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Urticaria (hives) is defined by the rapid appearance of lesions called wheals, which consist of dermal swelling presenting as pruritic papules or plaques with or without surrounding erythema. Wheals are smooth with no surface changes. Individual wheals last for 1–24 hours. Wheals form when mast cells release histamine in response to various stimuli. Urticaria is divided into acute (duration less than 6 weeks) and chronic (duration greater than 6 weeks) forms. Chronic urticaria can occur spontaneously or as a result of physical stimuli.



Key Points

  • ✓ Individual lesions of urticaria last for less than 24 hours.

  • ✓ Urticaria may persist beyond 6 weeks in 20% of patients.

  • ✓ Angioedema is often present in conjunction with urticaria.

  • ✓ H1 non-sedating antihistamines are the first line of therapy for urticaria.

Acute spontaneous urticaria is the most common form of urticaria. Acute spontaneous urticaria is defined as spontaneous urticaria of less than 6 weeks duration, whereas chronic spontaneous urticaria lasts more than 6 weeks. The majority of patients with spontaneous urticaria will fall in this category. The lifetime prevalence of urticaria is estimated to be approximately 9–20% and it can present in patients ranging in age from infants to the elderly.1 Associated angioedema can sometimes be seen in patients with urticaria. It is defined as swelling of the deeper dermis and subcutaneous tissue lasting up to 72 hours. Angioedema is seen in conjunction with classic wheals in 30–40% of patients with urticaria.1 When angioedema is seen without wheals this is frequently the result of drug therapy as with angiotensin-converting enzyme (ACE) inhibitors.


The underlying event leading to urticaria is mast cell degranulation, with release of histamine and other pro-inflammatory molecules including cytokines, prostaglandins, leukotrienes, and arachidonic acid metabolites causing rapid vasodilation and swelling of the surrounding tissue with plasma and activation of local itch sensory nerves.1,2 There are numerous stimuli that can lead to mast cell activation through various pathways. More than 50% of acute spontaneous urticaria is idiopathic.

Among cases with a known cause, the most common cause is viral infections, particularly in children.3 Drugs including beta-lactams, nonsteroidal anti-inflammatory drugs (NSAIDs), and ACE-inhibitors are another frequent cause,1,2 (Table 16-1). Food-induced type I hypersensitivity reactions are a rare cause of acute urticaria in adults, but are a more common cause in children. In type I hypersensitivity reactions (food and latex allergies), antigen specific immunoglobulin IgE causes a cross linking of the high-affinity (Ig)E receptors leading to mast cell degranulation.1 The exact mechanism leading to mast cell degranulation in non-type I forms of acute urticaria appears to be multifactorial and is less well-defined.

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