What does level 1 peanut allergy mean
Medical history and examination
Your doctor may suspect that you own a nut allergy from your symptoms. Your doctor may then enquire a lot of questions. For example, the quantity and type of food that you ate which caused a reaction, how quickly the symptoms started, how severe they were, how endless they lasted, etc.
Skin prick test
A skin prick test may be done to assist confirm the allergy. For this test, a drop of nut extract solution is placed on the skin, generally on the forearm.
Then, a needle prick is made through the drop. This is generally painless as just the extremely surface of the skin is pricked. However, it is enough to let a tiny quantity of solution into your skin. If a reaction occurs, it happens within 20-30 minutes.
- A reaction is considered to be ‘positive’ when the skin under the solution becomes red and itchy.
A white, raised swelling called a wheal surrounds the red central area. A wheal takes about 15-20 minutes to reach its full size, and then fades over a few hours.
- A reaction is considered to be ‘negative’ when the skin remains normal. This means that you are not allergic to the substance in the solution.
Do not take antihistamines on the day of the test as they may dampen any allergic response during the test.
You may also own a blood test.
This measures the quantity of a protein called IgE antibody which is produced as a result of an allergic reaction.
You can read more about IgE reactions in the separate leaflet called Food Allergy and Intolerance
If other tests are not conclusive then your doctor may enquire you to take part in a food challenge. For this test you are given foods to eat that may or may not contain nuts. You will then be watched closely for 15-30 minutes to see whether you own a reaction. Food challenges are always done at a hospital or specialised setting because of the risk of a severe reaction.
If you are found to be allergic to one type of nut, you may be tested for allergy to other nuts as well.
If you own an allergy to peanuts, you are more likely to own an allergy to tree nuts than a person who does not own a peanut allergy. Once an allergy has been confirmed, an allergy specialist will generally assist you to devise a plan to manage it. This plan will be individual to you and will take into account how severe your reaction is.
The immune system plays an integral role in the maintenance of tolerance to innocuous antigens. IgE-mediated food allergies happen as a result of a loss of integrity in the key immune components that maintain a state of tolerance and prevent benign food antigens from being recognized as pathogens.
More specifically, oral tolerance to foods is defined as the crossing of food antigen across the mucosal barrier, processing by dendritic cells in a non-activated state, and the induction of suppressive cytokines, such as interleukin 10, by those antigen-presenting cells. This in turn results in the differentiation of naïve T cells into T regulatory cells and suppression of food antigen-specific Th2 cells, as well as increased IgA and IgG4 production and a decrease in IgE by B cells.
Finally, there is immune suppression of eosinophils, basophils, and mast cells, effector cells which cause symptoms.
Sensitization is defined as the state of having detectable food-specific IgE which can be a precursor to the development of clinical food allergy.
It occurs when food crosses disrupted barrier and as a result of this disruption, harm signals and inflammatory cytokines are released which activate dendritic cells into phenotypes that are normally acquired during the defense against pathogens. These activated dendritic cells in turn activate naïve T cells into acquiring a T helper cell 2 (Th2) phenotype, which in turn promote inflammatory signals which induce food Ag-specific B cells to class switch and produce food antigen-specific IgE. In short, sensitization is mistaken identification of food antigen as pathogen. Every patients with IgE-mediated food allergies are sensitized to food allergen. This section will discuss five key components of the immune system involved in the development of tolerance and sensitization or allergy to food: the epithelium, innate immune cells, T cells, B cells, and finally, the effector cells of the allergic response, mast cells, eosinophils, and basophils (Fig.
The immune system plays an integral role in the maintenance of tolerance to innocuous antigens. IgE-mediated food allergies happen as a result of a loss of integrity in the key immune components that maintain a state of tolerance and prevent benign food antigens from being recognized as pathogens. More specifically, oral tolerance to foods is defined as the crossing of food antigen across the mucosal barrier, processing by dendritic cells in a non-activated state, and the induction of suppressive cytokines, such as interleukin 10, by those antigen-presenting cells.
This in turn results in the differentiation of naïve T cells into T regulatory cells and suppression of food antigen-specific Th2 cells, as well as increased IgA and IgG4 production and a decrease in IgE by B cells. Finally, there is immune suppression of eosinophils, basophils, and mast cells, effector cells which cause symptoms.
Sensitization is defined as the state of having detectable food-specific IgE which can be a precursor to the development of clinical food allergy.
