their scheduled outpatient visits, as documented in our computerized outpatient database; (4) were lost to follow-up before September 2008; (5) were followed for <2 years beyond age 3 years; or (6) had cystic fibrosis or immunodeficiency. Patients with peanut allergy were excluded if they had a clinical history suggestive of peanut allergy but did not have a confirmatory ImmunoCAP radioallergosorbent test (ICAP RAST; Pharmacia Diagnostics AB, Portage, Michigan) value >15, the 95% PPV to peanut,16, 17, 18 and an SPT 3 mm greater than negative control.19, 20, 21 Children diagnosed with egg, milk, and shellfish allergy also fulfilled the strict inclusion criteria for food allergy, including a suggestive clinical history, IgE >95% PPV for each specific food,16, 17, 18 and SPT 3 mm greater than negative control.19, 20, 21

Predictors 

Demographic information was gathered, including race, sex, age (documented in months), history of atopic dermatitis, family history of asthma, gastroesophageal reflux, history of food allergy, history of aeroallergen sensitivity, and passive smoke exposure in the home. Atopic dermatitis was defined according to the diagnostic criteria of Hannifin and Rajka.22 Gastroesophageal reflux was defined based on clinical signs and symptoms as well as diagnostic test results (ie, pH probe, gastric emptying scan, endoscopy with biopsy, or upper gastrointestinal series). Most of the covariates were organized into categorical variables, including sex (male or female), race (Caucasian, African American, or others), and the presence or absence of the following: atopic dermatitis; family history of asthma; gastroesophageal reflux; adenoidal hypertrophy; passive smoke exposure in the home; allergy to milk, egg, or shellfish; and the presence or absence of sensitization to dust mite, aspergillus, alternaria, grass, weed, cat, dog, and tree. Age was recorded at 3 points in time: at the first visit to the food allergy clinic, at the onset of persistent asthma symptoms, and at the end of the review period in September 2008. Chronologic age was included in the regression as a continuous variable.

IgE Level and Skin Testing 

The results of previous skin tests and food-specific IgE levels (ICAP RAST) to peanuts, egg, milk, and shellfish were obtained in addition to the results of skin testing to aeroallergens. All SPTs were performed using the GreerPick method (Greer Lab, Lenoir, North Carolina) and allergen extract (provided by Hollister-Stier Laboratories, Spokane, Washington). A SPT was considered positive when the wheal diameter was 3 mm and 50% larger than negative control, and the negative control remained negative.

All children with a history suggestive of allergic rhinitis or atopic dermatitis underwent skin testing with the same panel of aeroallergens (Table II). Data were recorded in a Microsoft Excel file and later transferred to an SPSS data set (SPSS version 17.0; SPSS Inc, Chicago, Illinois).

Table II. Univariate Poisson regression model of the effect of peanut allergy and other factors/covariates on the hospitalization of pediatric patients with asthma in a sample from a large tertiary hospital
VariablesRR95% CIP∗
Peanut allergy
No1.0ReferenceReference
Yes2.881.86-4.47<.001
Race
Caucasian1.0ReferenceReference
African American2.361.47-3.81<.001
Others3.241.69-6.22<.001
Sex
Female1.0ReferenceReference
Male1.731.03-2.89.037
Family history of atopy
No1.0ReferenceReference
Yes2.550.35-18.32.353
Smokers at home
No1.0ReferenceReference
Yes2.011.29-3.13.002
Atopic dermatitis
No1.0ReferenceReference
Yes1.560.98-2.47.058
Gastroesophageal reflux
No1.0ReferenceReference
Yes1.791.16-2.78.009
Adenoidal hypertrophy
No1.0ReferenceReference
Yes0.470.26-0.83.01
Aspergillus sensitization
No1.0ReferenceReference
Yes2.931.86-4.62<.001
Alternaria sensitization
No1.0ReferenceReference
Yes1.430.91-2.23.12
Dust mite sensitization
No1.0ReferenceReference
Yes2.911.78-4.76<.001
Milk allergy
No1.0ReferenceReference
Yes0.920.53-1.62.780
Egg allergy
No1.0ReferenceReference
Yes1.530.97-2.41.064
Shellfish allergy
No1.0ReferenceReference
Yes3.412.09-5.58<.001
Grass sensitization
No1.0ReferenceReference
Yes1.571.01-2.44.043
Weed sensitization
No1.0ReferenceReference
Yes0.730.42-1.26.251
Tree sensitization
No1.0ReferenceReference
Yes2.021.31-3.15.002
Cat sensitization
No1.0ReferenceReference
Yes2.611.61-4.23<.001
Dog sensitization
No1.0ReferenceReference
Yes1.200.75-1.92.453
Age, months1.011.00-1.01.120

