Peanut allergy is a type of food allergy to peanuts. It is different from tree nut allergies, because peanuts are legumes and not true nuts. Symptoms of allergic reaction typically occur within 2 hours of peanut ingestion. Allergic symptoms can involve the skin (hives, swelling), gastrointestinal (vomiting, diarrhea), respiratory system (cough, wheeze) or cardiovascular system (drop in blood pressure, shock). Anaphylaxis may occur. The risk of death from anaphylaxis is low, approximately 1 in 10 million.
It is due to a type I hypersensitivity reaction of the immune system in susceptible individuals.
Prevention may be partly achieved through early introduction of peanuts to the diets of pregnant women and babies.Patient page: It is recommended that babies at high risk be given peanut products in areas where medical care is available as early as 4 months of age. Oral immunotherapy results in some degree of tolerance in about 65% of children, though side effects are frequent. The principal treatment for anaphylaxis is the injection of epinephrine.
Peanut allergy occurs in about 1.4–2% in Europe and the United States as of 2021, increasing 3.5-fold over the preceding two decades. Among children in the Western world, rates of peanut allergy are between approximately 1.5% and 3% and have increased over time. It is a common cause of food-related fatal and near-fatal allergic reactions.
Signs and symptoms
Most symptoms of peanut allergy are related to the action of immunoglobulin E (IgE) and other anaphylatoxins which act to release histamine and other mediator substances from mast cells (degranulation). In addition to other effects, histamine induces vasodilation of arterioles and constriction of bronchioles in the lungs, also known as bronchospasm. Symptoms of allergic reaction typically occur within 2 hours of peanut ingestion. Allergic symptoms can involve the skin (itchiness, hives, swelling), gastrointestinal (vomiting, diarrhea), respiratory system (cough, wheeze) or cardiovascular system (drop in blood pressure, shock). Anaphylaxis may occur. The risk of death from anaphylaxis is low, approximately 1 in 10 million.
Cross-reactivity with other food People with confirmed peanut allergy may have cross-reactivity to tree nut, soy, and other legumes, such as peas, lentils, and lupinus. The cause of cross-reactivity results from similarity in the structures of storage proteins between the food sources. Allergenic proteins are grouped by protein families: cupins, prolamins, profilin and others. Peanuts and soybeans have proteins in the cupin, prolamin, and profilin families, while lentils contain cupin proteins.
A 2008 cohort study found no linkage between soy consumption and peanut allergy. Instead, the appearance of an association is likely due to confounding, as children with a milk allergy, who are at an increased risk of peanut allergy, are more likely to consume soy products.
Reviews of human clinical trials report that 6–40% of people with a confirmed peanut allergy will have allergic symptoms when challenged with tree nuts or legumes.
Causes Oral consumption is the most common route of exposure, but topical (skin) and inhalation can also trigger minor allergic reactions. There are at least 11 peanut proteins identified as allergenic. The condition is associated with several specific proteins categorized according to four common food allergy superfamilies: Cupin (Ara h 1), Prolamin (Ara h 2, 6, 7, 9), Profilin (Ara h 5), and Bet v-1-related proteins (Ara h 8). Among these peanut allergens, Ara h 1, Ara h 2, Ara h 3 and Ara h 6 are considered to be major allergens which means that they trigger an immunological response in more than 50% of the allergic population. These peanut allergens mediate an immune response via release of Immunoglobulin E (IgE) antibody as part of the allergic reaction.
Some of the peanut allergens can undergo enzymatic and non-enzymatic modifications, which makes them more likely to bind to ligands on antigen-presenting cells. Ara h 1 can undergo glycosylation modifications which have been shown to induce immunomodulatory responses; it stimulates lectin receptors MR and DC-SIGN on dendritic cells which further propagate cytokines and bias the immune system towards a Th2 type response. Peanut proteins that undergo non-enzymatic changes through Maillard reactions when cooked or exposed to room temperature have an increase in AGE modifications on their structure. These changes have been shown to stimulate RAGE receptors and SR-AI/II on dendritic cells and thus lead to an increase in IL-4 and IL-5-releasing Th2 cells.
Peanut allergies are uncommon in children of developing countries where peanut products have been used to relieve malnutrition. The hygiene hypothesis proposes that the relatively low incidence of childhood peanut allergies in developing countries is a result of exposure to peanuts early in life, increasing immune capability.
Desensitization through exposure In infants with a family history of peanut allergy, consuming peanut proteins at 4 to 11 months old has been shown to reduce the risk of developing an allergic response by 11–25%. From these results, the American Academy of Pediatrics rescinded their recommendation to delay exposure to peanuts in children, also stating there is no reason to avoid peanuts during pregnancy or breastfeeding. A later study by the National Institutes of Health provided further evidence supporting this. The study involved giving children diagnosed as "high allergic" small portions of peanut flour daily for several years, with some children randomly assigned placebo flour. The results were 71% of the children receiving peanut flour became desensitized to peanuts, while 2% receiving placebo flour became desensitized.
