A variety of tests now exist to diagnose allergic conditions; these include skin and blood testing. Blood tests (such as ELISAs) can be qualitative or quantitative for the detecting of IgE, IgM, IgA, or IgG specific mediated responses to known allergens. AlerCHEK, Inc. ELISA based testing allows for the accurate qualitative analysis of hypersensitive-driven responses to known allergens of interest. ALerCHEK uses its own unique proprietary technology based on colloidal gold which substantially optimizes the three dimensional expression of allergens. This ensures a high degree of sensitivity and reduces the number of false positives and false negative test results.
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- Human Allergen Specific IgE
IgE test, IgE allergy blood testing, human allergen IgE
- Human Allergen Specific IgG
IgG testing kit, IgG allergy blood testing, human allergen IgG
- Human Allergen Specific IgA
IgA test, IgA allergy blood testing, human allergen IgA
- Human Allergen Specific IgM I
gM test, IgA allergy blood testing, human allergen IgM
- Human Total IgE
Immunoglobulin E, immunoglobulin e IgE levels, IgE test
- Human Total IgM
Immunoglobulin M, immunoglobulin m IgM levels, IgM test
- Human Total IgG
Immunoglobulin G, immunoglobulin g IgG levels, IgG test
- Human Total IgA
Immunoglobulin A, immunoglobulin a IgA levels, IgA test
- Purified T-Cell Recall Antigen
Candida allbicans, delayed type hypersensitivity (DTH) assay
Allergy Testing and understanding of Allergic Reactions
Allergyis an immunological response often referred to as “atopy”. Hypersensitivity refers to an inappropriate or harmful immune-mediated response to an allergen. Allergens fall into groups of proteins or proteases such as grasses, pollens, animal dander, house dust mites, and food to list a few. Exposure to allergens generally occurs at mucosal membranes in the respiratory and digestive tracts. The initial exposure to allergen is called sensitization and does not usually result in allergy symptoms. Subsequent secondary exposures to the same allergen allows for an immediate allergic response. Hypersensitivities are classified based on the time required to initiate an immune response, mediators, and mechanism of tissue damage:
- Type I: Immediate hypersensitivity-occurs within minutes to a few hours after secondary antigen exposure (typically antibody mediated). Most allergies are Type I, in which IgE is produced in response to an antigen (allergen). Most IgE is present on mast cell membranes in the connective tissues around the respiratory and digestive tracts.
- Type II: Delayed-occurs within 48-72 hours typically after secondary antigen exposure (typically T cell mediated). Type II hypersensitivity is mediated by IgG antibodies and on occasion, IgM antibodies. This hypersensitivity results when antibody binds to cell surface antigen, creating an antigen-antibody complex that activates a complement cascade. Classical complement activation by IgG releases inflammation-promoting anaphylatoxins and leads to the formation of membrane attack and lysis of the antibody-coated cell and against the body’s own cells. Most food allergies are IgG-mediated.
- Type III: Delayed hypersensitive response also occurs within 48-72 hours after antigen exposure. This reaction occurs when IgG or IgM antibody-antigen complexes get trapped in capillaries. The antibodies are able to recruit inflammatory mediators resulting in vasculitits and tissue death. Some examples of type III reactions include autoimmune disorders such as Systemic Lupus Erythematosus (SLE), rheumatoid arthritis, and serum sickness.
- Type IV: Delayed hypersensitivity allergic reactions are cellular processes in which cell-mediated responses occur within 24-48 hours after antigen exposure. Antigen presenting cells stimulate CD4+ T cells to activate other inflammatory cells, damaging presenting cells and nearby tissues.
Mild allergic responses are most common among the human population and cause symptoms such as sneezing, itching of eyes and skin, rashes, hives, indigestion, diarrhea, or difficulty breathing. Allergies can play a major role in conditions such as asthma. Severe allergies to environmental and dietary allergens or to medication may result in life-threatening anaphylactic reactions and potentially death.
Allergic responses can be divided into two phases. The first is an acute response that occurs immediately after exposure to an allergen. This phase can either subside or progress into a ‘late phase reaction’ which can substantially prolong the symptoms of a response, and result in tissue damage. In the early stages of an allergic response, a type I hypersensitivity reaction against an allergen causes a response by T helper 2 (TH2) lymphocytes which produce a cytokine called interleukin 4 (IL-4). TH2 cells interact with B cells which have the role of producing antibodies. In the presence of IL-4, B cells begin the production of large amounts of IgE antibodies. Secreted IgE circulates in the blood and binds to an IgE-specific receptor on the surface of other immune cells known as mast cells and basophils which induce an inflammatory response. IgE-coated cells, at this stage, are sensitized to the allergen. If later exposure to the same allergen occurs, the allergen can bind to IgE-coated mast cells or basophils, activating the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, releasing histamines and other inflammatory mediators into the surrounding tissue causing systemic effects such as vasodilation, bronchoconstriction, mucous secretion, nerve stimulation, and smooth muscle contraction.