∗P <.05.

Response Variables 

The primary outcome for the study was the frequency of systemic steroid use for an asthma exacerbation, and the secondary outcome was the frequency of hospitalizations for an asthma exacerbation. Systemic steroids and hospital admissions for systemic food or other allergic reactions were excluded. All courses of systemic steroids and hospitalizations administered at our institution and at any other outside facility, including a primary care physician, between age 3 years to September 2008 were accounted for and documented in the medical record. Records from outside primary care offices and hospitals were scanned into our system documenting clinical findings, hospital admissions, and medications, including the use of systemic steroids.

Statistical Analysis 

Categorical variables were described using frequency and percentages, and continuous variables were summarized using mean and standard deviation. Pearson's χ2 test and the 2-sample t test were used to examine the balance of the distribution of peanut allergic pediatric patients with respect to the distribution of other covariates and 2 outcome variables of asthma morbidity. The associations between the outcome variables and the main predictor variable—peanut allergy—as well as other covariates were examined using univariate Poisson regression model. A multivariate Poisson regression model was used to adjust for the mixing effects of the potential confounding variables on the association between asthma morbidity (outcome variable) and peanut allergy. To enter into the multiple regression model, a variable must have been significant at P <.10. Due to their biological/clinical relevance, atopic dermatitis, gastroesophageal reflux, and adenoidal hypertrophy were used in the multivariate Poisson regression without consideration of their significance in the univariate model. An interaction effect was not tested for because of the small sample size. All analyses were 2-tailed at a .05 significance level. All analyses were performed using SPSS version 17.0 (SPSS Inc., Chicago, Illinois).

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Results 

A total of 160 patients met the inclusion criteria, 46 (28.75%) with asthma and peanut allergy and 114 (71.25%) with asthma but without peanut allergy. The patients ranged in age from 5 years to 18 years. Table I presents the distribution of covariates between the children with peanut allergy and those without peanut allergy. The 2 groups differed significantly (P <.05) in terms of mean chronologic age, mean age at onset of persistent asthma symptoms, and mean age at first presentation to the allergy practice. The 2 groups were similar in terms of sex and race distributions (P = .06 and .768, respectively). The cohort was predominately male (65%) and Caucasian (68.8%).

There were significant differences in the distribution of atopic features between the children with and without peanut allergy. Those with peanut allergy were more likely to have atopic dermatitis (P = .001) and to be sensitive to specific aeroallergens, including dust mite (P = .012), aspergillus (P = .032), grass (P = .013), weed (P = .001), and cat (P = .022). They also were more likely to have another food allergy, including milk (P = .011), egg (P <.001), and shellfish (P = .048). Differences between the 2 groups in the distributions of gastroesophageal reflux (P = .103), adenoidal hypertrophy (P = .099), and smoke exposure at home (P = .299) were not statistically significant (Table I).

Table II illustrates the association between the frequency of hospitalization and peanut allergy, as well as other covariates. There was a statistically significant association between the frequency of hospitalization and peanut allergy (risk ratio [RR] = 2.88; 95% confidence interval [CI] = 1.86-4.47). Race, sex, smoke exposure at home, gastroesophageal reflux, adenoidal hypertrophy, shellfish allergy, and sensitization to aspergillus, dust mite, grass, tree, and cat were significantly (P <.05) related to the frequency of hospitalization, but family history of atopy, age, milk allergy, and sensitization to alternaria, weed, and dog were not related (P >.05). Although not quite reaching the level of significance, atopic dermatitis (P = .058) and egg allergy (P = .064) also had a considerable association with the frequency of pediatric hospitalizations. Compared with Caucasian subjects, African-American subjects were 2.36-times more likely and Asian, Hispanic, and American Indian subjects were 3.24-times more likely to have an increased rate of hospitalization.

