Epidemiology

In the United States, food allergies affect almost 2 % of the general population. Over the past two decades, the prevalence and severity of food allergies as increased in this country. Among all food allergies, peanut allergy is the third most prevalent allergy occurring among young children and the most common food allergy in older children, adolescents and adults, with the median age of first allergic reaction being 14 months. Among children who have peanut allergies, approximately 75% will experience a reaction on their first exposure with the potential outcome being severe or fatal. There is an estimated 2 fold increase in reported peanut allergies among Westernized nations, with the most likely culprits being peanuts used as a source of protein in health foods, the popularity of vegetarianism and the increased used of prepared foods. In 2002, the prevalence of peanut allergy among children under the age of 5 was 0.8% as compared to 1997 when the prevalence was 0.4%; however, the prevalence among adults has remained constant over this five-year period. The reasons why peanut allergies are increasing are unknown.

Pathogenesis

Food allergies are mostly attributed to IgE mediated and or cell mediated mechanisms. When exposed to a particular allergen, food specific IgE antibodies are formed which bind to the Fce receptors on mast cells, basophils, macrophages and dendritic cells. Mediators are released as the allergens reach the IgE antibodies and the result is the production of vasodilatation, smooth muscle contraction, and mucus secretion. Mast cells and macrophages release cytokines that attract and activate other cells which produces an inflammatory response that is more prolonged. Systems that are affected during an acute IgE mediated reaction include the skin, gastrointestinal tract, respiratory tract and cardiovascular system. Lymphocytes, more specifically food allergen-specific T cells, can also play a role by secreting cytokines that lead to a delayed inflammatory response affecting the skin, GI or respiratory tract. Infants and children are more susceptible to food allergies because of the immaturity of the immune system.

The allergenic proteins in peanut allergies are vicilin (Ara h1) and conglutin (Ara h2). Exposure and sensitization to these proteins occur early in life with passage through maternal breast milk, and thereafter introduction of solid foods. Mixed IgE cellular responses can also lead to chronic disorders such as atopic dermatitis, asthma, and allergic eosinophilic gastroenteritis.

Clinical Manifestations

Skin

• Uticaria
• Angioedema
• Flushing
• Erythmatous rash

• Shortness of breath
• Rhinitis
• Laryngeal edema
• Nasal congestion
• Prutritis
• Sneezing
• Dyspnea
• Wheezing
• Food induced pulmonary hemosiderosis

• Oral prurits
• Early satiety
• Nausea
• Vomiting
• Diarrhea
• Abdominal pain

• Dysrhythmias
• Hypotension
• Loss of consciousness

Diagnosis

The diagnosis of a peanut allergy is dependent on a careful history, skin tests, in vitro measurement of food specific IgE, and appropriate exclusion diet. In order to establish a diagnosis it is important to determine the time interval between ingestion and the development of symptoms, the type of symptoms manifested, reproducible symptoms on other occasions of ingestion, and time interval from last reaction. A prick skin test and radioallergosorbent test are used to illicit IgE sensitization, with a negative skin test excluding an IgE mediated food allergy. Food challenges are also an appropriate way to diagnosis food allergies. Prior to initiating a food challenge, the peanut allergen must be eliminated from the diet for 10-14 days for IgE mediated food allergy and up to 8 weeks for cell-mediated allergic reaction. If symptoms remain unchanged and appropriate elimination diets have been utilized, a peanut allergy is not likely responsible for the child’s clinical presentation.

Treatment

Although the complete elimination of peanuts from the diet can be difficult, identification and elimination of foods are the most appropriate treatment for peanut allergy. Injectable epinephrine and a written emergency plan in case of accidental ingestion should be given to children with asthma and IgE mediated food allergies. Patients should be aware of the biphasic nature of the reaction and they should contact their physician after the emergency treatment is completed. Current recommendations include promoting breast-feeding with the exclusion of peanut and nut products from mom’s diet and delay the introduction of peanut and tree nuts from a child’s diet until the age of three.
The patients should have a Medic-Alert Bracelet or Necklace
 
 
 
 

References
 

Adkinson: Middleton’s Allergy: Principles and Practice, 6th ed., Copyright 2003 Mosby, Inc.  Fleisher, DM et al. The natural Progression of Peanut allergy: Resolution and the possible Recurrence. 2003; 112 (1): 183-189 Marx: Rosen’s Emergency Medicine: Concepts and Clinical Practice, 5th ed., Copyright 2002 Mosby, Inc.  Nowak-Wegrzyn, A et al. Food Allergy Therapy. Immunology and Allergy Clinics of North America. 2004; 24(4): 702-725. Perry, T. et al. Distribution of Peanut Allergen in the Environment. Journal of Allergy and Clinical Immunology. 2004; 113( 5):973-976 Sampson, H., Leung, D. Adverse Reactions to Foods. Behrman: Nelson Textbook of Pediatrics, 17the ed., Copyright 2004 Elsevier.  Sicherer, SH et al. Prevalence of Peanut and Tree Nut Allergy in the United States Determined by Means of a Random Digital Dial Telephone Survey: A 5-year Follow-up Study. Journal of Allergy and Clinical Immunology. 2003; 112 (6): 1203-1207. Leaung D.Y.M.et al. Effect of Anti-IgE Therapy in Peanut Allergy NEJM March 13, 2003  Lack G etal. Factors Associated with the Development of Peanut Allergy in Children NEJM March 13 2003 Behind the Research: Studying Peanut Anaphylaxis. NEJM March 13, 2003