It occurs when food crosses disrupted barrier and as a result of this disruption, harm signals and inflammatory cytokines are released which activate dendritic cells into phenotypes that are normally acquired during the defense against pathogens. These activated dendritic cells in turn activate naïve T cells into acquiring a T helper cell 2 (Th2) phenotype, which in turn promote inflammatory signals which induce food Ag-specific B cells to class switch and produce food antigen-specific IgE.
In short, sensitization is mistaken identification of food antigen as pathogen. Every patients with IgE-mediated food allergies are sensitized to food allergen. This section will discuss five key components of the immune system involved in the development of tolerance and sensitization or allergy to food: the epithelium, innate immune cells, T cells, B cells, and finally, the effector cells of the allergic response, mast cells, eosinophils, and basophils (Fig. 3).
The epithelial barrier serves a major role in defense against pathogens. In the context of IgE-mediated food allergies, the epithelial barrier prevents unnecessary entry of antigens.
An intact epithelial barrier is significant in the maintenance of tolerance, as it prevents the entry of harm signals and subsequently prevent the production of inflammatory cytokines, in conjunction with food antigens. Antigens cannot freely pass an intact epithelial barrier. Instead, in an intact epithelium, antigen is often transported through “assisted” mechanisms. These mechanisms include: paracellular diffusion, athletic transport via the enterocytes, microfold (M) cells, or goblet cells, and by specialized macrophages projecting through epithelial .
Food antigens recognized by specialized antigen presenting cells in the absence of pro-inflammatory or harm signals will further promote the maintenance of tolerance through the release of chemical mediators such as interleukin 10 (IL-10) and/or transforming growth factor beta (TGF-β), which will promote the development of regulatory T cells [4, 5, 6].
When the integrity of the epithelial barrier is compromised, sensitization to food allergens can happen, leading to the development of food allergy. Epithelial damage or inflammation can permit antigens to pass freely through the gut barrier, along with other pathogens.
Damaged epithelium also promotes the release of pro-inflammatory epithelial cytokines, such as interleukin 25 (IL-25), IL-33, and thymic stromal lymphopoeitin (TSLP) [7, 8].
The epithelial cytokines released can foster the activation of an allergic phenotype by signaling to antigen presenting cells and other innate immune cells at or under the epithelial barrier. When food antigen uptake occurs by activated antigen presenting cells in the presence of inflammatory cytokines, the benign antigen is now seen as a “threat.”
Antigen Presenting Cells and Innate Lymphoid Cells
In the absence of sensitizing chemical mediators, CX3CR1+ macrophages can sample antigen and produce the cytokine IL-10, which will permit for the differentiation of naïve T cells to regulatory T cells.
CD103+ dendritic cells can also capture antigen directly or from transfer by the macrophage . CD103+ DCs will migrate to draining lymph nodes and present the antigenic peptide along with the class 2 major histocompatibility complicated (MHC) to naïve T cells. Furthermore, in the presence of TGF-β and retinoic acid secreted from the DCs, naïve T cells are promoted toward a tolerant phenotype and can differentiate to T regulatory cells .
Conversely, the breakdown of tolerance due to a compromised epithelial barrier, promotes the epithelial release of pro-inflammatory chemical mediators, such as IL-25, IL-33, and TSLP [7, 8].
These mediators act upon antigen presenting cells and innate lymphoid cells, to further promote sensitization by a Th2 phenotype. Activated dendritic cells promoting allergy, express surface OX40L, also known as tumor necrosis factor ligand superfamily member 4 (TNFSF4) and migrate to the draining lymph node where they encounter and present antigen to naïve T cells . The MHC of the dendritic cell presents antigenic food peptides to naïve T cells and with the interaction between OX40L on DCs and OX40 on naïve T cells, differentiation occurs from naïve T cells into Th2 T cells, thus promoting the allergic state.
In addition to activated dendritic cells, type 2 innate lymphoid cells (ILC2) own also been shown to frolic a critical role in the induction of food allergy.
ILC2s expand in an antigen-independent manner while in the presence of the cytokines TSLP, IL-25, and IL-33 and promote a Th2 cell-mediated immune response . As a result, ILC2s produce large quantities of TH2 cytokines, such as IL-5, IL-13, IL-4, and IL-9 [12, 13, 14]. The secretion of the cytokine IL-4 and IL-13 from ILC2s can disrupt allergen-specific T regulatory cell induction and their suppressive functions, as well as enhance mucosal mast cell activation, thereby sustaining dysregulation and promoting the induction of food allergies .
The appropriate milieu of cytokine and innate cell mediators promote the development of tolerance through naïve T cells.
