Peanut allergy.
Peanut allergies have become a major health concern in the United States. Peanuts are one of the most common causes of food allergies and along with tree nuts they account for most of the cases of fatal and near-fatal anaphylactic reactions to food. Not only is there a rise in the prevalence of peanut allergies in Westernized countries but also most patients with peanut allergies have lifelong clinical sensitivities to peanuts. Patient management involves strict avoidance; recognition of the early symptoms of anaphylaxis; and usage of an emergency treatment plan; including the self-administration of epinephrine in case of an accidental ingestion. Future treatment strategies may include recombinant peanut protein immunotherapy and anti-Immunoglobulin E therapy to modulate clinical reactivity to peanuts. This article reviews the current understanding of the clinical characteristics; pathogenesis; diagnosis; and management of the peanut allergy.
Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts
BACKGROUND: Allergy to peanut is common. However; it is not known whether the prevalence of sensitization and clinical allergy to peanut is increasing. OBJECTIVE: We sought to determine any change in the prevalence of peanut sensitization and reactivity in early childhood in 2 sequential cohorts in the same geographic area 6 years apart. METHODS: Of 2878 children born between September 1; 1994; and August 31; 1996; living on the Isle of Wight; 1273 completed questionnaires; and 1246 had skin prick tests at the age of 3 to 4 years. Those with positive skin prick test responses to peanut were subjected to oral peanut challenges; unless there was a history of immediate systemic reaction. These data were compared with information on sensitization and clinical allergy to peanut available from a previous cohort born in 1989 in the same geographic area. RESULTS: There was a 2-fold increase in reported peanut allergy (0.5 % [6/1218] to 1.0 % [13/1273]); but the difference was nonsignificant (P =.2). Peanut sensitization increased 3-fold; with 41 (3.3 %) of 1246 children sensitized in 1994 to 1996 compared with 11 (1.1 %) of 981 sensitized 6 years ago (P =.001). Of 41 sensitized children in the current study; 10 reported a convincing clinical reaction to peanut; and 8 had positive oral challenge results; giving an overall estimate of peanut allergy of 1.5% (18/1246). CONCLUSIONS: Sensitization to peanut had increased between 1989 and 1994 to 1996. There was a strong but statistically nonsignificant trend for increase in reported peanut allergy.
Purification; crystallization and initial crystallographic characterization of brazil-nut allergen Ber e 2. Acta Crystallogr Sect F Struct Biol Cryst Commun
Peanut and tree-nut allergies have attracted considerable attention because of their frequency and their lifelong persistence. Brazil-nut (Bertholletia excelsa) allergies have been well documented and the 11S legumin-like seed storage protein Ber e 2 (excelsin) is one of the two known brazil-nut allergens. In this study; Ber e 2 was extracted from brazil-nut kernels and purified to high purity by crystalline precipitation and gel-filtration chromatography. Well diffracting single crystals were obtained using the hanging-drop vapour-diffusion method. A molecular-replacement structural solution has been obtained. Refinement of the structure is currently under way.
Long-term prospective observational study of patients with peanut and nut allergy after participation in a management plan in England.
BACKGROUND: Peanut and nut allergy is common and the most frequent cause of severe or fatal reactions to foods. Current advice is poor--doctors give an epinephrine injector to patients; without training or advice on nut avoidance--so that further reactions are common and deaths occur. We devised and assessed a management programme providing advice on nut avoidance and emergency medication. METHODS: Unselected referrals with confirmed peanut or tree-nut allergy were recruited. Severity of nut allergy was graded 1-5 and emergency medication allocated accordingly: oral antihistamine with or without inhaled or injected epinephrine. Patients; parents; and school staff received verbal and written advice on nut avoidance as well as training in recognition and self-treatment of reactions; with a written treatment plan. At follow-up (more than 13610 patient months) retraining was given and details of further reactions obtained. FINDINGS: 88 (15%) of 567 patients had a follow-up reaction of reduced severity. 62 of 88 were mild (grades 1-3; mainly cutaneous) and 49 patients used oral antihistamine; six inhaled adrenaline; and ten took no treatment. 12 of 12 patients with a moderate follow-up reaction improved after inhaled epinephrine. Only three (0.5%) of 567 patients; aged 27-40 years; had a severe follow-up reaction (involving dyspnoea) compared with 12% initially. Only one of 567 changed from a mild index reaction to a severe follow-up reaction. Patients with a moderate/severe (grade 4-5) reaction were older (median 18 years vs 9 years; p=0.03) and nine of 26 received injected epinephrine which was always effective. 85% of patients had no further reactions. Severity was related to the amount of nut eaten. INTERPRETATION: Self-treatment was effective (inhaled epinephrine for early laryngeal oedema and an epinephrine injector for severe reactions) but provision of this treatment; including who should carry epinephrine; required assessment of allergy severity. Our management plan was effective; and our results indicate that patients should be referred to specialist allergy centres for advice on nut avoidance.
