Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PEANUTS”

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.

At least 19 recordsLinked to original sources
PubMed2001

Final report on the safety assessment of Peanut (Arachis hypogaea) Oil, Hydrogenated Peanut Oil, Peanut Acid, Peanut Glycerides, and Peanut (Arachis hypogaea) Flour.

Peanut (Arachis Hypogaea) Oil is the refined fixed oil obtained from the seed kernels of Arachis hypogaea. Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides are all derived from Peanut Oil. Peanut Flour is a powder obtained by the grinding of peanuts. The oils and glycerides function in cosmetic formulations as skin-conditioning agents. The acid functions as a surfactant-cleansing agent, and the flour functions as an abrasive, bulking agent and/or viscosity-increasing agent. In 1998, only Peanut Oil and Hydrogenated Peanut Oil were reported in use. When applied to the skin, Peanut Oil can enhance the absorption of other compounds. Hepatic changes were noted at microscopic examination of rats fed diets containing 15% edible Peanut Oil for 28 days, although no control group was maintained and the findings were also noted in rats fed fresh corn oil. United States Pharmacopeia (USP)-grade Peanut Oil was considered relatively nonirritating when injected into guinea pigs and monkeys. Technical-grade Peanut Oil was moderately irritating to rabbits and guinea pigs and mildly irritating to rats following dermal exposure. This same oil produced reactions in < or = 10% of 50 human males. Peanut Oil was not an ocular irritant in rabbits. Peanut Oil, either "laboratory expressed" or extracted using a food-grade solvent, was not carcinogenic to mice. Peanut Oil exerted anticarcinogenic activity when tested against known carcinogens. Peanuts are the food most likely to produce allergic and anaphylactic reactions. The major allergen is a protein that does not partition into Peanut Oil, Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides. Aflatoxins can be produced in stored agricultural crops such as peanuts, but do not partition into the oils, acids, or glycerides. Manufacturers were cautioned to make certain that the oils, acids, and glycerides are free of aflatoxins and protein. Formulators were cautioned that the oils, acids, or glycerides may enhance penetration and can affect the use of other ingredients whose safety assessment was based on their lack of absorption. The available studies on Peanut Oil supported the conclusion that Peanut Oil, Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides are safe for use in cosmetic formulations. Peanut (Arachis Hypogaea) Flour, however, is sufficiently different from the above ingredients such that its safety can not be supported by studies using the oil. The additional data needed for Peanut (Arachis Hypogaea) Flour are (1) concentration of use; (2) chemical specifications (i.e., aflatoxin and protein levels); (3) method of preparation; and (4) contact urticaria and dermal sensitization at concentration of use. Although data on aflatoxin levels are sought, it is expected that concentrations of aflatoxin should comply with U.S. government stipulations. Absent the additional data, it was concluded that the available data are insufficient to support the safety of Peanut (Arachis Hypogaea) Flour for use in cosmetic products.

Administration, Cutaneous↗
PubMed2000

The psychological burden of peanut allergy as perceived by adults with peanut allergy and the parents of peanut-allergic children.

BACKGROUND: Peanut-allergic patients are affected by a condition which forces them and their families to exercise extreme dietary vigilance and experience constant uncertainty throughout their lives. OBJECTIVE: To compare the quality of life and family relations of children and adults with a peanut allergy to that of children and adults with a rheumatological disease. METHODS: Patients with a confirmed diagnosis of peanut allergy or a rheumatological disease completed (for children less than 18 years, by proxy) self-report questionnaires regarding the impact of their condition on their quality of life and family relations. A vertical visual analogue scale and the Impact on Family Questionnaire (IFQ) served as outcome measures. RESULTS: One hundred and fifty-three peanut-allergic children were compared with 69 children with a rheumatological disease while 37 peanut-allergic adults were compared with 42 adults with a rheumatological disease. The parents of peanut-allergic children, compared to the parents of children with a rheumatological disease, reported that their children had significantly more disruption in their daily activities. Furthermore, the parents of peanut-allergic children reported more impairment in the familial-social dimension of the IFQ. Conversely, adults with a chronic rheumatological disease reported more disruption in their family relations than peanut-allergic adults. CONCLUSION: Given the considerable disruption in daily activities and family relations reported by the parents of peanut-allergic children, accurate diagnosis of peanut allergy is essential. Our work should make health care professionals dealing with children with confirmed peanut allergy more aware of the support that these families may require. Furthermore, we hope to motivate food industries to offer more 'peanut free' products to decrease the dietary restrictions of these patients while minimizing their potential for accidental ingestion.