Naïve T cells reside in the draining lymph nodes and await for the upstream signals, and, in combination with the presented antigens, promote the development of T regulatory cells. Specifically, antigen presenting cells secreting TGF-β, retinoic acid, or IL-10, foster the development of antigen-specific T regulatory cells from the naïve T cells [4, 5, 6]. Specifically, retinoic acid from DCs promotes the expression of homing receptor α4β7 on T regulatory cells thereby allowing for the translocation to the intestinal lamina propria, where they exhibit suppressive activity via CTLA-4 binding to effector [15, 16].
Furthermore, cytokines secreted from T regulatory cells, such as IL-10 and TGF-β, can also suppress effector cells .
Th2-differentiated cells can migrate out of the draining lymph nodes into the lamina propria and secrete pro-inflammatory cytokines, such as IL-5 and IL-13 to further promote the differentiation of downstream pro-inflammatory effector cells such as eosinophils and basophils. IL-4, which is produced by Th2 cells, promotes B cell class switching to produce IgE in order to further establish sensitization and an allergic response to food.
In addition to Th2 cell activation, naïve T cells own also been shown to differentiate to T helper 9 cells. Th9 cells contribute to the development of the allergic response by secreting IL-9, which further promotes the accumulation of tissue residing mast cells .
Effector Cells (Mast Cells and Basophils)
Tissue residing mast cells and circulating basophils are significant in the allergic process. In the presence of IL-10 and TGF-β, B cells can produce IgA antibodies which are significant in the maintenance of tolerance. Elevated food-specific IgA antibodies are associated with desensitization and the state of sustained unresponsiveness in patients who own oral immunotherapy to food.
The exact mechanism of the facilitation of tolerance by IgA is not known but seems dependent upon the innate immune system [19, 20]. Furthermore, tolerance occurs in the absence of food-specific IgE. In its absence, the effector mast cells and basophils cannot degranulate.
In the presence of IL-4, B cell class switching occurs and food-specific IgE is produced, thereby promoting a state of sensitization and allergy. Antigen food-specific IgE binds to the FcεRI receptors on mast cells and basophils. Upon exposure to antigen, cross-linking of IgE and the IgE receptors happen on the surface of mast cells and basophils resulting in the release of preformed mediators into circulation.
The mediators involved in anaphylaxis include: histamine, tryptase, platelet activating factor, prostaglandins, and leukotrienes .
Histamine is one of the most significant preformed mediators of anaphylaxis. Once released from the activated mast cell or basophil, histamine’s onset of action is rapid (within 5 min); however, it is quickly metabolized (half-life 30 min). In anaphylaxis, histamine acts upon H1 and H2 receptors and stimulation of these receptors leads to vasodilation, increased vascular permeability, increased heart rate, increased cardiac contraction, and increased glandular secretion.
Tryptase, another preformed mediator primarily stored in mast cells, has limited diffusion from an activated mast cell because it is secreted as an athletic proteoglycan complicated .
Tryptase levels peak at 60–90 min after the onset of .
In anaphylaxis, tryptase can cause angioedema by the activation of the contact (kallikrein-kinin) system. Platelet activating factor is a potent mediator of anaphylaxis. It causes bronchoconstriction, increased vascular permeability, chemotaxis, and degranulation of eosinophils and neutrophils.
Prostaglandins are lipid mediators that are released from activated mast cells during anaphylaxis. Basophils do not produce prostaglandin D2 (PGD2), a prostaglandin only produced in mast cells. PGD2 causes bronchoconstriction, peripheral vasodilation, and coronary and pulmonary artery vasoconstriction, acting to recruit basophils, eosinophils, dendritic cells, and Th2 cells and enhance the release of histamine from basophils.
Leukotrienes are also lipid mediators with a slow onset of action. They cause smooth muscle contraction, mucus secretion and cause increase vascular permeability. They are also significant in the recruitment of allergic inflammatory cells and modulating the production of inflammatory cytokines.
The five components of the immune system, the epithelium, innate immune cells, T cells, B cells, and effector cells (mast cells, eosinophils, and basophils), can either promote tolerance to food antigens or sensitization, leading to allergic manifestations.
Genetic and environmental factors can influence the immune system. As more is discovered about these influences, the underlying pathophysiology of IgE-mediated food allergy may be altered to promote tolerance or a state of desensitization (absence of clinical symptoms on exposure to food).
What is nut allergy?
An allergy occurs when your body’s immune system, which normally fights infection, overreacts to a substance called an allergen.