Perceived prevalence of peanut allergy in Great Britain and its association with other atopic conditions and with peanut allergy in other household members.
BACKGROUND: Despite increasing awareness of peanut allergy; little is known of its prevalence. We report on a two-stage interview survey conducted in Great Britain. METHODS: A total of 16434 adults (aged 15+ years) reported their own allergies and atopies and named cohabitants with peanut allergy (stage 1). Follow-up interviews were conducted with identified sufferers from peanut allergy (stage 2). RESULTS: At stage 1; peanut allergy was reported in 58 respondents and 205 other household members. When we accounted for cases where peanut allergy was unconfirmed or newly reported at stage 2; the prevalence; based on 124 confirmed sufferers; was estimated as 0.48% (95% confidence interval 0.40%-0.55%). The prevalence in children (0.61%; 0.41%-0.82%) was slightly higher than in adults; age-of-onset was strikingly earlier. Prevalence was strongly associated with other atopies; particularly tree-nut allergy. Cases tended significantly to cluster in households. Half of cases had never consulted a doctor. Exactly 7.4% reported being hospitalized after a reaction. CONCLUSIONS: Peanut allergy is reported by 1 in 200 of the population and is commoner in those reporting other atopies. The fact of similar rates in children and adults argues against a recent marked rise in prevalence. The frequency and potential lethality of this disorder emphasize the need for sufferers to demographic factors; other food allergies; atopic conditions; and allergy in family/household members. Our study comprised a screening survey and detailed interviews with sufferers identified. The frequency and potential lethality of this disorder emphasize the need for sufferers to receive correct medical advice on management [corrected].
Influence of plant lipids on immune responses in mice to the major Brazil nut allergen Ber e 1
BACKGROUND: Lipids; particularly bacterial lipopolysaccharide; can impact on immune responses to proteins; with low doses enhancing type 2 responses. OBJECTIVE: We have examined the influence of natural plant lipid extracts on antibody responses provoked in mice by recombinant Ber e 1; the major allergen in Brazil nuts. METHODS: BALB/c strain mice were immunized (by intraperitoneal injection) with natural or recombinant Ber e l produced in Pichia pastoris and admixed with various lipid fractions isolated from Brazil nuts. Serum samples were analysed for specific IgE antibody by homologous passive cutaneous anaphylaxis assay and for IgG by enzyme-linked immunosorbant assay. RESULTS: Exposure to recombinant (lipid-free) Ber e 1 alone failed to induce detectable IgG or IgE antibody. Co-administration of the total lipid fraction (with reduced triglyceride levels); sterol-rich; or polar lipid fractions; resulted in marked adjuvant effects on IgG and IgE. However; the beta-sitosterol and glycolipid-rich fractions were associated with only low-level IgG antibody; and had little impact on IgE antibody production. Natural Ber e 1 containing endogenous lipids also provoked IgG and IgE antibody responses. Identical IgE and IgG antibody responses were detected regardless of whether natural or recombinant Ber e 1 was used as substrates for analyses. CONCLUSION: Endogenous Brazil nut lipids are required for the induction of optimal antibody responses to Ber e 1 in the BALB/c strain mouse. Appropriate antibody binding sites are present on both natural and recombinant forms of Ber e 1; suggesting that the impact of lipid is at the induction phase; rather than antibody recognition; and is possibly required for efficient antigen presentation.