Adolescent↗
PubMed2003

Characterization of lymphocyte responses to peanuts in normal children, peanut-allergic children, and allergic children who acquired tolerance to peanuts.

Comparing lymphocyte responses to allergenic and nonallergenic foods could reveal the differences between pathogenic and normal immune responses to foods. Defining the cytokine-producing phenotypes of peanut-specific lymphocytes from peanut-allergic children, children who outgrew peanut allergy, and children who have always tolerated peanuts may be useful for understanding the mechanisms of food tolerance. Investigating immune responses against foods is hindered, however, by the fact that circulating food antigen-specific lymphocytes are very rare. In a novel approach we used carboxyfluorescein succinimidyl ester to detect peanut-specific lymphocytes by flow cytometry. We confirmed that these cells are indeed peanut specific by cloning. Peanut-allergic donors show Th2 polarization of cytokine production by peanut-specific cells (IFN-gamma (low), TNF-alpha (low), IL-4 (high), IL-5 (high), IL-13 (high)). Conversely, nonallergic children and children who have outgrown their allergy show Th1 skewing to peanut antigens (IFN-gamma(high), TNF-alpha (high), IL-4 (low), IL-5 (low), IL-13(low)), similarly to nonallergenic food antigens (beta-lactoglobulin, OVA). This finding suggests that peanut antigens do not intrinsically induce Th2 skewing, but that the type of response depends upon the donor's allergic status. In conclusion, food allergic status is characterized by a Th2 response whereas Th1-skewed responses underlie oral tolerance.

Adolescent↗
PubMed2004

Specific immunoglobulin E antibodies to peanut over time in relation to peanut intake, symptoms and age.

The clinical outcome of peanut allergy and some factors associated with development of peanut allergy remain unsolved. It has not been clarified to what extent peanut intake affects immunoglobulin (IgE) antibody formation in peanut sensitized individuals. The aim of the study was to investigate the development of peanut hypersensitivity in children and adolescents with specific IgE antibodies to peanut, using questionnaires and current serum tests and comparing it to information obtained 5-6 yr earlier, to investigate how peanut intake during this period related to subject age, IgE antibody levels and symptoms and to investigate what information this patient group was given at the time of diagnosis regarding avoidance of peanut related food. All patients with detectable peanut-specific IgE antibodies investigated during 1994-1996 deriving from two allergy laboratories in the western region of Sweden were traced and reinvestigated (n=132). A total of 111 subjects (63 with peanut allergy and 48 peanut sensitized) participated in the questionnaire. Eighty-six of them consented to be enrolled in a further interview and renewed testing of specific IgE antibody to peanut 5 yr later. All tests were done using the Pharmacia CAP system. Increased IgE antibody levels during follow-up was related to age; subjects 0-6 yr at initial test occasion were more likely to have higher IgE antibody class than the older individuals (p=0.018). Exposure to peanut during the study, i.e. 5-6 yr since diagnosis, did not seem to affect the result. During the follow-up period, 29 out of 86 (34%) increased their IgE antibody class. At the second test occasion the remaining subjects had similar (28%) or lowered (38%) levels of IgE antibodies. Exposure to peanut during follow-up was more common in subjects with IgE antibody class 1-3 compared to subjects with high value (> 3) at the initial test (p=0.003). Reported symptoms during follow-up were also more common in subjects with initially high IgE antibody value. Individuals with initially high IgE antibodies to peanut had been given more information about peanut allergy and cross-reacting allergens than other individuals. The subjects over 6 yr of age showed a decrease in peanut-specific IgE class over a 5-yr period. Together with the literature, our result suggest that follow-up and renewed testing is recommended, since there may be a change in IgE antibody classes and clinical sensitivity over time. Even in Sweden, with a low consumption of peanuts, the youngest individuals with peanut sensitization experienced a similar course of events that has been reported in other countries.

Age Factors↗
PubMed1999

Exposure to peanuts in utero and in infancy and the development of sensitization to peanut allergens in young children.

