Peanut gallery delights peanut-sized patients in Houston.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Conventional management of peanut-induced anaphylaxis is composed of administration of epinephrine, antihistamine, and steroid and stabilization of airway, ventilatory, and circulatory function. Therapies directed toward slowing or preventing further absorption of peanut protein from the gastrointestinal tract after accidental ingestion have not been a routine part of management. OBJECTIVE: The purpose of this study was to determine the ability of activated charcoal to complex with peanut protein, thereby preventing its binding to either peanut-specific IgE or peanut-specific IgG. METHODS: Peanut protein was coincubated with micronized activated charcoal suspension at pH 3.5 or 7.4. Peanut protein complexed with charcoal was removed by centrifugation. Binding of residual peanut protein to peanut-specific IgG was measured by a sandwich ELISA assay. Also, ability of uncomplexed peanut protein to bind to peanut-specific IgE was determined by Western blot and by skin prick testing in subjects with peanut allergy. RESULTS: Activated charcoal (AC) formed complexes with peanut protein, effectively competing for binding with peanut-specific IgG in a sandwich ELISA assay. AC complexed efficiently with peanut protein at both neutral and acidic pH in as little as 60 seconds. AC was also able to remove IgE-binding peanut allergens from solution as determined by Western blot and by skin prick testing in subjects with peanut allergy. A ratio of 200 mg of AC to 1 mg peanut protein was required for complete removal of peanut protein from solution. AC was able to complex with peanut protein within food matrices such as ice cream and chocolate. CONCLUSION: The data presented herein show that AC removes both IgE-binding and IgG-binding peanut proteins from solution rapidly at both neutral and acidic pH. These data suggest that administration of AC may be useful as an adjunct to slow or to prevent further absorption of peanut protein from the gastrointestinal tract after accidental ingestion by individuals with peanut allergy.
BACKGROUND: Peanut and tree nuts are a major cause of food-induced anaphylaxis with an appreciable mortality. Co-sensitization to peanuts and tree nuts is a common clinical observation and may be because of peanut-specific serum IgE antibodies that cross-react with tree nut allergens. It is, however, unclear whether these cross-reactive IgE antibodies are involved in effector-cell activation. OBJECTIVE: To determine if cross-reactivity of peanut-specific IgE antibodies with tree nuts can cause effector cell activation using an in vitro basophil activation assay. METHODS: Two peanut allergic subjects with positive specific IgE for peanut and tree nuts (as measured by CAP-FEIA) were studied. Basophil activation to peanut and tree nuts, as indicated by CD63 expression, was assessed by flow cytometry to confirm co-sensitization to peanut and tree nuts. Inhibition ELISA using sera from the subjects was performed to detect peanut-specific IgE antibodies that cross-reacted with tree nut proteins. To determine whether cross-reactive tree nut allergens can induce effector-cell activation, peanut-specific antibodies were affinity purified from the subject sera and used to resensitize non-peanut/tree nut allergic donor basophils stripped of surface IgE. Basophil activation was then measured following stimulation with peanut and tree nut extracts. RESULTS: The two peanut allergic subjects in this study showed positive basophil activation to the peanut and tree nut extracts. Inhibition ELISA demonstrated that pre-incubation of the peanut allergic subject sera with almond, Brazil nut and hazelnut extracts inhibited IgE binding to peanut extract. IgE-stripped basophils from non-peanut/tree nut allergic subjects resensitized with affinity-purified peanut-specific antibodies from the peanut allergic subject sera became activated following stimulation with peanut, almond and Brazil nut extracts, demonstrating biological activity of cross-reactive IgE antibodies. CONCLUSION: Peanut-specific IgE antibodies that cross-react with tree nut allergens can cause effector-cell activation and may contribute to the manifestation of tree nut allergy in peanut allergic subjects.
