| Background |
Patients with atopic allergic diseases such as atopic asthma, atopic dermatitis, and hay fever have been shown to exhibit increased total immunoglobulin E (IgE) levels in blood. In general, elevated levels of IgE indicate an increased probability of an IgE-mediated hypersensitivity, responsible for allergic reactions. Parasitic infestations such as hookworm, and certain clinical disorders including aspergillosis, have also been demonstrated to cause high levels of IgE. Decreased levels of IgE are found in cases of hypogammaglobulinemia, autoimmune diseases, ulcerative colitis, hepatitis, cancer, and malaria. Cord blood or serum IgE levels may have prognostic value in assessing the risk of future allergic conditions in children. Certain groups of white blood cells, including basophils and tissue mast cells, have membrane receptors for the IgE molecule. These target cells, through a series of complex reactions, form a combination of a specific allergen with antibody-sensitized basophils such as histamine, into the blood stream. As a result of these biochemical mediators, there is a constriction of smooth muscles, dilation of small blood vessels, activation of blood platelets, and irritation of skin nerve endings characteristic of allergic reactions.Typical clinical symptoms of immediate hypersensitivity are inflammation and itching in a skin reaction, or congestion in a bronchial reaction. The IgE serum concentration in a patient is dependent on both the extent of the allergic reaction and the number of different allergens to which patient is sensitized. Nonallergic normal individuals have IgE concentrations that vary widely and increase steadily during childhood, reaching their highest levels at age 15 to 20, and thereafter remaining constant until about age 60, when they slowly decline. |