This study attempted to determine the underlying factors that may influence the development of peanut sensitization in young children in South Africa. One of our objectives was to ascertain whether the consumption of peanuts or peanut-containing foods during pregnancy and lactation by mothers from atopic families impacted upon the development of an allergic response to peanuts in the child. Forty-three children between the ages of 0 and 3 yr participated in this study. There were 25 peanut-sensitized subjects and 18 control subjects (children sensitized to milk and/or egg, but not to peanuts). A significant association was found between peanut sensitization and sensitivity to soya (p=0.0002), wheat (p=0.03), and cod fish. We found that mothers who consumed peanuts more than once a week during pregnancy were more likely to have a peanut-allergic child than mothers who consumed peanuts less than once a week (odds ratio=3.97, 98% confidence interval 0.73-24). Peanuts or peanut butter was introduced into the child's diet from a significantly younger age in the peanut-allergic subjects (p<0.03). There was a positive correlation in the peanut-allergic subjects between age of introduction of peanuts and age at the onset of symptoms (r=0.63). Exclusive breast feeding did not protect against the development of peanut sensitization. Peanut allergy is associated with an increased risk of sensitization to other foods. It is more likely to occur if mothers eat peanuts more frequently during pregnancy and introduce it early to the infant's diet. These features highlight potentially avoidable factors that might prevent sensitization.

Animals↗
PubMed2005

Peanut-lupine antibody cross-reactivity is not associated to cross-allergenicity in peanut-sensitized mouse strains.

BACKGROUND: Peanut hypersensitivity is one of the most common food allergies and one of the most common causes of death by food anaphylaxis in children and adults. Cross-reactivity of peanut-specific antibody (Ab) with other legumes is frequently demonstrated but it still remains to be demonstrated whether these responses could lead to clinical signs of cross-allergenicity. OBJECTIVE: We sought to evaluate peanut-specific serum IgE and IgG1 antibody (Ab) responses and anaphylactic reaction in mice strains and to assess both cross-reactivity and cross-allergenicity of peanut and lupine. METHODS: Four mice strains (i.e., C3H, BALB/c, CBA and SJL) were sensitized to peanut by intraperitoneal (ip) injection of crude peanut protein extract with alum. Other groups were given oral peanut extract without adjuvant. Peanut-specific antibodies (Abs) and anaphylactic responses to peanut challenge were examined. RESULTS: The C3H, CBA (H-2(k)) and BALB/c (H2-(d)) mice exhibited high levels of peanut-specific serum IgE, IgG1 Ab responses after the intra-peritoneal sensitization. Only the two strains of mice in the H-2(k) background developed anaphylactic symptoms upon intra-peritoneal challenge with crude peanut protein extract. While cross-reactivity of peanut and lupine was confirmed by ELISA, no clinical symptom of cross-allergenicity was seen after challenge with lupine. Mice that were given oral peanut showed only increase in peanut-specific IgG2a, but no IgE or IgG1 Abs and failed to develop anaphylactic reactions following injection of either peanut or lupine protein. CONCLUSION: These results show that mice of different genetic backgrounds can be sensitized to peanut by ip injection to develop anti-peanut Abs that cross react with lupine. In addition, cross-allergenicity may not directly correlate with the presence of cross-reactive Abs since no clinical symptoms of cross-allergenicity was seen after ip challenge with lupine.

Allergens↗
PubMed2004

Soy immunotherapy for peanut-allergic mice: modulation of the peanut-allergic response.

BACKGROUND: Allergen-specific immunotherapy (IT) is an effective therapeutic modality to prevent further anaphylactic episodes in patients with insect sting hypersensitivity and is being investigated for peanut allergy. So far, peanut-specific IT has been unsuccessful because of the side effects of therapy. Soybean seed storage proteins share significant homology with the respective peanut allergens. OBJECTIVE: This study was undertaken in mice to investigate whether specific doses of soybean would desensitize peanut-allergic mice. METHODS: C3H/HeJ mice were sensitized to peanut with 3 intraperitoneal (IP) injections of crude peanut extract. The mice were desensitized by IP injections with either crude peanut or soybean extract for 4 weeks, 3 times a week. Controls included placebo desensitization with PBS and naive mice. After 2 weeks of rest, mice were challenged IP with crude peanut extract. Thirty minutes later, symptom scores and body temperatures were recorded. Serum immunoglobulins, peanut-induced splenocyte proliferation, and secreted cytokines were measured before and after desensitization. RESULTS: The clinical symptoms in the soybean- and peanut-desensitized animals were markedly reduced compared with the placebo-treated mice. Specific IgG1 levels to crude peanut were significantly lower in the soy IT group than in the peanut IT group. The cellular response to crude peanut was also downregulated in the soy IT group, as shown by decreased peanut-specific stimulation indices and a cytokine profile skewed toward a T H 1 response. CONCLUSIONS: Soy IT can be used to desensitize/downregulate peanut-specific response in peanut-allergic mice and could provide a new therapeutic intervention for peanut allergy.

