On the other hand, simple organic substances are more commonly known to cause delayed reactions. An individual may be exposed to these allergens through inhalation, ingestion, injection, or skin contact. (Porth, 2002)
The classifications of hypersensitivity are not dependent on severity, but the type of cells, and location of tissues that is affected. Hypersensitivity reactions are classified into four types: type I (mediated by IgE), type II (tissue-specific), type III (immune-complex mediated), and type IV (cell-mediated) (Holmes, 2003). The first three types are mediated by antibodies, and the fourth type is mediated by T-cells, which produce a delayed reaction or onset of symptoms. However, it is seldom that one type occurs in isolation from the other (Nowak & Handford, 2004).
During a hypersensitivity reaction or allergic reaction, an individual is usually prescribed with bronchodilators, steroids, and antihistamines. This paper will discuss type I hypersensitivity or anaphylactic hypersensitivity, as well as the pharmacokinetics and pharmacodynamics of the three agents mentioned above. In addition, Chinese herbal medicines will also be briefly discussed.
This type describes the allergy as the immediate hypersensitivty or anaphylactic hypersensit...
In addition, Chinese herbal medicines will also be briefly discussed.
Type I Hypersensitivity
This type describes the allergy as the immediate hypersensitivty or anaphylactic hypersensitivity. It is mediated by the IgE antibody, which results to mast cell degranulation (Porth, 2003). The most common examples are systemic anaphylaxis, hay fever, allergic rhinitis, eczema, and asthma.
The mucous membranes of the organs are very richly supplied with mast cells that are filled with IgE antibodies, and these mast cells are ideally located to be able to detect the entry of antigens. Upon initial entry, the individual or host will not manifest any symptoms or reactions. However, the cells have already captured and processed the allergen, and the antigen has then bound with IgE on mast cells, which have caused the cells to degranulate. These granules then spread into the circulation and binds with the mast cells throughout the body. Subsequently, the host is ready for the next contact with the allergen. (Nowak & Handford, 2004)
Now during the second exposure, the mast cells are activated, causing the release of mediators, which then result to the immediate responses of the immune system, and this response is mostly cause by the release of preformed histamines (Ewan, 1998; Nowak & Handford, 2004).
Kay (2001) gave a concise aetiology of acute allergy. She summarized that immediate hypersensitivity is brought about by the release of preformed granule-associated mediators, membrane derived lipids, cytokines, and chemokines when an allergen interacts with IgE that is bound to mast cells or basophils by the high affinity IgE receptors. In addition, the primary inducers of IgE are interleukin-4 and