Showing papers by "Scott H. Sicherer published in 2003"
TL;DR: For example, this paper found that the prevalence of self-reported peanut and tree-nut allergy increased from 0.4% in 1997 to 0.8% in 2002 by a factor of 1.04% (95% CI, 0.9-1.24%).
Abstract: Background Allergy to peanuts and tree nuts (TNs) is the leading cause of fatal and near-fatal food allergic reactions. Peanut allergy appears to be increasing in prevalence. Objectives We sought to determine the prevalence of self-reported peanut and TN allergy among the general population of the United States in 2002 by sex and age and to compare the results with prevalence estimates obtained 5 years earlier. Methods We performed a nationwide, cross-sectional, random telephone survey by using a standardized questionnaire. Results A total of 4855 households participated (53% participation rate), representing a census of 13,493 individuals. Peanut allergy, TN allergy, or both was self-reported in 166 (1.2%; 95% CI, 1.0%-1.4%) individuals in 155 (3.2%; 95% CI, 2.7%-3.7%) households, overall prevalence rates similar to those reported in 1997. Also similar to the 1997 survey, the severity level was high, with 79% reporting respiratory or multiple organ system reactions and 66% experiencing more than 5 lifetime reactions. Despite the severity and reaction frequency, only 74% of the children and 44% of the adults sought evaluation for the allergy, and fewer than half who did were prescribed self-injectable epinephrine. Applying conservative rules to adjust for persons with unconvincing reactions and a false-positive rate of the survey instrument (7%), a final prevalence estimate of 1.04% (95% CI, 0.9%-1.24%) was obtained. A male predominance of peanut-TN allergy was reported in children younger than 18 years (1.7% vs 0.7%, P = .02), and a female predominance was reported among adults (1.7% vs 0.9%, P = .0008). Although the rate of peanut allergy, TN allergy, or both was not significantly different from 1997 to 2002 among adults, the rate increased from 0.6% to 1.2% among children, primarily as a result of an increase in reported allergy to peanut (0.4% in 1997 to 0.8% in 2002, P = .05). Conclusions Self-reported peanut allergy has doubled among children from 1997 to 2002, and peanut allergies, TN allergies, or both continue to be reported by more than 3 million Americans. Considering that reactions are severe and the allergy is persistent, these allergies represent an increasing health concern.
729 citations
TL;DR: Cereals, vegetables, and poultry meats, typically regarded as of low allergenic potential, must be considered in the evaluation of FPIES, particularly in infants previously diagnosed with FPIES to cow's milk or soy, and as an initial cause in patients who have been exclusively breastfed.
Abstract: Background. Infantile food protein-induced enterocolitis syndrome (FPIES) is a severe, cell-mediated gastrointestinal food hypersensitivity typically provoked by cow’s milk or soy. Solid foods are rarely considered a cause. Objective. To describe the clinical characteristics and natural history of FPIES provoked by solid foods. Methods. Patients with FPIES induced by solid foods were identified and their clinical course compared with a control group with FPIES caused by cow’s milk and/or soy evaluated over the same time period. Results. Fourteen infants with FPIES caused by grains (rice, oat, and barley), vegetables (sweet potato, squash, string beans, peas), or poultry (chicken and turkey) were identified. Symptoms were typical of classical FPIES with delayed (median: 2 hours) onset of vomiting, diarrhea, and lethargy/dehydration. Eleven infants (78%) reacted to >1 food protein, including 7 (50%) that reacted to >1 grain. Nine (64%) of all patients with solid food–FPIES also had cow’s milk and/or soy-FPIES. Initial presentation was severe in 79% of the patients, prompting sepsis evaluations (57%) and hospitalization (64%) for dehydration or shock. The diagnosis of FPIES was delayed, after a median of 2 reactions (range: 2–5). Thirty patients with typical cow’s milk- and/or soy-FPIES were identified for comparison. Overall, 48% of the 44 infants with FPIES were reactive to >1 food protein, and the risk for multiple food hypersensitivity approached 80% in the infants with solid food or soy-induced FPIES. None of the patients developed FPIES to maternally ingested foods while breastfeeding unless the causal food was fed directly to the infant. Conclusions. Cereals, vegetables, and poultry meats, typically regarded as of low allergenic potential, must be considered in the evaluation of FPIES, particularly in infants previously diagnosed with FPIES to cow’s milk or soy, and as an initial cause in patients who have been exclusively breastfed. Infants with FPIES are at risk for multiple dietary protein hypersensitivities during an apparent period of immunologic susceptibility. Pediatricians should consider FPIES in the differential diagnosis of shock and sepsis.
312 citations
TL;DR: This review catalogs the spectrum of gastrointestinal food allergies that affect children and provides a framework for a rational approach to diagnosis and management.