Animals↗
PubMed2006

Human subjects without peanut allergy demonstrate T cell-dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression.

BACKGROUND: Peanut allergy is a major cause of anaphylaxis. Regulation of immune responses to peanut allergen, particularly why sensitization does not usually progress to allergic reactions, is not well investigated. Most studies focus exclusively on serologic responses and individuals with peanut allergy. OBJECTIVE: We sought to determine the existence, prevalence, and nature of peanut-specific, T cell-dependent cytokine and chemokine responses of adults who eat peanut without having symptoms. METHODS: We developed systems to examine specific immunity in peanut-tolerant individuals who had (1) negative histories and negative peanut skin test responses, (2) negative histories and positive peanut skin test responses, and (3) clinically apparent peanut allergy. After primary culture of PBMCs restimulated with whole peanut extract, we quantified responses characteristic of TH1 (IFN-gamma and CXCL10) and TH2-like immunity (IL-5, IL-13, CCL17, and CCL22) using ultrasensitive ELISAs. Antigen-presenting cell costimulatory requirements (CD4, HLA-DR, CD80/86, and cytotoxic T lymphocyte-associated antigen 4 [CTLA4] Ig) were determined. RESULTS: T cell-dependent, peanut-specific IL-5, IL-13, and CCL22 were common in peanut-tolerant individuals, regardless of whether they had positive or negative skin test responses. These were blocked by anti-CD4 and were dependent on CD28/CD86 costimulation. None of the 70 individuals studied had demonstrable IFN-gamma or CXCL10 responses to peanut. All demonstrated TH1 and TH2 responses to the ubiquitous recall antigen streptokinase. CONCLUSIONS: Qualitatively similar and quantitatively increasing peanut-specific TH2 responses in the consistent absence of putatively protective TH1 immunity were found in both peanut-tolerant individuals and those with peanut allergy. CLINICAL IMPLICATIONS: The continuum of responses between individuals with negative and individuals with positive skin test results, rather than TH1 versus TH2 bias, might be important in peanut allergy.

Adolescent↗
PubMed2000

A murine model of peanut anaphylaxis: T- and B-cell responses to a major peanut allergen mimic human responses.

BACKGROUND: Peanut allergy affects 0.6% of the US population. At the present time, allergen avoidance is the only therapeutic option. Animal models of food-induced anaphylaxis would facilitate attempts to design novel immunotherapeutic strategies for the treatment of peanut allergy. OBJECTIVE: The purpose of this study was to develop a murine model of IgE-mediated peanut hypersensitivity that closely mimics human peanut allergy. METHODS: C3H/HeJ mice sensitized orally with freshly ground whole peanut and cholera toxin as adjuvant were challenged orally 3 and 5 weeks later with crude peanut extract. Anaphylactic reactions were determined. T- and B-cell responses to Ara h 1 and Ara h 2, the major peanut allergens, were characterized by evaluating splenocyte proliferative responses and IgE antibody concentrations. Furthermore, IgE antibodies in the sera of patients with peanut allergy and mice were compared for antibody binding to Ara h 2 isoforms and allergenic epitopes. RESULTS: Peanut-specific IgE was induced by oral peanut sensitization, and hypersensitivity reactions were provoked by feeding peanut to sensitized mice. The symptoms were similar to those seen in human subjects. Ara h 1- and Ara h 2-specific antibodies were present in the sera of mice with peanut allergy. Furthermore, these Ara h 2-specific IgE antibodies bound the same Ara h 2 isoforms and major allergenic epitopes as antibodies in the sera of human subjects with peanut allergy. Splenocytes from mice with peanut allergy exhibited proliferative responses to Ara h 1 and Ara h 2. CONCLUSION: This murine model of peanut allergy mimics the clinical and immunologic characteristics of peanut allergy in human subjects and should be a useful tool for developing immunotherapeutic approaches for the treatment of peanut allergy.