Peanuts are one of the most common and severe food allergens. Nevertheless, the occurrence of peanut allergy varies between countries and depends on both the exposure and the way peanuts are consumed. Processing is known to influence the allergenicity of peanut proteins. The aim of this study was to assess the effect of thermal processing on the IgE-binding capacity of whole peanut protein extracts and of the major peanut allergens Ara h 1 and Ara h 2. Whole proteins, Ara h 1, and Ara h 2 were extracted and purified from raw, roasted and boiled peanuts using selective precipitation and multiple chromatographic steps, and were then characterized by electrophoresis and mass spectrometry. The immunoreactivity of whole peanut extracts and purified proteins was analyzed by the enzyme allergosorbent test (EAST) and EAST inhibition using the sera of 37 peanut-allergic patients. The composition of the whole protein extracts was modified after heat processing, especially after boiling. The electrophoretic pattern showed protein bands of low molecular weight that were less marked in boiled than in raw and roasted peanuts. The same low-molecular-weight proteins were found in the cooking water of peanuts. Whole peanut protein extracts obtained after the different processes were all recognized by the IgE of the 37 patients. The IgE-binding capacity of the whole peanut protein extracts prepared from boiled peanuts was 2-fold lower than that of the extracts prepared from raw and roasted peanuts. No significant difference was observed between protein extracts from raw and roasted peanuts. It is noteworthy that the proteins present in the cooking water were also recognized by the IgE of peanut-allergic patients. IgE immunoreactivity of purified Ara h 1 and Ara h 2 prepared from roasted peanuts was higher than that of their counterparts prepared from raw and boiled peanuts. The IgE-binding capacity of purified Ara h 1 and Ara h 2 was altered by heat treatment and in particular was increased by roasting. However, no significant difference in IgE immunoreactivity was observed between whole protein extracts from raw and roasted peanuts. The decrease in allergenicity of boiled peanuts results mainly from a transfer of low-molecular-weight allergens into the water during cooking.
BACKGROUND: Peanuts are a common cause of food-induced anaphylaxis and fatalities. Previous studies have demonstrated that rush immunotherapy to crude peanut extract reduces clinical symptoms triggered by oral peanut challenges, but the immunotherapy was associated with an unacceptably high incidence of systemic allergic reactions. One approach to reduce the frequency of allergic reactions would be to use a modified peanut antigen with low allergenic properties. OBJECTIVE: We sought to determine the immunologic characteristics of crude intact peanut extract before and after pepsin digestion. METHODS: We used IgE immunoblotting and assessment of T-lymphocyte responses to intact and peptic digests of peanut extracts. RESULTS: Western blot analysis of sera from 5 subjects with peanut allergy showed multiple IgE-reactive proteins in crude intact peanut extract that were eliminated after pepsin treatment of the peanut extract. In contrast, pepsin-digested peanut induced significant T-cell proliferation responses (stimulation index = 30) in vitro in PBMCs from 7 subjects with peanut allergy, albeit at lower levels than that induced by intact peanut (stimulation index = 66). Furthermore, IFN-gamma production was induced by intact peanut and pepsin-digested peanut in a concentration-dependent manner. Importantly, T-cell lines generated in response to intact peanut also reacted to pepsin-digested peanut, indicating cross-reactive T-cell epitopes in intact and pepsin-digested peanut. CONCLUSION: These findings suggest that pepsin-digested peanut may be useful in peanut immunotherapy because pepsin digestion eliminates IgE reactivity but maintains T-cell reactivity.
BACKGROUND: Peanut allergy creates great fear in many families because it is one of the leading causes of fatal and near-fatal food-induced allergies. Earlier reports suggested that peanut allergy was life-long, but a recent study described resolution of peanut allergy in some children. OBJECTIVE: Tolerance to peanut allergy in childhood was studied. Examination of the natural history of childhood peanut allergy was explored. METHODS: A retrospective review of all children with peanut allergy seen at the Children's Hospital of Philadelphia in a 3-year period (n = 293). Children with histories of peanut allergy were challenged at the mean age [3.8 years; range 1.5 to 8 year] which was 1.8 years [range: 0.5 to 6.8 years], following their last known clinical reaction. Food allergy or tolerance was confirmed by open challenges. RESULTS: Thirty-three patients with histories of peanut allergy and a positive skin test to peanut underwent oral challenges. Not one patient (n = 5) with a history of peanut anaphylaxis developed tolerance to peanuts. In comparison, 9 of 17 patients with history of urticaria upon ingestion to peanuts developed tolerance. Also, 4 of 10 patients with flaring of their atopic dermatitis upon ingestion to peanuts developed tolerance. The 14 patients with a negative challenge to peanut had a significantly smaller wheal and flare reaction than the 19 patients with positive challenges. Tolerance to peanut was documented by a positive challenge reverting to a negative challenge in one patient. Oral challenge of 13 additional patients with positive skin tests and histories of only refusing to eat peanut resulted in 5 (39%) positive challenges. CONCLUSION: A selected group of peanut-allergic children, who do not have a history anaphylaxis to peanut, may develop tolerance to peanuts.
