Excerpt from Urticaria, Acute


Synonyms, Key Words, and Related Terms: hives, allergy, allergic reaction, anaphylaxis, anaphylactoid reaction, angioedema, immune-mediated urticaria, nonimmune-mediated urticaria, non-immune-mediated urticaria, urticaria, rash, drug rash, viral rash

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Background: Urticaria was first described in the English literature in 1772, although the disease has been recognized throughout history. The disorder is marked by the onset of evanescent wheals (hives) associated with pruritus. Acute urticaria is a common disorder that often prompts patients to seek treatment in the emergency department (ED). In fact, it is the most common cutaneous disease treated in the ED. The eruption is symptomatic and can be visually apparent over many different parts of the skin. The natural course of the acute disease lasts from a one-time event of several hours’ duration up to 6 weeks, depending on the etiology. If urticaria is present continuously over a 6-week period, it is categorized as chronic urticaria. Information on this entity is available in Urticaria, Chronic.

Individual lesions appear at different locations and fade without scarring, often in a matter of hours. In 50% of patients, a specific etiology can be identified. Brief episodes of urticaria can be associated with identifiable causes, and the method of exposure (ie, direct contact, oral or intravenous routes) is usually known. If the location of the wheals remains fixed for longer than 24 hours, the diagnosis may be urticarial vasculitis or bullous pemphigoid.

Pathophysiology: The release of histamine and other compounds by mast cells and basophils causes the appearance of urticaria. Immune Immune-mediated urticaria is from immunoglobulin E (IgE) binding specific antigen and the complex binding to FcER1 receptors to activate mast cells. Mast cell activation from crosslinking of FcER1 receptor causes degranulation of intracellular vesicles that contain histamine, leukotriene C4, prostaglandin D2, and other chemotactic mediators that recruit eosinophils and neutrophils into the dermis. Histamine and chemokine release lead to extravasation of fluid into the dermis (edema). Histamine effects account for many of the clinical and histologic findings of urticaria.

Histamine is the ligand for at least 2 types of membrane-bound receptors, H1 and H2 receptors, which are present on numerous cells. The activation of H1 histamine receptors on smooth muscle cells and endothelial cells leads to cellular contraction and increased vascular permeability. The activation of H2 histamine receptors causes vasodilation. Urticaria is a reaction pattern that reflects the activation of mast cells and basophils. The exact mechanism of action resulting in the release of the intracellular contents of mast cells and basophils is varied and can occur through immune-mediated or non–immune-mediated mechanisms.

Immune-mediated urticaria

Immune-mediated urticaria can be caused by 3 of 4 types of immune mechanisms.

  • The type I allergic IgE response is initiated by antigen-mediated IgE immune complexes that bind and cross-link Fc receptors on the surface of mast cells and basophils. The types of antigens that bind to IgE are varied and include proteins, polysaccharides, and other immunogenic molecules.

  • Type II responses are mediated by cytotoxic T cells. The disease process activates byproducts that cause urticarial vasculitis or bullous pemphigoid.

  • Type III immune-complex disease is associated with systemic lupus erythematosus and other connective tissue disorders that activate urticaria.

Non–immune-mediated

Chemicals that can directly induce mast cell degranulation, presumably by altering the membrane properties, cause non–immune-mediated urticaria. Common agents associated with direct mast cell activation are opiates, antibiotics, curare, radiocontrast media, azo dyes, aspirin, and aspirin derivatives.

Frequency:

  • In the US: Urticaria affects 15-20% of the population at some point in their lives.