2S Albumins, Plant↗
PubMed2003

Relevance of casual contact with peanut butter in children with peanut allergy.

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).

Administration, Inhalation↗
PubMed1998

Peanut allergic subjects' peripheral blood mononuclear cell proliferative responses to crude peanut protein.

BACKGROUND: Peanut allergy is characterized by a high frequency of severe and occasionally fatal reactions. OBJECTIVE: To determine if there are features of the in vitro cellular response that may account for the observed severity of peanut allergy. METHODS: Skin-prick testing (SPT), RAST assay of serum peanut-specific and total IgE and mixed peripheral blood mononuclear cells (PBMC) proliferative responses to crude peanut protein were measured in 44 peanut allergics with varying severity of clinical reactions. PBMC responses of 13 non-peanut allergic controls (six atopic) were also studied. RESULTS: Subjects' PBMCs proliferated more than controls', even without stimulation. Subjects' PBMC proliferative responses did not correlate with clinical severity, SPT weal size or peanut-specific IgE levels. Controls' PBMCs did not respond to peanut. There was no correlation between PBMC response and time since last reaction to peanut. Subjects' PBMCs responded more than controls, to mitogen as well as allergen. Proliferation increased with increasing concentration of peanut protein (P < 0.0001). CONCLUSION: PBMCs of peanut allergics demonstrate a dose-dependent response to peanut which does not correlate with clinical severity, SPT reaction or levels of peanut specific IgE. The response is antigen-specific. Peanut protein is not mitogenic and is not acting as a superantigen. While there are non-specific differences in the PBMC responses of peanut allergic individuals compared with atopic and non-atopic controls, these differences do not explain the unique severity of peanut allergy.

Adolescent↗
PubMed2002

High-oleic peanuts are not different from normal peanuts in allergenic properties.

High-oleic peanuts are known for a high content of oleic fatty acid. However, it is not known whether high-oleic peanuts are different from normal chemistry peanuts in levels of allergenicity and end-product adducts (i.e., products cross-linked with proteins). For this purpose, four different peanut cultivars (Florunner, Georgia Green, NC 9, and NC 2) were evaluated and compared with high-oleic peanuts (SunOleic 97R). Adducts such as AGE/CML from Maillard reactions and MDA/HNE from lipid oxidation were determined, respectively, in ELISA, using polyclonal antibodies. Allergenicity was determined based on IgE binding and T-cell proliferation. Results showed that raw high-oleic peanuts were not different from normal peanuts in adduct levels. After roasting, CML and HNE levels remained unchanged, but an increased and similar amounts of AGE adducts were found in all peanuts. MDA also increased but not in high-oleic peanuts. This suggests that high-oleic peanuts are more stable to lipid oxidation than others during heating. Despite this, high-oleic peanuts did not differ from normal peanuts in IgE binding and T-cell proliferation. It was concluded that a high content of oleic fatty acid has no effect on peanut allergenicity and that high-oleic peanuts do not give a higher or lower risk of allergy than normal peanuts.

Aldehydes↗
PubMed1997

Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract.

BACKGROUND: Immediate hypersensitivity to peanuts is a frequent cause of anaphylactic reactions and deaths in children and adults. Currently, preventive treatment consists of avoidance, which is difficult because of the widespread and often disguised use of peanuts in the food industry. METHODS: Twelve patients with immediate hypersensitivity to ingestion of peanuts were recruited. Half were treated with injections of peanut extract: a maintenance level of tolerance was first achieved by a rush protocol, then maintained with weekly injections for at least 1 year. The other six were untreated control subjects. All patients underwent double-blind, placebo-controlled, oral peanut challenges initially, after approximately 6 weeks, and after 1 year. RESULTS: All treated patients achieved the maintenance dose of 0.5 ml of 1:100 wt/vol peanut extract by the rush injection protocol. All experienced increased tolerance to double-blind, placebo-controlled peanut challenge and decreased sensitivity on titrated skin prick testing with peanut extract, whereas the threshold to oral peanut challenge and cutaneous reactivity to peanut extract were unchanged in the untreated control subjects. Systemic reactions were common in the treated group both during rush immunotherapy and with maintenance injections. Only three patients remained tolerant of the full maintenance dose. The increased tolerance to oral peanut challenge was maintained in the three subjects who received full maintenance doses, but there was partial (n = 2) or complete (n = 1) loss of protection in the patients who required dose reduction because of systemic reactions. CONCLUSIONS: Injections of peanut extract increase the tolerance of patients with peanut allergy to oral ingestion of peanuts. Injections result in repeated systemic reactions in most patients, even during maintenance injections. For clinical application of this method of treatment, a modified peanut extract is needed.