Table III illustrates the association between the frequency of systemic steroid use and peanut allergy, as well as other covariates. There was a statistically significant association between the frequency of systemic steroid use and peanut allergy (RR = 1.72; 95% CI = 1.41-2.10). Children with peanut allergy were 1.72-times more likely to require more courses of oral steroids compared with those without peanut allergy. African-American race; age; sex; smoke exposure at home; gastroesophageal reflux; sensitivity to aspergillus, dust mite, tree, grass, and cat; and allergy to egg and shellfish also were significantly (P <.05) related to the frequency of hospitalization, but family history of atopy, atopic dermatitis, adenoidal hypertrophy, milk allergy, and sensitization to alternaria, weed, and dog were not (P >.05). Compared with Caucasian subjects, African-American subjects were 2.21-times more likely to receive more courses of systemic steroids.

Table III. Univariate Poisson regression model of the effect of peanut allergy and other factors/covariates on the use of number of oral steroids of pediatric patients with asthma in a sample from a large tertiary hospital
VariablesRR95% CIP∗
Peanut allergy
No1.0ReferenceReference
Yes1.721.41-2.10<.001
Race
Caucasian1.0ReferenceReference
African American2.211.80-2.72<.001
Others1.420.96-2.10.76
Sex
Female1.0ReferenceReference
Male2.281.78-2.94<.001
Family history of atopy
No1.0ReferenceReference
Yes1.780.84-3.76.13
Smokers at home
No1.0ReferenceReference
Yes1.741.42-2.13<.001
Atopic dermatitis
No1.0ReferenceReference
Yes1.040.85-1.26.74
Gastroesophageal reflux
No1.0ReferenceReference
Yes1.551.27-1.89<.001
Adenoidal hypertrophy
No1.0ReferenceReference
Yes1.010.82-1.26.897
Aspergillus sensitization
No1.0ReferenceReference
Yes1.711.36-2.15<.001
Alternaria sensitization
No1.0ReferenceReference
Yes1.180.96-1.45.111
Dust mite sensitization
No1.0ReferenceReference
Yes1.441.18-1.75<.001
Milk allergy
No1.0ReferenceReference
Yes1.210.95-1.52.118
Egg allergy
No1.0ReferenceReference
Yes1.251.01-1.54.039
Shellfish allergy
No1.0ReferenceReference
Yes2.481.95-3.16<.001
Grass sensitization
No1.0ReferenceReference
Yes1.521.25-1.86<.001
Weed sensitization
No1.0ReferenceReference
Yes1.140.92-1.42.235
Tree sensitization
No1.0ReferenceReference
Yes1.501.22-1.84<.001
Cat sensitization
No1.0ReferenceReference
Yes1.531.25-1.87<.001
Dog sensitization
No1.0ReferenceReference
Yes1.080.87-1.34.503
Age, months1.0031.00-1.01.048

∗P <.05.

After adjusting for all other significant covariates, children with peanut allergy were 1.59 times more likely to have an increased rate of systemic steroid use for asthma beyond age 3 years (P <.001; 95% CI = 1.24-2.04). Other covariates significant in the regression included African-American race (P <.001), other minority (P = .015), male sex (P <.001), atopic dermatitis (P = .005), gastroesophageal reflux (P <.001), sensitization to aspergillus (P <.001), and shellfish allergy (P = .032). Smoke exposure at home, adenoidal hypertrophy, age, egg allergy, and sensitization to dust, grass, tree, and cat were not significant predictors (data available on request).

After adjusting for all other significant covariates, children with peanut allergy were 2.32-times more likely to have an increased hospitalization rate for asthma beyond age 3 years (P = .003; 95% CI = 1.33-4.05). Other significant factors in the regression included African-American race (P = .024), other minority (P <.001), male sex (P = .03), gastroesophageal reflux (P = .003), egg allergy (P = .029), shellfish allergy (P = .025), and sensitization to aspergillus (P <.001). Smoke exposure at home, atopic dermatitis, and sensitization to dust mite, grass, tree, and cat were not significant covariates (data available on request).

