True allergic reaction (IgE mediated) to food must be differentiated from food intolerance, which is rarely multisystemic, not necessarily found among atopic patients, with no positive skin prick tests or in vitro responses (RAST). A nonallergic reaction that typifies food intolerance would be an acute gastrointestinal response in a lactose-intolerant individual.. This patients does not have the enzyme lactase and, therefore, cannot breakdown sugar lactose in milk and other foods into glucose and galactose. Profound diarrhea or vomiting usually results without any other system involved (respiratory or skin, for example). Food avoidance is the treatment of choice, as it is with food allergy, and over time, food intolerance may resolve. Lactaid is a brand of milk in which the enzyme lactase is added so that the milk may be consumed.
Approximately 20 percent of the U.S. population may perceive food as causative reaction in food allergies, whereas the true prevalence of food allergies is approximately 1 percent. Food allergies are usually found in individuals with a strong personal and family history of allergies. Atopic responses are associated with many foods. In children under the age of 2, 90 percent of the incriminating foods are eggs, milk, legumes (such as peanuts, which are not nuts), and soy. In adult. fish, shellfish, fruits, and tree nuts might be added to the list.
Diagnosis of food allergy and intolerance
The gold standard of food allergy testing is the double-blinded, placebo-controlled food challenge, which will establish whether the patient is truly allergic to a specific food. Because this method of testing for food allergies is time consuming, expensive, and potentially dangerous, in vivo testing is usually performed in food allergy centers. Occacionally, straight food challenges may be tried when the chances of reactions are minimal and the serum IgE (radioallergosorbent test, or RAST) specific for the allergen is low or negative.
FOOD ALLERGY AND INTOLERANCE
Perhaps of all allergic reactions, the public, clinicians, and medical personnel misunderstand food allergy most. as little as 1 percent of the U.S. population has true food allergies compared with 20 percent who are perceived to have them. True food allergy is a typical, and sometimes catastrophic, type I, IgE-mediated reaction, which preferably must be proven by in vitro or in vivo testing.
A major topic of current research has revolved around airway changes in the chronic asthmatic. This process, known as remodeling, is believed to result in irreversible changes in the lung. McMillan and Lloyd induced acute pulmonary eosinophilia and bronchial hyperactivity in mice using multiple allergen challenges. They subsequently induced a chronic phase in a subset of mice using Ova challenge showed significant changes in Ova-challenged mice. Compared with the acutely challenged mice, the Ova group showed deposition of collagen as well as airway smooth muscle and goblet cell hyperplasia. Cytokine profiles in the chronic phase revealed increases of IL-4, transforming growth factor beta 1 (TGF-β1). and IFN-γ. These findings strongly support the concept of airway remodeling and reveal a dual TH1 and TH2 cytokine profile in the chronic phase of asthma.
Treatment is multifactorial. Environmental measures to eliminate allergen exposure should always be attempted. Inhaled corticosteroids remain the mainstay of medical treatment as they down-regulate multiple inflammatory reactions in the lungs. Other adjuncts such as leukotriene receptor antagonists modify significant mediators of allergic inflammation present in asthmatic airways. Newer treatments include monoclonal antibodies directed against IgE (anti-IgE therapy), which have shown some success in decreasing asthma symptoms and the need for oral or inhaled corticosteroids.
Immunology of asthma
From a histopathological standpoint, the inflammation in allergic asthma involves the entire thickness of the airway. Findings include generalized edema, denudation of the epithelium, subbasement membrane thickening, and smooth muscle and mucous gland hyperthropy. This pocess begin when dendritic cells, a subset of antigen-presenting cells found in the lung tissue, process inhaled antigens and present them to T lymphocytes through the interaction of the receptor molecule CD28 on T cells and its ligand CD80 on dendritic cells. This interactions result in T lymphocyte development down the TH2 pathway. TH2 lymphocytes are characterized by release of a family of proinflammatory cytokines, including IL-3, IL-4, IL-5, IL-13, tumor necrosis factor-α (TNF-α), and granulocyte-macrophage colony-stimulating factor. These cytokines promote development, activation, and survival of eosinophils. In addition, IL-4, IL-5, IL-13 and TNF-α activate endothelial cell adhesion proteins, ICAM-1 and VCAM-1, which assist inflammatory cell movement from blood vessels into the airway. IL-4 and IL-13 are key stimuli of B cells for antigen-specific IgE production, which initiates the allergic cascade. as a whole, these complex immunological processes lead to the pathologic processes that characterize asthma.