Most allergens are not obviously harmful and they own no effect on people who are not allergic to them. Allergic reactions to allergens can vary from mild to life-threatening.
Both peanuts and tree nuts (for example, walnuts, hazelnuts, almonds, cashews, pecans, Brazils and pistachios) can act as allergens, and can cause an allergic reaction in some people. When you come into contact with something that you are allergic to (an allergen), a group of cells in your body, called mast cells, release a substance called histamine.
Histamine causes the tiny blood vessels in the tissues of your body to leak fluid which causes the tissues to swell. This results in a number of diverse symptoms.
Strictly speaking, peanuts are not nuts, they are legumes, in the same family as peas and beans. Peanuts grow underground whereas other nuts grow on trees. The expression nut in this leaflet can mean either tree nuts or peanuts.
See also the separate leaflets calledAllergies and Food Allergy and Intolerance for more information about allergy in general.
What are the symptoms of a nut allergy?
Both peanuts and tree nuts can cause allergic reactions.
Allergic reactions to nuts can vary from mild to extremely severe, and are sometimes life-threatening. Symptoms often start extremely quickly, within an hour of having come into contact with a nut, and sometimes within minutes. Reactions that take put more than four hours after coming into contact with nuts are unlikely to be an allergy.
Signs and symptoms of a mildallergic reaction can include:
- Your face swelling.
- Feeling sick.
- Colicky pains in your tummy (abdomen).
- Your mouth and lips tingling.
- Nettle rash, or hives (urticaria).
- A feeling of tightness around your throat.
Signs and symptoms of a more severeallergic reaction can include:
- General redness of your skin.
- A quick heart rate.
- Low blood pressure, which can cause you to feel faint or to collapse.
This severe reaction is called anaphylaxis and without quick treatment you would soon become unconscious.
A little number of people die every year as a result of this helpful of severe reaction, generally because they do not obtain treatment quickly enough. If you ponder you are having an anaphylactic reaction you need to call an ambulance straightaway and obtain immediate medical help.
About 1 in 3 people with a nut allergy own an initial reaction to the nut, followed by a second reaction between one and eight hours after the first. This is why it is significant to stay in hospital after an initial anaphylactic reaction.
What causes nut allergy?
If you are allergic to nuts, when you first come into contact with nuts your immune system reacts and prepares to fight.
However, you don’t get any symptoms of a reaction. It is only when you come into contact with nuts for a second time that a full allergic reaction happens. Most children who are allergic to nuts own the symptoms of an allergic reaction when they appear to be exposed to nuts for the first time. However, this is probably not their first exposure, but their second. They may already own come into contact with nuts through their mom, through either of the following:
- Whilst they were in the womb (uterus).
- Through breast milk if they were breast-fed.
Most people with nut allergy react after contact with little amounts (less than one nut) and some people may react to trace amounts.
This means that you don’t always own to eat nuts to own a reaction. A few people are so sensitive to nut allergens that a tiny quantity on their lips, or even standing next to someone eating peanuts, can be enough to start a reaction.
There are lots of diverse allergens but nuts cause some of the strongest and most severe reactions. Doctors don’t yet know why this is.
How common is nut allergy and who gets it?
In the UK about 2 in 100 children and about 1 in 200 adults own an allergy to nuts.
The number of people with peanut allergy is growing.
Nut allergy is the most common type of severe food allergy. It often starts when children are extremely young. Most first allergic reactions take put when a kid is between 14 months and two years ancient. Unlike other food allergies such as milk allergy, nut allergy is something that you are unlikely to grow out of. Only about 1 in 5 people with a nut allergy will grow out of it, and these tend to be the people who own mild reactions.
If you own what is called atopy, or if atopy runs in your family, then you are more at risk of developing an allergy to nuts.
Atopy is the name for a group of allergic conditions that include hay fever, asthma and eczema. In specific, children who own eczema are more likely to develop a nut allergy. If you own an allergy to peanuts then you may also react to tree nuts.
What are the treatment options for nut allergy?
Avoid nuts wherever possible
Preventing an allergic reaction from happening in the first put is a key part of living with a nut allergy. So, study to recognise foods that may contain nuts and avoid them. You may be referred to a dietician to assist with this. Advice may include:
1. Check the ingredients:
- Always check food labels, even for products you know, as ingredients can change.
- Nuts and nut oils are used as ingredients in a wide range of foods.
Take care with biscuits, cakes, pastries, desserts, ice cream, breakfast cereals, cereal bars, nut butters and spreads, confectionery, vegetarian dishes and salad dressings.