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Discussion 

Coexistent peanut allergy and asthma is a growing problem in school-age children, with the prevalence of both disorders on the rise. We found an association between peanut allergy and asthma morbidity after controlling for known risk factors for asthma morbidity.23, 24, 25 We chose the use of systemic steroids as our primary outcome because previous studies have accepted worsening asthma symptoms requiring the intervention of systemic steroids by a medical professional as a practical working definition for an asthma exacerbation.23 We accounted for many of the known risk factors associated with asthma morbidity, including sex; age; race; family history of atopy; exposure to smoke in the home; atopic dermatitis; gastroesophageal reflux; adenoidal hypertrophy; milk, egg, or shellfish allergy; and sensitization to grass, tree, cat, or aspergillus.23, 24, 25, 26 Children with peanut allergy were 2.32-times more likely to have an increased rate of hospitalization (P = .03) and 1.59 times more likely to require more courses of oral steroids (P <.001). Many of the young school-age children included in our study presented with peanut allergy before tree nut exposure.27, 28, 29, 30 We advised these high-risk children to avoid tree nuts, because peanut and tree nut allergies are highly coreactive (20%-50%).27, 28, 29, 30 We did not include tree nut allergy, because many of the subjects did not fulfill the strict clinical criteria for our study. Shellfish allergy also was associated with asthma morbidity, which may reflect the persistence of both peanut and shellfish allergies throughout school age and adolescence.

Previously known risk factors for asthma morbidity23, 24, 25, 26 also were associated with increased asthma and reflect the recent trends in racial disparities.31 Sensitization to aspergillus (P <.001 for both), gastroesophageal reflux (P = .003 and <.001, respectively), and African-American race (P <.001 and .015) were associated with increased hospitalization rate and increased systemic steroid use. Surprisingly, we did not find a significant association between asthma morbidity and the following variables: atopic dermatitis, egg allergy, and milk allergy. This may reflect the early anticipatory guidance given to these children.

The strengths of our study include the provision of treatment for persistent asthma according to NAEPP guidelines,15 good compliance and access to health care, and the strict inclusion criteria for food allergy and persistent asthma. All children with food allergy had a suggestive clinical history supported by an IgE level >95% PPV16, 17, 18 and a SPT 3 mm greater than negative control.19, 20, 21 This distinguishes our study from those that have examined only the relationship between food sensitivity and asthma morbidity. Although a double-blinded food challenge is the gold standard for diagnosing peanut allergy, this type of study would be unethical in such a high-risk patient population. All children with persistent asthma continued to wheeze and to need treatment with inhaled corticosteroids according to the NAEPP guidelines beyond age 5, which helps exclude children with bronchiolitis.

Our study has some limitations. The study's retrospective nature makes it susceptible to bias, including different thresholds for prescribing systemic steroids among primary care or emergency physicians. The study also excluded children who may have had peanut allergy but did not fulfill our strict inclusion criteria,16, 17, 18 and it did not include a significant number of adolescents. Thus, our findings may not apply to all children with peanut allergy presenting in the outpatient practice.

In conclusion, our findings suggest that peanut allergy may be a risk factor for increased asthma morbidity in school-age children. Early prevention and intervention can improve the quality of care. Instructing parents about tangible risk factors for an exacerbation may help improve compliance and reduce the need for oral steroids. Further studies are needed to validate our findings in large populations using prospective methods.

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Table I. 