Allergy to cashew nuts and peanuts. Article in Dutch; Ned Tijdschr Geneeskd
Anaphylaxis due to the ingestion of peanuts is a serious; common condition; known to both the general public and physicians. Recently; an increasing number of patients with an anaphylactic reaction after eating small amounts of cashew nuts have been reported. In three children; a boy aged 7 and two girls aged 9 and 10 years; respectively; with heterogeneous case histories involving allergic upper airway and conjunctival symptoms and constitutional eczema; allergy for cashew nuts was diagnosed in the first two and allergy for peanuts in the third. They were given dietary advice and an adrenaline auto-injector for emergencies. In most cases; a detailed food history; together with the demonstration of IgE against cashew nuts by means of serology or skin prick tests; are sufficient to establish the diagnosis. If the clinical relevance of a sensitisation to cashew nuts is unknown; a food provocation test may be necessary. The treatment consists of dietary intervention; and an adrenaline auto-injector is prescribed for a serious anaphylactic reaction. So far; three major allergens from the cashew nut (Anacardium occidentale) have been identified and purified.
IgE cross-reactivity between the major peanut allergen Ara h 2 and tree nut allergens
Allergy to peanut and tree nuts is characterised by a high frequency of life-threatening anaphylactic reactions and typically lifelong persistence. Although peanut is the most common cause of nut allergy; peanut allergic patients are frequently also sensitive to tree nuts. It is not known if this is due to cross-reactivity between peanut and tree nut allergens. In this study; the major peanut allergen Ara h 2 was cloned from peanut cDNA; expressed in E. coli cells as a His-tag fusion protein and purified using a Ni-NTA column. Immunoblotting; ELISA and basophil activation indicated by CD63 expression all confirmed the IgE reactivity and biological activity of rAra h 2. To determine whether or not this allergen plays a role in IgE cross-reactivity between peanut and tree nuts; inhibition ELISA was performed. Pre-incubation of serum from peanut allergic patients with increasing concentrations of almond or Brazil nut extract inhibited IgE binding to rAra h 2. Purified rAra h 2-specific serum IgE antibodies also bound to proteins present in almond and Brazil nut extracts by immunoblotting. This indicates that the major peanut allergen; Ara h 2; shares common IgE-binding epitopes with almond and Brazil nut allergens; which may contribute to the high incidence of tree nut sensitisation in peanut allergic individuals.
Food allergy: nuts and tree nuts
Nuts are a well-defined cause of food allergy; which affect approximately 1 % of the general population in the UK and the USA. There do appear to be differences in the frequency of nut allergy between different countries because of different dietary habits and cooking procedures. For example; in the USA and France; peanuts are one of the most frequent causes of food allergy; but in other countries; it seems to be less common. Genetic factors; in particular; appear to play a role in the development of peanut allergy. While the majority of nut allergens are seed storage proteins; other nut allergens are profilins and pathogenesis-related protein homologues; considered as panallergens because of their widespread distribution in plants. The presence of specific IgE antibodies to several nuts is a common clinical finding; but the clinical relevance of this cross-reactivity is usually limited. Allergic reactions to nuts appear to be particularly severe; sometimes even life-threatening; and fatal reactions following their ingestion have been documented. Food allergy is diagnosed by identifying an underlying immunological mechanism (i.e. allergic testing); and establishing a causal relationship between food ingestion and symptoms (i.e. oral challenges). In natural history investigations carried out in peanut-allergic children; approximately 20 % of the cases outgrew their allergy or developed oral tolerance. The treatment of nut allergies should include patient and family education about avoiding all presentations of the food and the potential for a severe reaction caused by accidental ingestion. Patients and families should be instructed how to recognise early symptoms of an allergic reaction and how to treat severe anaphylaxis promptly.
Purification; identification and preliminary crystallographic studies of Pru du amandin; an allergenic protein from Prunus dulcis
Food allergies appear to be one of the foremost causes of hypersensitivity reactions. Nut allergies account for most food allergies and are often permanent. The 360 kDa hexameric protein Pru du amandin; a known allergen; was purified from almonds (Prunus dulcis) by ammonium sulfate fractionation and ion-exchange chromatography. The protein was identified by a BLAST homology search against the nonredundant sequence database. Pru du amandin belongs to the 11S legumin family of seed storage proteins characterized by the presence of a cupin motif. Crystals were obtained by the hanging-drop vapour-diffusion method. The crystals belong to space group P4(1) (or P4(3)); with unit-cell parameters a = b = 150.7; c = 164.9 A.