Abstract: Gastrointestinal food allergies are a spectrum of disorders that result from adverse immune responses to dietary antigens. The named disorders include immediate gastrointestinal hypersensitivity (anaphylaxis), oral allergy syndrome, allergic eosinophilic esophagitis, gastritis, and gastroenterocolitis; dietary protein enterocolitis, proctitis, and enteropathy; and celiac disease. Additional disorders sometimes attributed to food allergy include colic, gastroesophageal reflux, and constipation. The pediatrician faces several challenges in dealing with these disorders because diagnosis requires differentiating allergic disorders from many other causes of similar symptoms, and therapy requires identification of causal foods, application of therapeutic diets and/or medications, and monitoring for resolution of these disorders. This review catalogs the spectrum of gastrointestinal food allergies that affect children and provides a framework for a rational approach to diagnosis and management.
187 citations
TL;DR: Allergists' estimates of the prevalence of OAS in patients with pollen allergy are lower than the prevalence reported in the published studies of these patients, perhaps reflecting a low index of suspicion, underdiagnosis, or both.
Abstract: Background There is no consensus on the diagnosis and therapy of oral allergy syndrome (OAS; also known as pollen-food allergy syndrome), a disorder caused by IgE antibody-mediated reactions to homologous proteins in pollens and fruits and vegetables. Objective We sought to determine how practicing allergists define and treat OAS. Methods A questionnaire was mailed to 226 randomly selected US allergists from the American Academy of Allergy, Asthma and Immunology directory. Results One hundred twenty-two (54%) returned surveys were analyzed. Median estimates of the prevalence of OAS among the patients with pollen allergy were 5% among children and 8% among adults. Twenty percent of allergists reported that some patients progressed to systemic symptoms. Fifty-three percent of allergists recommended complete avoidance of causal foods to all patients, whereas 9% did not advocate any restrictions. Thirty percent never prescribed epinephrine for OAS, 3% always did, and the remainder did so on the basis of symptoms. When presented with clinical cases, 20% diagnosed systemic reactions to peach as OAS, 13% believed peanut could cause OAS, and 25% did not prescribe epinephrine for peanut allergy manifested by oral symptoms. Conclusion Allergists' estimates of the prevalence of OAS in patients with pollen allergy (5%-8%) are lower than the prevalence reported (approximately 50%) in the published studies of these patients, perhaps reflecting a low index of suspicion, underdiagnosis, or both. The wide range of responses regarding diagnosis and management indicates the need for a better definition for the disorder and standard therapeutic guidelines. Discrepancies might be related to the term OAS, and therefore use of the more specific term "pollen-food allergy syndrome" is suggested.
167 citations
TL;DR: It can be stated with 96% confidence that at least 90% of highly sensitive children with peanut allergy would not experience a systemic-respiratory reaction from casual exposure to peanut butter.
Abstract: Background: Casual skin contact or inhalation of peanut butter fumes is reported and feared to cause allergic reactions in highly sensitive children with peanut allergy but has not been systematically studied. Objective: We sought to determine the clinical relevance of exposure to peanut butter by means of inhalation and skin contact in children with peanut allergy. Methods: Children with significant peanut allergy (recent peanut-specific IgE antibody concentration >50 kIU/L or evidence of peanut-specific IgE antibody and one of the following: clinical anaphylaxis, a reported inhalation-contact reaction, or positive double-blind, placebo-controlled oral challenge result to peanut) underwent double-blind, placebo-controlled, randomized exposures to peanut butter by means of contact with intact skin (0.2 mL pressed flat for 1 minute) and inhalation (surface area of 6.3 square inches 12 inches from the face for 10 minutes). Placebo challenges were performed by using soy butter mixed with histamine (contact), and scent was masked with soy butter, tuna, and mint (inhalation). Results: Thirty children underwent the challenges (median age, 7.7 years; median peanut IgE level, >100 kIU/L; 13 with prior history of contact and 11 with inhalation reactions). None experienced a systemic or respiratory reaction. Erythema (3 subjects), pruritus without erythema (5 subjects), and wheal-and-flare reactions (2 subjects) developed only at the site of skin contact with peanut butter. From this number of participants, it can be stated with 96% confidence that at least 90% of highly sensitive children with peanut allergy would not experience a systemic-respiratory reaction from casual exposure to peanut butter. Conclusions: Casual exposure to peanut butter is unlikely to elicit significant allergic reactions. The results cannot be generalized to larger exposures or to contact with peanut in other forms (flour and roasted peanuts). (J Allergy Clin Immunol 2003;112:180-2.)
137 citations
TL;DR: Overall, the typical allergens of infancy and early childhood are egg, milk, peanut, wheat, and soy, whereas allergens that are responsible for severe reactions in older children and adults are primarily caused by peanut, tree nuts, and seafood.