Demographic and other study variable characterizations by group
VariablePeanut allergyNo peanut allergyTotalP value
Patients, n (%)46 (28.75)114 (71.25)160 (100)
Age, months
Mean (SD)111.33 (33.33)126.26 (37.3)121.97 (36.7).019
Median104.5124115
Minimum-maximum67-19459-22259-222
Mean age of first allergy visit, months40.2851.4148.21.018
Mean age of persistent asthma symptoms, months27.7841.6837.68.002
Sex .062
Male35 (76.1)69 (60.5)104 (65.0)
Female11 (23.9)45 (39.5)56 (35.0)
Race .768
Caucasian30 (65.2)80 (70.2)110 (68.8)
African American13 (28.3)26 (22.8)39 (24.4)
Other (Asian, Hispanic, Indian)3 (6.5)8 (7.0)11 (6.8)
Presence of atopic features
Atopic dermatitis <.001
Yes37 (80.4)50 (43.9)87 (54.4)
No9 (19.6)64 (56.1)73 (45.6)
Family history .149∗
Yes46 (100.0)109 (95.6)155 (96.9)
No0 (0.0)5 (4.4)5 (3.1)
Sensitization to aeroallergens
Dust mite .012
Yes29 (63.0)47 (41.2)76 (47.5)
No17 (37.0)67 (58.8)84 (52.5)
Aspergillus .032
Yes12 (26.1)14 (12.3)26 (16.3)
No34 (73.9)100 (87.7)134 (83.7)
Alternaria .104
Yes19 (41.3)32 (28.1)51 (31.9)
No27 (58.7)82 (71.9)109 (68.1)
Grass .013
Yes26 (56.5)40 (35.1)66 (41.2)
No20 (43.5)74 (64.9)94 (58.8)
Weed .001
Yes20 (43.5)20 (18.4)41 (25.6)
No26 (56.5)93 (81.6)119 (74.4)
Cat .022
Yes29 (63.0)49 (43.0)78 (48.8)
No17 (37.0)65 (57.0)82 (51.2)
Dog .597
Yes14 (30.4)30 (26.3)44 (27.5)
No32 (69.6)84 (73.7)116 (72.5)
Tree allergy <.001
Yes21 (45.7)25 (21.9)46 (28.8)
No25 (54.3)89 (78.1)114 (71.2)
Risk factors for asthma morbidity
Gastroesophageal reflux
Yes13 (28.3)48 (42.1)61 (38.1).103
No33 (71.7)66 (57.9)99 (61.9)
Adenoidal hypertrophy
Yes10 (21.7)40 (35.1)50 (31.2).099
No36 (78.3)74 (64.9)110 (68.8)
Smoke exposure at home
Yes15 (32.6)28 (24.6)43 (26.9).299
No31 (67.4)86 (75.4)117 (73.1)
Associated food allergies
Milk
Yes15 (32.6)17 (14.9)32 (20.0).011
No31 (67.4)97 (85.1)128 (80.0)
Egg
Yes26 (56.5)19 (16.7)45 (28.1)<.001
No20 (43.5)95 (83.3)115 (71.9)
Shellfish
Yes8 (17.4)8 (7.0)16 (10.0).048
No38 (82.6)106 (93.0)144 (90.0)

P values are generated from either the χ2 statistic or a 2-sample t test.

∗P value from Fisher's exact test.

