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Food allergy is estimated to affect 6 of young children and 3-4 of adults in westernized countries. The most common causes of food allergy in children are cow's milk, eggs, peanuts, tree nuts and sesame seeds. While the majority of those allergic to milk, egg, wheat or soy, outgrow their allergies by school age, those allergic to nuts, peanuts, seeds or seafood usually have persistent allergy. In Australia 1.9% of infants and young children are estimated to have peanut allergy. The prevalence of peanut allergy in childhood in other countries varies between 0.5% and 1.8%. Peanut allergy resolves for approximately 20% of young children by school age and degenerates for approximately 20% of young children over time. Recent studies from the UK and USA suggest that peanut allergy has doubled in the last five years. Admissions to hospital with anaphylaxis (which have been mainly attributed to food allergy) have also doubled in the last decade in both Australia and the UK, particularly in young children. Ambulance Services have also reported a record number of call outs for anaphylaxis with a 33% increase since 2001 in Australia. However, anaphylaxis mortality rates remain low and stable, despite increasing anaphylaxis prevalence. In January 1997 through December 2005 there were 112 fatalities from anaphylaxis in Australia, 7 (6.3%) were attributed to food anaphylaxis and peanuts were the offending allergen in 3 cases.
Peanut allergy is a severe, usually rapid, allergic reaction to the ingestion of peanuts or peanut products. It is caused by an overreaction of the body's immune system to peanut protein. When the body detects the peanut protein it stimulates the immune system to produce Immunoglobulin E (IgE) antibodies. These antibodies then bind mast cells, causing them to release histamine and other mediator substances that cause inflammation in tissues of the body, such as the lungs causing constriction of bronchioles, also known as bronchospasm. Peanut allergy can be diagnosed by either a blood test or skin prick test. A blood test (called a radioallergosorbent or RAST test) can measure your immune system's response to peanuts by measuring the concentration of IgE antibodies. The skin prick test involves the piercing of the skin and exposure to small amounts of the proteins found in peanuts intradermally to see the skins response. If the patient is allergic to peanuts, a hive will develop at the test location on the skin. However, these tests don't indicate the severity of the allergic reaction. Risk factors that are associated with peanut allergy include age, environmental exposure through the food we eat, maternal exposure during pregnancy and lactation, use of skin creams containing peanut oil, and also the presence of atopy which is an allergic hypersensitivity affecting parts of the body not in direct contact with the allergen eg. Atopic dermatitis. Food allergy is also at least in part genetically determined. Peanut allergy is about tenfold more likely to occur in a child with a sibling who is allergic to peanuts compared to the general population risk; however, specific genes have not yet been identified. Recent epidemiological studies also identify potential environmental influences on immune function favouring allergic responses, including reduced exposures to bacteria and infections, a rise in consumption of omega-6 and decreased consumption of omega-3 polyunsaturated fatty acids, reduced dietary antioxidants, and excess or deficiency of vitamin D.
The allergic reaction to peanut occurs soon after exposure usually through ingestion. Typical immediate allergic reactions include the development of hives (itchy bumps) on the face or body; blotching around the mouth, acute urticaria, angioedema, skin rash ; immediate runny nose, sneezing and itchy-watery eyes; coughing; coughing, choking or gagging; wheezing, voice changes trouble breathing; and abdominal pain, vomiting and diarrhoea. The child's behaviour may also change during an allergic reaction. Although allergic reactions are usually mild to moderate in severity and usually terminate spontaneously or after the administration of an antihistamine, severe reactions known as anaphylaxis can occur. Anaphylaxis is a type I hypersensitivity response that results from the release of histamine, leukotrienes, heparin, PGD2, platelet activating factor, nerve growth factor and some interleukins from degranulated mast cells. Degranulation of mast cells is caused by the binding of IgE antibodies to its antigen. Mast cells are large cells found in particularly high concentrations in vascularized connective tissues just beneath epithelial surfaces, including the submucosal tissues of the gastrointestinal and respiratory tracts, and the dermis that lies just below the surface of the skin. Histamine that is released during an allergic reaction act via H1 receptors to cause dilation of blood vessels and increased vascular permeability, and contraction of smooth muscle in the bronchi and bronchioles. Anaphylaxis is associated with systemic vasodilation which results in hypotension and dysrhythmia. It is also associated with severe bronchoconstriction to the point where the individual is unable to breathe. Approximately 80% of anaphylactic reactions occur on first known ingestion.
Peanuts are widely used in processed western foods and oriental cooking. This poses significant problems for people with severe peanut allergy. Laws require that any product, which contains peanuts, must be labelled to that effect, so the labels of all foods can be checked before purchase. Some manufacturers will also label their products as possibly containing traces of nuts, or with similar phrases such as manufactured on the same machinery. This labelling is not a legal requirement but may be added by the manufacturer. In such situations, multiple products may be made on the same production line and cross contamination with traces of nuts can occur. The risk of having a severe allergic reaction from cross contamination is greatest for those with a history of severe food allergies. Occasionally nut products or oils have been used as unlabelled ingredients in cosmetics such as massage oils and even toothpaste and moisturisers eg. Arachnis oil is the scientific term for peanut. The increasing consumption of take away food has also lead to a rise in anaphylactic episodes as not enough caution is taken when eating foods prepared outside the family home or they are not alerting whoever is cooking their food of their allergy so that the right precautions are taken to minimise contamination with peanuts or use of peanut oil in cooking.