Abstract: Food allergy seems to be increasing in prevalence, 1 significantly decreases the quality of life for patients and their families, 2 and has become a common diagnostic and management issue for the pediatrician. 3 Studies now a decade old showed that 6% to 8% of children younger than 3 years experience documented adverse reactions to foods. Several studies have defined the prevalence of allergy to specific foods in childhood. Population-based studies document a prevalence of cow milk allergy in 1.9% to 3.2% of infants and young children, 4 egg allergy 5–7 in 2.6% of children by age 2.5 years, 8 and peanut allergy in 0.4% to 0.6% of those younger than 18 years. 9,10 Overall, the typical allergens of infancy and early childhood are egg, milk, peanut, wheat, and soy, whereas allergens that are responsible for severe reactions in older children and adults are primarily caused by peanut, tree nuts, and seafood. Allergy to fruits and vegetables are prominent but usually not severe. 11–13 For diagnostic purposes, it is instructive to consider the prevalence of food allergy as a cause of specific disorders. For example, food allergy accounts for 20% of acute urticaria, 14,15 is present in 37% of children with moderate to severe atopic dermatitis 16,17 and approximately 5% with atopic asthma, 18 and is the most frequent cause of anaphylaxis outside the hospital setting. 19–22
50 citations
49 citations
TL;DR: To determine if physician-administered physical examination and screening questionnaire accurately detects exercise-induced bronchoconstriction in adolescent athletes, adolescents participating in organized sports from 3 suburban high schools are examined.
Abstract: Hallstrand TS, Curtis JR, Koepsell TD, et al. J Pediatr. 2002;141:343–349
To determine if physician-administered physical examination and screening questionnaire accurately detects exercise-induced bronchoconstriction (EIB) in adolescent athletes.
Two hundred fifty-six adolescents participating in organized sports from 3 suburban high schools.
The number screened positive from the examination and questionnaire was compared with EIB diagnosed by the …
39 citations
TL;DR: These studies reviewed the clinical features of patients with hyper-IgE syndrome and report clinical features that could lead to earlier diagnosis.
Abstract: Conley ME, Howard V. J Pediatr. 2002;141:566–571
Hyper-immunoglobulin E (HIE) syndrome is an immunodeficiency disorder characterized by recurrent skin abcesses, pneumonia, elevated serum IgE, and increased incidence of dental abnormalities (retained primary teeth), bone fractures and scoliosis. X-linked agammaglobulinemia (XLA) attributable to a mutation in the gene for Bruton’s tyrosine kinase (BTK) typically results in recurrent bacterial infections in the first few years of life. These studies reviewed the clinical features of patients with these diagnoses and report clinical features that could lead to earlier diagnosis.
Eight children with hyper-IgE syndrome were …
24 citations
TL;DR: This review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insect venom that were reported primarily in this Journal from 2001 to 2002.
Abstract: This review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insect venom that were reported primarily in this Journal from 2001 to 2002. Among the topics highlighted: Epinephrine injected intramuscularly into the thigh provides the most efficient absorption profile for adults and children; determination of serum IgE antibody-specific food allergen concentrations and atopy patch tests with foods show promise for enhanced diagnostic accuracy; numerous food allergens are now characterized on the molecular level, allowing for improved diagnostic and treatment modalities; the complex immunologic mechanisms underlying drug hypersensitivity reactions are being elucidated; venom immunotherapy improves quality of life for sufferers, and increased venom immunotherapy doses are useful in recalcitrant cases.
20 citations
TL;DR: The atopy patch test (APT), in which foods are applied to the skin under Finn chambers in a manner similar to that used with classic contact allergens in patch testing, has been investigated to address limitations, but this methodology is also limited by relatively low positive predictive accuracy.
Abstract: The most definitive tool to diagnose food allergy is the double-blind, placebo-controlled oral food challenge [1,2]. This methodology is labor-intensive, time-consuming and, like any test in medicine, even this ‘gold standard’ is subject to false positive (51%) and false negative (*3%) results [3]. Of course, the history and physical examination are key to an accurate diagnosis, but the correlation of food allergies suspected by history, with the results of double-blind, placebo-controlled oral food challenges is notoriously poor (*30–40%) [4–6]. Currently available laboratory tests include the prick skin test (PST) and serum tests for concentrations of food-specific IgE antibody. Unfortunately, the presence of food-specific IgE antibody does not necessarily indicate that an allergic reaction would occur upon ingestion of the tested food. Furthermore, a number of food allergic disorders, particularly those solely involving the gastrointestinal tract, are not associated with detectable IgE antibodies. The atopy patch test (APT), in which foods are applied to the skin under Finn chambers in a manner similar to that used with classic contact allergens in patch testing, has been investigated to address these limitations. However, this methodology is also limited by relatively low positive predictive accuracy (40–63%) [7–9]. Each diagnostic method has significant limitations.
Journal Article•
TL;DR: Improved gene therapy techniques are used to correct adenoside deaminase (ADA)-deficient severe combined immunodeficiency (SCID) in patients who lacked an HLA-identical sibling donor and for whom polyethylene glycol conjugated (PEG)-ADA was unavailable.
Abstract: Aiuti A, Slavin S, Aker M, et al. Science. 2002;296:2410–2413
To use improved gene therapy techniques to correct adenoside deaminase (ADA)-deficient severe combined immunodeficiency (SCID).
Two patients (7 months old and 2.5 years) with ADA-SCID who lacked an HLA-identical sibling donor and for whom polyethylene glycol conjugated (PEG)-ADA was unavailable.
Patients underwent collection of autologous CD34+ cells (stem cells) from bone marrow that were …