Administration, Oral↗
PubMed2000

The natural history of peanut allergy in young children and its association with serum peanut-specific IgE.

OBJECTIVES: To observe the nature and frequency of adverse reactions caused by accidental peanut exposure in young children with clinical peanut hypersensitivity and to determine the value of serum peanut-specific IgE levels during follow-up. STUDY DESIGN: Eighty-three children with clinical peanut hypersensitivity diagnosed before their fourth birthdays were contacted yearly to track adverse peanut reactions. Serum peanut-specific IgE levels were determined in 51 of 83 subjects. RESULTS: Fifty-eight percent (31/53) of subjects followed up for 5 years experienced adverse reactions from accidental peanut exposure. Regardless of the nature of their initial reaction, the majority with subsequent reactions (52%, 31/60) experienced potentially life-threatening symptoms. The group with isolated skin symptoms (11/51, 22%) had lower serum peanut-specific IgE levels than the group with respiratory and/or gastrointestinal symptoms (40/51, 78%) (median: 1.25 kU(A)/L vs 11. 65 kU(A)/L, P =.004, Wilcoxon rank sums test). Despite this, there was no threshold level below which only skin symptoms appeared to occur. Four selected subjects had negative double-blind placebo-controlled food challenge responses to peanuts during follow-up. CONCLUSIONS: The majority of children with clinical peanut hypersensitivity followed up for 5 years will have adverse reactions from accidental peanut exposure. Symptoms experienced during subsequent adverse peanut reactions may not be consistent with symptoms reported during initial reactions. Therefore proper education regarding peanut avoidance and treatment of adverse reactions is necessary in all cases of clinical peanut hypersensitivity. Young children who are allergic to peanuts can lose clinical hypersensitivity.

Allergens↗
PubMedDate not supplied

Can commercial peanut assay kits detect peanut allergens?

Peanut is the food group mostly associated with severe and fatal allergic reactions. In the United States, more than 90% of peanut-allergic individuals' serum IgE recognized peanut proteins Ara h 1 and Ara h 2, thus establishing these proteins as major peanut allergens. The amount of Ara h 1 and Ara h 2 in 3 varieties of peanut cultivars that are commonly processed in the industrialized countries was determined to be 12-16 and 6-9%, respectively. Current commercial peanut test kits use polyclonal peanut-specific antibodies to detect soluble or buffer extractable peanut proteins. Because the 2 major peanut allergens Ara h 1 and Ara h 2 are isolated from soluble peanut proteins, it is generally assumed that these commercial kits can detect peanut allergens, although none of these kits claims to detect peanut allergen. This study showed for the first time that the peanut test kits could, in fact, detect major peanut allergens Ara h 1 and Ara h 2 in both native or heat-denatured structures; therefore, these kits qualified to be classified as peanut allergen enzyme-linked immunosorbent assays.

2S Albumins, Plant↗
PubMed2003

The predictive value of a positive prick skin test to peanut in atopic, peanut-naïve children.