Risk factors for allergy development can be determined by the host’s heredity along with sex, race, age and environmental exposures. Genetic factors cannot explain all cases of allergic responses. Environmental factors such as exposure to infectious diseases during early childhood, pollution, allergen levels, and dietary changes also contribute allergic disorders.
The risk of allergic senstitization and the development of allergies vary with age, with young children most at risk. Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years of age. Overall, boys have a higher risk of developing allergies than girls. However, certain diseases, such as asthma, in young adults are more likely to conflict females. Differences in sex decrease in adulthood. Racial factors have been more difficult to separate from environmental influences and changes due to migration. Further research has suggested that different genetic loci are responsible for asthma, primarily in people of Caucasian, Hispanic, Asian, and African origins.
Signs and Symptoms
Many allergens such as dust or pollen are airborne particles. In these cases, allergens are introduced to areas in contact with air such as the eyes, skin, nose, and lungs. Inhaled allergens may also lead to asthmatic symptoms. Allergic responses may also result from foods, insect stings, medications, soaps and detergents. The most common food allergies are: Cow’s milk, Hen’s eggs, Fish, Peanuts, Shellfish, Tree Nuts, Soybeans, and Wheat.
Certain medications including antibiotics and insect bites and/or stings produce a systemic allergic response that is also called anaphylaxis, affecting multiple organ systems including the digestive system, respiratory, and circulatory system. Depending on the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered instantly or with a delayed onset. Severe reactions usually require injections of epinephrine. Substances that come into contact with skin, such as latex, are also common causes of allergic responses.
|Type I: Immediate-IgE Mediated Response
||Type II & III – Delayed Reactions (IgG-mediated primarily)
||Irritable Bowel Syndrome
||Ulcers and malabsorbtion
||Dark circles under the eyes
Routes of Entry/Contact with Allergens
A variety of tests now exist to diagnose allergic conditions; these include skin and blood testing.
Skin testing (known as puncture testing and prick testing) involves a series of pin puncture or pricks made into the patient’s skin to asses for the presence of allergen specific IgE antibodies. Small amounts of suspected allergens and/or extracts are introduced to sites on the skin, and at times, injected intradermally. If a patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes.
Various blood testing methods are also available for detecting allergies to specific substances. These include radiometric and colormetric immunoassays. A number of laboratories have set up ELISA (enzyme-linked Immunoassay) to test the presence of antibodies for particular allergen antigens. Blood tests can be qualitative or quantitative for the detecting on IgE, IgM, IgA, or IgG specific mediated responses to known allergens.
Testing Allergic Responses
Treatments for allergies include allergen avoidance, use of anti-histamines, steroids or other oral medications, immunotherapy to desensitize the response to allergen, and targeted therapies. Traditionally treatment and management of allergies involved avoidance of allergen in question. While this approach may help to reduce the symptoms, it is difficult to achieve for those allergens to pollens and other air-borne sources. Strict avoidance is often used in managing food allergies.
Several antagonistic drugs are used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes. These include antihistamines, cortisones, dexamethasone, hydrocortisone, epinephrine (adrenaline), theophylline, and cromolyn sodium. These drugs help to alleviate the symptoms of allergies and are essential in the recovery of acute anaphylaxis, but are not effective in chronic treatment of allergic disorders.
Immunotherapy, also known as desensitization or hyposensitization, is a treatment in which the patient in gradually vaccinated with progressively larger doses of the diagnosed allergen. This can either reduce the severity of reaction or eliminate hypersensitivity altogether. It relies on progressive IgG skewing to block excessive IgE production. The person builds up immunity to the increasing allergen. Studies have demonstrated the long-term efficiency and the preventive effects of immunotherapy in reducing the development of new allergies. A second form of immunotherapy is intravenous injections of monoclonal anti-IgE antibodies. The bind to free and B cell associated IgE, signaling their destruction. It is not recommended for the treatment of food allergies but has been very effective in treating several types of atopy. The third type is Sublingual immunotherapy, which is administered orally and takes advantage of oral immune tolerance to non-pathogenic allergens such as foods and resident bacteria. This is more popular in Europe but gaining support in America among allergen specialists.