Allergen specific therapies
Currently, the only proven therapy for the treatment of peanut allergy, and food allergy in general, is strict avoidance of the peanut-containing foods and education of patients to recognize and treat allergic reactions caused by accidental exposure. Oral immunotherapy (OIT) continues to be the most highly investigated therapy. OIT offers a promising therapeutic option for peanut allergy. OIT is based on the concept that contact of an antigen with the oral mucosa/gut-associated lymphoid system leads to the induction of oral tolerance. In OIT protocols allergic patients are desensitized to the allergic food, which protects them against reactions caused by accidental Ingestions. Patients are started on minute amounts of allergen orally and over time are given increasing quantities of allergen in an attempt to develop generalized tolerance. OIT also has the potential to induce tolerance so that an allergic food can be reintroduced into the diet on a regular basis without fear of reaction. Given that during OIT an allergic patient is given an allergen that could potentially cause a serious reaction, the safety of OIT is a particular concern. To date, only a few uncontrolled trials, mostly case reports, have been reported using OIT in patients with peanut allergy. A study performed by Jones et al treated 29 patients suffering with peanut allergy. By 6 months, titrated skin prick tests and activation of basophils significantly decreased and peanut-specific IgE levels decreased by 12 to 18 months. Analysis of safety data revealed that allergic reactions to treatment were more common on the escalation days. Further studies are needed in larger populations of children with peanut allergy to ensure the safety of this protocol. Studies are underway to determine the efficacy of peanut OIT and its duration of effect. The question remains whether peanut OIT will simply lead to desensitization or to true immune tolerance. If only desensitization is achieved, patients who are being treated with peanut OIT and who have an accidental ingestion will likely be protected from an allergic reaction. However, similar to drug desensitization, if peanut OIT only causes desensitization and is discontinued, the patient would be at risk for reactions if accidental ingestions occur. If immune tolerance is achieved by means of peanut OIT, then patients might be able to discontinue therapy and reintroduce peanut into their diet without fear of reaction. Even if peanut OIT only results in desensitization and not immune tolerance, it might offer protection for those who might have accidental peanut ingestions. Until appropriate safety, dosing regimens, and efficacy studies are completed routine treatment using OIT should not be used.
Therapies using engineered proteins to avoid activating mast cells during specific allergen immunotherapy are planning clinical studies in humans. It has identified IgE binding sites on proteins and has been able to mutate the sites to ablate IgE binding, while preserving the protein's ability to stimulate T cells.
Another promising strategy is peptide immunotherapy. It aims to create a vaccine composed of numerous small peptides that span the sequence of native allergenic proteins with sequential overlap. This strategy presents T cell epitopes but avoids cross-linking of IgE. Preliminary studies in a murine model show promise, but the practical problem of validating the stability and uniformity of a complex peptide vaccine has stalled development.
Another promising approach is the utilization of bacterial plasmid DNA encoding an allergen for immunotherapy. This approach goes on the hypothesis that endogenously produced antigen would not stimulate an allergic immune response. However, there have been no published reports of successful plasmid DNA-based immunotherapy reversing established peanut or other food allergy.
Non- Allergen specific therapies
A nonspecific immunomodulatory approach, anti-IgE therapy has been investigated for the treatment of peanut allergy in human beings. A double-blind placebo controlled dose-ranging clinical trial of a humanized monoclonal anti-IgE, TNX-901, was carried out in 84 volunteers with peanut allergy. TNX- 901 significantly increased the threshold of reactivity to peanut by oral food challenge from 178 mg to 2.8 g. However, the therapeutic response was not uniform, approximately 25% of subjects experienced no change in their threshold of reactivity and another 25% tolerated at least 10 g. It is not clear as to why differences occurred. As IgE antibodies are centrally involved in acute allergic reactions it is thought that anti-IgE blocking antibodies may interfere with the allergic immune mechanisms, not only preventing the IgE-triggered mast cell degranulation but also preventing facilitated antigen presentation that maintains the ongoing allergic immune response. This raises the question whether therapeutic use of anti-IgE in peanut allergy may lead to long-term resolution of this allergy by interrupting the IgE dependent pro-allergic feedback loop caused by facilitated antigen presentation. However, additional studies of anti-IgE therapy are needed to confirm its level of protection and utility in peanut allergy.
A nine herb preparation designated Food Allergy Herbal Formula (FAHF)-2 has been developed by Li and colleagues which has been shown to completely block anaphylactic symptoms in the peanut-sensitized murine model of peanut allergy. Anaphylactic symptoms occurred with each peanut challenge in placebo-treated mice, whereas the FAHF-2-treated mice were fully protected until the sixth month, when retreatment afforded renewed protection. Compared to controls, the FAHF-2-treated mice had significantly lower plasma levels of peanut specific IgE following therapy, and splenocytes cultured in vitro with peanut protein produced less IL-4, IL-5, and IL-13 and more IFN-γ.
We are only beginning to recognize potential genetic, environmental, and immunologic influences on the development and progression of peanut allergy and the occurrence of peanut allergy is increasing at an alarming rate. Recent studies have provided insights for improved diagnosis, management and patient education and also have increased our understanding of the immune mechanisms underlying peanut allergic responses and how tolerance may be abolished or avoided to result in an allergic response. Although there seems to be a genetic disposition toward atopy and peanut allergy, the explanations for the rise in prevalence of peanut allergy must lie in environmental factors that presumably include global influences on immune responses. Understanding of these risk factors will lead toward improved diagnosis and prevention. Clinical trials are now or soon will be investigating promising immunotherapeutic approaches to peanut allergy such as OIT, anti-IgE, Chinese herbal medicine, and engineered recombinant proteins. Although much remains to be learned about the underlying immunologic effects of these various therapeutic approaches, it is hoped that at least one will provide the means to treat peanut allergy.