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References 

  1. Moorman JE, Rudd RA, Johnson CA, King M, Minor P, Bailey C, et al. National surveillance for asthma—United States, 1980-2004. MMWR Surveill Summ. 2007;56:1–54
  2. Bloom B, Dey AN, Freeman G. Summary health statistics for US children: National Health Interview Survey, 2005. Vital Health Stat. 2006;231:1–84
  3. National Center for Health Statistics, Office of Analysis and Epidemiology. Asthma prevalence, health care use and mortality, United States, 2003–05. Available from: http://www.cdc.gov/nchs/products/pubs/pubd/hestats/ashtma03-05/asthma03-05.html. Accessed September 10, 2008.
  4. Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med. 1992;327:380–384
  5. Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007;119:1016–1018
  6. Bock SA, Muñoz -Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. 2001;107:191–193
  7. Roberts G, Lack G. Food allergy and asthma—what is the link?. Paediatr Respir Rev. 2003;4:205–212
  8. Oehling A, Baena Cagnani CE. Food allergy and child asthma. Allergol Immunopathol (Madr). 1980;8:7–14
  9. Wang J, Visness CM, Sampson HA. Food allergen sensitization in inner-city children with asthma. J Allergy Clin Immunol. 2005;115:1076–1080
  10. Roberts G, Patel N, Levi-Schaffer F, Habibi P, Lack G. Food allergy as a risk factor for life-threatening asthma in childhood: a case-controlled study. J Allergy Clin Immunol. 2003;112:168–174
  11. Simpson AB, Yousef EJ, Glutting J. Food allergy and asthma morbidity in children. Pediatr Pulmonol. 2007;42:489–495
  12. Skolnick HS, Conover-Walker MK, Koerner CB, Sampson HA, Burks W, Wood RA. The natural history of peanut allergy. J Allergy Clin Immunol. 2001;107:367–374
  13. Hourihane JO, Roberts SA, Warner JO. Resolution of peanut allergy: case-control study. BMJ. 1998;316:1271–1275
  14. Fleischer DM, Conover-Walker MK, Christie L, Burks AW, Wood RA. The natural progression of peanut allergy: resolution and the possibility of recurrence. J Allergy Clin Immunol. 2003;112:183–189
  15. National Asthma Education and Prevention Program Coordinating Committee, US Department of Health and Human Services. National Asthma Education and Prevention Program Expert Panel Report 3. Guidelines for the Diagnosis and Management of Asthma: Full Report 2007. Bethesda, MD: National Institutes of Health; 1997;p. 20-100
  16. Sampson HA. Update on food allergy. J Allergy Clin Immunol. 2004;113:805–819
  17. Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol. 2001;107:891–896
  18. Sampson HA, Ho DG. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol. 1997;100:444–451
  19. Knight AK, Shreffler WG, Sampson HA, Sicherer SH, Noone S, Mofidi S, et al. Skin prick test to egg white provides additional diagnostic utility to serum egg white-specific IgE antibody concentration in children. J Allergy Clin Immunol. 2006;117:842–847
  20. Sporik R, Hill DJ, Hosking CS. Specificity of allergen skin testing in predicting positive open food challenges to milk, egg and peanut in children. Clin Exp Allergy. 2000;30:1540–1546
  21. Roberts G, Lack G. Diagnosing peanut allergy with skin prick and specific IgE testing. J Allergy Clin Immunol. 2005;115:1291–1296
  22. Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol (Stockh). 1980;114(Suppl 92):44–47
  23. Sears MR. Epidemiology of asthma exacerbations. J Allergy Clin Immunol. 2008;122:662–668
  24. Chen Y, Stewart P, Johansen H, McRae L, Taylor G. Sex differences in hospitalization due to asthma in relation to age. J Clin Epidemiol. 2003;56:180–187
  25. ten Brinke A, Sterk PJ, Masclee AAM, Spinhoven P, Schmidt JT, Zwinderman AH, et al. Risk factors of frequent exacerbations in difficult-to-treat asthma. Eur Respir J. 2005;26:812–818
  26. Murray CS, Poletti G, Kebadze T, Morris J, Woodcock A, Johnston SL, et al. Study of modifiable risk factors for asthma exacerbations: virus infection and allergen exposure increase the risk of hospital admissions in children. Thorax. 2006;61:376–382
  27. 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. 2003;112:1203–1207
  28. Skripak JM, Wood RA. Peanut and tree nut allergy in childhood. Pediatr Allergy Immunol. 2008;19:368–373
  29. Clark AT, Ewan PW. The development and progression of allergy to multiple nuts at different ages. Pediatr Allergy Immunol. 2005;16:507–511
  30. de Leon MP, Drew AC, Glaspole IN, Suphioglu C, O'Hehir RE, Rolland JM. IgE cross-reactivity between the major peanut allergen ara h 2 and tree nut allergens. Mol Immunol. 2007;44:463–471
  31. Ginde AA, Espinola JA, Camargo CA. Improved overall trends but persistent racial disparities in emergency department visits for acute asthma, 1993–2005. J Allergy Clin Immunol. 2008;122:313–318

 The authors declare no conflicts of interest.

PII: S0022-3476(09)01215-3

doi:10.1016/j.jpeds.2009.11.080

The Journal of Pediatrics
Volume 156, Issue 5 , Pages 777-781.e1, May 2010

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