Diet during pregnancy There is conflicting evidence on whether maternal diet during pregnancy has any effect on development of allergies due to a lack of good studies. A 2010 systematic review of clinical research indicated that there is insufficient evidence for whether maternal peanut exposure, or early consumption of peanuts by children, affects sensitivity for peanut allergy.
Routes of exposure
While the most obvious route for an allergic exposure is unintentional ingestion, some reactions are possible through external exposure. Peanut allergies are much more common in adults who had oozing and crusted skin rashes as infants. Sensitive children may react via ingestion, inhalation, or skin contact to peanut allergens, which have persistence in the environment, possibly lasting over months.
Airborne particles in a farm- or factory-scale shelling or crushing environment, or from cooking, can produce respiratory effects in exposed allergic individuals. Empirical testing has discredited some reports of this type and shown some to be exaggerated. Residue on surfaces has been known to cause minor skin rashes, though not anaphylaxis. In The Peanut Allergy Answer Book, Harvard pediatrician Michael Young characterized this secondary contact risk to allergic individuals as rare and limited to minor symptoms. Some reactions have been noted to be psychosomatic, the result of conditioning, and belief rather than a true chemical reaction. Blinded, placebo-controlled studies were unable to produce any reactions using the odor of peanut butter or its mere proximity.
Rarely, allergic reactions have been triggered by exposure from kissing and sexual contact, especially if the partner has eaten peanuts within the last hour.
Pathophysiology The allergy arises due to dendritic cells recognizing peanut allergens as foreign pathogens. They present the antigens on MHC class II receptors, and these antigens are recognized by cell receptors on T cells. The contact, along with the release of the cytokine IL-4, induces their differentiation into CD4+ Th2 cells. The Th2 cells proliferate and release pro-inflammatory cytokines, such as IL-4, IL-5, and IL-13, which can be bound to receptors on undifferentiated B cells or B cells of the IgM subtype. The receptor-cytokine binding causes their differentiation into IgE which can then be bound onto FcεRI on mast cells, eosinophils and basophils. This elicits degranulation of the aforementioned cells, which release potent cytokines and chemokines, thus triggering inflammation and causing the symptoms characteristic of allergy.
Diagnosis Diagnosis of food allergies, including peanut allergy, begins with a medical history and physical examination. Skin prick test or blood test, when used in addition to a medical history suggesting of peanut allergy (allergic symptoms within 2 hours of peanut ingestion), can be used to confirm peanut allergy. National Institute of Allergy and Infectious Diseases (NIAID) guidelines recommend that parent and patient reports of food allergy be confirmed by a doctor because "multiple studies demonstrate 50% to 90% of presumed food allergies are not allergies".
Skin prick test Skin prick tests are designed to identify specific IgE bound to cutaneous mast cells. During the test, a glycerinated allergen extract drop is placed on the patient's skin. The patient's skin is then pricked with the drop. This procedure is repeated with two controls: a histamine drop designed to elicit an allergic response, and a saline drop designed to elicit no allergic response. The wheal that develops from the glycerinated extract drop is compared against the saline control. A positive allergic test is one in which the extract wheal is 3 mm larger than the saline wheal. A positive skin prick test is about 50% accurate, so a positive skin prick test alone is not diagnostic of food allergies.
Blood test Blood test for specific IgE antibodies to peanuts may indicate allergic sensitization to peanut. A positive blood test is about 50% accurate, so a positive blood test alone is not diagnostic of peanut allergy.
Oral food challenge The "gold standard" of diagnostic tests is a double-blind placebo-controlled oral food challenge. At least two weeks before an oral food challenge, the person is placed on an elimination diet where the suspected allergen is avoided. During the oral food challenge, they are administered a full age-appropriate serving of a suspected allergen in escalating size increments. They are continuously monitored for allergic reaction during the test, and the challenge is stopped and treatment administered at the first objective sign of allergic reaction.
Oral food challenges pose risks. In a study of 584 oral food challenges administered to 382 patients, 48% (253) of challenges resulted in allergic reactions. 28% (72) of these challenges resulted in "severe" reactions, which were defined by the study as a patient having: lower respiratory symptoms; cardiovascular symptoms; or any four other, more minor, symptoms. Double-blind placebo-controlled oral food challenges are also time-consuming and require close medical supervision. Because of these drawbacks to the double-blind placebo-controlled oral food challenge, open food challenges are the most commonly used form of food challenge. Open food challenges are those in which a patient is fed an age-appropriate serving of a suspected food allergen in its natural form. The observation of objective symptoms resulting from ingestion of the food, such as vomiting or wheezing, is considered diagnostic of food allergy if the symptoms correlate with findings from the patient's medical history and laboratory testing, such as the skin prick test.
Prevention
A 2008 joint United Kingdom-Israel study by George Du Toit et al. observed that Jewish children in the UK have a 10-fold higher prevalence of peanut allergy compared to Jewish children of similar ancestry in Israel, where solid food introduction during infancy commonly includes a popular peanut butter-based snack.