BACKGROUND: Although allergy testing before food ingestion is generally not recommended, many peanut-naive children undergo prick skin tests (PSTs) to peanut because of atopy. Children with positive PSTs are generally advised to avoid peanuts either indefinitely or until a definitive diagnosis is made through challenge. OBJECTIVE: To describe peanut challenges in atopic, peanut-naive children with PST to peanuts > or = 3 mm and the PST properties in this population. METHODS: Between 1994 and 2001, 47 patients were identified who had a positive peanut PST, no previous peanut ingestion, and had undergone a peanut challenge. RESULTS: Forty-nine percent of the challenges were positive. The mean of the largest wheal diameter (95% confidence interval [CI]) of the PST in children having a negative and positive challenge was 6.3 mm (CI, 5.3 to 7.3) and 10.3 mm (CI, 8.9 to 11.8), respectively. At a PST cutoff of > or = 5 mm, the sensitivity and negative predictive value (95% CI) was 100% (85.2 to 100) and 100% (29.2 to 100), whereas the specificity and positive predictive value (95% CI) was 12.5% (2.7 to 32.4) and 52.3% (36.7 to 67.5), respectively. CONCLUSIONS: We show that 49% of atopic, peanut-naïve children sensitized to peanut developed allergic symptoms during oral provocation with peanut. Although the sensitivity of the PST at > or = 5 mm for the detection of peanut allergy in this study was 100%, our small sample size limits the applicability of this value. Further investigation is needed to determine whether children with wheal diameters of 3 or 4 mm, perhaps coupled with low peanut-specific IgE, could undergo less resource-intensive, accelerated challenges.

Antibody Specificity↗
PubMedDate not supplied

Preparation of peanut butter suspension for determination of peanuts using enzyme-linked immunoassay kits.

Peanuts are one of the 8 most common allergenic foods and a large proportion of peanut-allergic individuals have severe reactions, some to minimal exposure. Specific protein constituents in the peanuts are the cause of the allergic reactions in sensitized individuals who ingest the peanuts. To avoid accidental ingestion of peanut-contaminated food, methods of analysis for the determination of the allergenic proteins in foods are important tools. Such methods could help identify foods inadvertently contaminated with peanuts, thereby reducing the incidence of allergic reactions to peanuts. Commercial immunoassay kits are available but need study for method performance, which requires reference materials for within- and between-laboratory validations. In this study, National Institute of Standards and Technology Standard Reference Material 2387 peanut butter was used. A polytron homogenizer was used to prepare a homogenous aqueous Peanut Butter suspension for the evaluation of method performance of some commercially available immunoassay kits such as Veratox for Peanut Allergen Test (Neogen Corp.), Ridascreen Peanut (R-Biopharm GmbH), and Bio-Kit Peanut Protein Assay Kit (Tepnel). Each gram of the aqueous peanut butter suspension contained 20 mg carboxymethylcellulose sodium salt, 643 microg peanut, 0.5 mg thimerosal, and 2.5 mg bovine serum albumin. The suspension was homogenous, stable, reproducible, and applicable for adding to ice cream, cookies, breakfast cereals, and chocolate for recovery studies at spike levels ranging from 12 to 90 microg/g.

Arachis↗
PubMed1999

Cross-allergenicity of peanut and lupine: the risk of lupine allergy in patients allergic to peanuts.

BACKGROUND: Peanut allergy is common, but cross-allergy between legumes is rare. Proteins from Lupinus albus are increasingly eaten in the form of seeds or additives to wheat flour. The risk of cross-allergenicity is still insufficiently known. OBJECTIVE: We sought to study the risk of cross-allergy to lupine in patients allergic to peanut and to study lupine allergenicity. METHODS: Twenty-four patients allergic to peanuts were studied by means of skin prick tests with native lupine flour from Lupinus albus. Double-blind oral challenge tests were performed with lupine flour and peanut in 8 of these patients. Specific IgEs were assayed for peanut, lupine flour, and pollen in 6 sera. RAST inhibition tests for lupine pollen by peanut were performed on 4 of these sera. Peanut and lupine flour immunoblots were carried out for 6 sera, and crossed immunoblot inhibitions for peanut by lupine flour and lupine flour by peanut were carried out for 2 sera. RESULTS: The skin prick test responses with lupine flour were positive in 11 (44%) subjects. The challenge test responses were positive in 7 of 8 subjects at the same doses as with peanut. The major lupine flour allergen (molecular mass, 43 kd) is present in peanuts. The RAST inhibition and immunoblot tests indicated cross-reactivity of peanut with the lupine flour and pollen. CONCLUSIONS: The risk of crossed peanut-lupine allergy is high, contrary to the risk with other legumes. The inclusion of 10% lupine flour in wheat flour without mandatory labeling makes lupine a hidden allergen, presenting a major risk of cross-reaction in subjects already allergic to peanut products. A high sensitizing potential can also be postulated for this legume.

Adolescent↗