Pathophysiology of Urticaria

Urticaria

Urticaria is common and results from mast cell degranulation (type 1 immunologic reaction) in response to antigens, with the release of histamine and other vasoactive mediators, leading to erythema and edema. Of these patients, 70% had idiopathic urticaria (where the antigen is unknown), the remainder had other forms of urticaria. Urticaria, if severe, can also affect the subcutaneous tissue and cause angioedema (swelling of the hands, lips, around the eyes, and although rare, it is important to pay attention to the tongue or larynx). (Davey, 2005)

The process of acute urticaria begins with the binding of antigens to interconnected IgE receptors and then attachment to mast cells or basophils. Furthermore, activation of mast cells and basophils will mediate the release of various inflammatory mediators. Mast cells produce histamine, tryptase, chyme, and cytokines. These substances increase the degranulation ability of mast cells and stimulate increased ELAM and VCAM activity, which triggers migration of lymphocytes and granulocytes to the site of urticarial lesions (Anonymous, 2007).

This event triggers an increase in vascular permeability and causes localized edema known as wheal. The patient feels itching and swelling in the dermal layer of the skin. Acute urticaria can occur systemically if the allergen is absorbed deeper into the skin and reaches the circulation. This condition occurs in contact urticaria, for example urticaria that occurs due to wearing latex gloves, where the latex is absorbed by the skin and enters the bloodstream, causing systemic urticaria.

Acute urticaria can also occur on stimulation of mast cells in the absence of IgE binding to allergens. For example, on exposure to radiocontrast media, where during the radiological process, there will be a change in osmolality in the environment which causes mast cells to degranulate (Anonymous, 2007).

Immunological and non-immunologic factors are able to stimulate mast cells or basophils to release these mediators. In the non-immunologic, cyclic AMP (adenosine mono phosphate) may play an important role in mediator release. Several chemicals such as amines and amide derivatives, drugs such as morphine, codeine, polymyxin, and some antibiotics play a role in this condition.

Cholinergic substances such as acetylcholine, released by cutaneous cholinergic nerves whose mechanism is not yet known, can directly influence mast cells to release mediators. Physical factors such as heat, cold, blunt trauma, X-rays, and massage can directly stimulate mast cells. Some conditions such as fever, heat, emotion, and alcohol can stimulate the capillaries directly, resulting in vasodilation and increased permeability (Djuanda, 2008).

Immunological factors play a more important role in acute urticaria than chronic, usually IgE binds to the surface of mast cells and/or basophil cells due to the presence of Fc receptors. This situation is clearly seen in type I reactions (anaphylaxis), such as drug and food allergies.

Complement also plays a role, classically or alternatively activation of complement causes the release of anaphylatoxins (C3a, C5a) which can stimulate mast cells and basophils, for example seen as a result of venom or bacterial toxins. Complement binding also occurs in urticaria due to cytotoxic reactions and immune complexes in this condition are also released anaphylatoxins. Urticaria due to contact occurs using insect ingredients, cosmetic ingredients, and cephalosporins.

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