- Chinese, Thai and Indonesian dishes often use nuts and nut oil, particularly peanuts or peanut oil.
- Avoiding whole nuts is relatively simple. What is more hard is avoiding nuts in processed foods. Nuts are not always obviously listed on ingredient labels. For example, peanut can be listed as groundnut, ground nut, monkey nut, mixed nuts, peanut butter, peanut oil, arachis oil and groundnut oil.
- Get a list of nut-free foods from your local supermarket.
Take care when you are not preparing your food:
- When eating out, enquire staff which foods contain nuts and the risk of contamination of other foods. If possible, speak to the chef, not the waiter or waitress.
- Do not eat anything you are unsure about.
- If friends or family prepare food for you, make certain they know what you can’t eat.
- Avoid eating foods at buffets or from delicatessens or bakeries where it is simple for food to be contaminated by touching other foods containing nuts.
- If your kid has an allergy to nuts then make certain that they do not share food with other children at parties and other group events. Take food for them.
Principles of treatment
It is unlikely that you will always be capable to avoid contact with nuts and you may be accidentally exposed to nuts at any time.
So, be prepared:
1. Make certain that you, and others around you love your friends and family, know that you are allergic to nuts and what to do if an allergic reaction starts:
- If your kid has a nut allergy then make certain that anyone else who looks after your kid knows about it and knows what to do if a reaction starts. For example, nursery staff, babysitters, teachers and other parents.
Your doctor — either your GP or a hospital doctor with special training in children’s medical care (a paediatrician) — will be capable to record a care plan. This care plan will tell anyone looking after your kid what they should do if the kid has an allergic reaction.
- You should (or your kid should if they own an allergy) wear a medical emergency identification bracelet or equivalent that tells other people about the allergy.
2. If an allergic reaction starts, get the correct treatment quickly:
- Mild reactions can be treated with an antihistamine medicine.
- Adrenaline (epinephrine) is given by an injection so that it can work straightaway.
If you own a severe reaction to nuts you will be given an adrenaline (epinephrine) injection (like a pen). You will carry this with you every the time. Brand names include EpiPen®, Emerade® and Jext®.
- If you own a severe allergy you must carry your adrenaline (epinephrine) injection with you at every times. Some people hold adrenaline (epinephrine) in the places where they spend most of their time. For example, they hold it at home, at school or at work.
Numerous people carry two injections ‘just in case’.
- It is vitally significant that if an allergic reaction starts you get treatment as quickly as possible. The sooner your reaction is treated, the better.
- More serious reactions are treated with adrenaline (epinephrine) which, if given quickly, can reverse the symptoms of the reaction.
- These adrenaline (epinephrine) injections come in diverse doses for adults and children.
They work by injecting adrenaline (epinephrine) into your thigh muscle when you press a button or jab it against your skin.
- Check the expiry date on the adrenaline (epinephrine) regularly. If it passes the expiry date, get a new one. Also, make certain that you know how to use it properly. Your family and friends should know how to use it too, in case you are not capable to.
Know what to do if you own an allergic reaction
1. Mild reactions:
- Take an antihistamine tablet as soon as possible. You can purchase these at pharmacies or obtain them on prescription.
Antihistamines block the action of histamine, the chemical released into your body during an allergic reaction. They generally take 15-30 minutes to start working.
- If your reaction gets worse then get medical assist straightaway.
2. Severe (anaphylactic) reactions:
- If you own an adrenaline (epinephrine) injection pen, use it.
- If you own asthma and own an inhaler, use it.
- In the ambulance or at the hospital you may also be given oxygen to assist your breathing, steroids to reduce any inflammation, and antihistamines to counter the allergic reaction.
- Get assist and call an ambulance straightaway.
If possible, always own someone with you at every times if you own a reaction, even if you need to go to the toilet. For example, do this even if you feel ill or are being ill (vomiting).
- Some people may need more intensive treatment if the reaction is extremely severe.
Mild symptoms can final up to an hour but severe symptoms can final longer. You will need to stay in hospital until your doctor is certain you own fully recovered.
Immunotherapy (desensitisation) is a treatment where you are given tiny amounts of the allergen which is then extremely gradually increased over time.
The purpose is to build up tolerance to the allergen. This treatment has been used with some success to treat pollen and insect poison (venom) allergies. But, at present it is not widely used to treat food allergy such as nut allergy because of the risk of anaphylaxis. However, some studies own shown some promising results, and the technique is used at some extremely specialist centres.