OBJECTIVES: To determine rates of other atopic manifestations in people with peanut allergy and the prevalence of such allergy in their families. DESIGN: A survey of people with self reported peanut allergy and people referred by their general practitioner for suspected peanut allergy; survey and skin testing of 50 children with reported peanut allergy and their available first degree relatives. SUBJECTS: 622 adults and children with reported, suspected, or known peanut allergy. MAIN OUTCOME MEASURES: Prevalence of peanut allergy and other allergies in the families of people with peanut allergy. RESULTS: 622 valid completed questionnaires were returned out of the 833 questionnaires dispatched (74.7%). All forms of atopy were both more common in successive generations (P < 0.0001) and more common in maternal than paternal relatives (P < 0.0001). Peanut allergy was reported by 0.1% (3/2409) of grandparents, 0.6% (7/1213) of aunts and uncles, 1.6% (19/1218) of parents, and 6.9% (42/610) of siblings. Consumption of peanuts while pregnant or breast feeding was more common among mothers of probands aged < or = 5 years than mothers of probands aged > 5 years (P < 0.001). Age of onset correlated inversely with year of birth (r = -0.6, P < 0.001). Skin prick testing of 50 children with reported peanut allergy and their families: 7 probands (14%) had a negative result for peanut. Peanut allergy was refuted by food challenge in all those tested (5/7). No parent and 13% (5/39) of siblings had a positive result on skin prick testing for peanut. Two of these siblings had negative challenge with peanuts. The prevalence of peanut allergy in siblings is therefore 3/39 (7%). CONCLUSIONS: Peanut allergy is more common in siblings of people with peanut allergy than in the parents or the general population. Its apparently increasing prevalence may reflect a general increase of atopy, which is inherited more commonly from the mother. Peanut allergy is presenting earlier in life, possibly reflecting increased consumption of peanut by pregnant and nursing mothers.
BACKGROUND: Although peanut allergy may recur, the frequency with which this occurs is unknown. OBJECTIVE: The goals of this study were to determine the rate of peanut allergy recurrence, identify risk factors for recurrent peanut allergy, and develop specific recommendations for the treatment of patients with resolved peanut allergy. METHODS: Children who outgrew peanut allergy were evaluated with questionnaires, skin tests, and peanut-specific IgE levels. Patients were invited to undergo a double-blind, placebo-controlled food challenge (DBPCFC) unless the history of a possible recurrence reaction was so convincing that a challenge would be potentially dangerous. RESULTS: Sixty-eight patients were evaluated. Forty-seven patients continued to tolerate peanut, of whom 34 ingested concentrated peanut products at least once per month and 13 ate peanut infrequently or in limited amounts but passed a DBPCFC. The status of 18 patients was indeterminate because they ate peanut infrequently or in limited amounts and declined to have a DBPCFC. After excluding 12 patients originally diagnosed with peanut allergy based solely on a positive skin prick test or peanut-specific IgE level, 3 of 15 patients who consumed peanut infrequently or in limited amounts had recurrences, compared with no recurrences in the 23 patients who ate peanut frequently ( P = .025). The recurrence rate was 7.9 (95% CI, 1.7% to 21.4%). CONCLUSION: Children who outgrow peanut allergy are at risk for recurrence, and this risk is significantly higher for patients who continue largely to avoid peanut after resolution of their allergy. On the basis of these findings, we now recommend that patients eat peanut frequently and carry epinephrine indefinitely until they have demonstrated ongoing peanut tolerance.
BACKGROUND: It was once thought that peanut allergy is a lifelong problem. We previously reported that about 20% of children outgrow their peanut allergy and that more than 60% of patients with a peanut-IgE level of 5 or less passed an oral challenge. OBJECTIVE: The goal of this study was to further describe the natural progression of peanut allergy by reviewing patients who have undergone oral peanut challenges since the previous study. METHODS: Patients with peanut-IgE levels of 5 or less were offered a peanut challenge. Those who passed were further evaluated by questionnaire to assess reintroduction of peanut into their diet and whether any recurrence has occurred. RESULTS: Eighty-four patients were evaluated, and 80 underwent complete analysis. Fifty-five percent with peanut-IgE levels of 5 or less and 63% with peanut-IgE levels of 2 or less passed challenges, compared to 61% and 67%, respectively, in our previous study. The 4 additional patients passed peanut challenges in this study after previously failing. Three patients with initial anaphylactic reactions and 2 patients with initial peanut-IgE levels greater than 70 passed their challenge. Follow-up of those who passed in both studies showed that the majority of patients reintroduced peanut into their diet, but that continued label reading, infrequent/limited ingestion, and aversion to peanut were all common in this population. Two patients had suspected subsequent reactions to peanut after passing their challenge. CONCLUSIONS: Patients with a history of peanut allergy and peanut-IgE levels of 5 or less have at least a 50% chance of outgrowing their allergy. Recurrence of peanut allergy may occur but appears to be uncommon.