eMedicine Specialties > Dermatology > Allergy & Immunology

Urticaria, Acute

Author: Henry K Wong, MD, PhD, Associate Professor of Dermatology, Ohio State University College of Medicine
Contributor Information and Disclosures

Updated: Sep 4, 2009

Introduction

Background

Urticaria was first described in the English literature in 1772, although the disease has been recognized throughout history. Urticaria 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, acute urticaria is the most common cutaneous disease treated in the ED.¹ The eruption is symptomatic and can be visually apparent over many different parts of the skin. The natural course acute urticaria 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.

Individual lesions of acute urticaria appear at different locations and fade without scarring, often in a matter of hours. In 50% of patients with acute urticaria, 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-mediated urticaria is from immunoglobulin E (IgE) binding specific antigen, and the IgE-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.^2,3 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.

Frequency

United States

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

International

The international frequency of acute urticaria is similar to the US frequency.

Mortality/Morbidity

Acute urticaria causes discomfort, but it does not cause mortality unless it is associated with angioedema involving the upper airways.^4,5,6

Race

No variation in race is reported for acute urticaria.

Sex

Females have a slightly higher prevalence (61%) of acute urticaria than males.

Age

Acute urticaria affects persons of all age groups. The mean age of persons who are affected is in the second to third decade of life.

Clinical

History

Acute urticaria is characterized by the onset of clinically apparent, edematous, evanescent, erythematous plaques. Individual acute urticaria lesions remain for less than 24 hours, exhibiting a transitory and migratory behavior. The etiology can be inferred in as many as 50% of new cases. In general, greater than 80% of new-onset urticaria resolves in 2 weeks and greater than 95% of new-onset cases resolve by 3 months. Atopy can often be identified in the patient or his or her family members. When urticaria persists for more than 6 weeks, it is considered chronic urticaria. Additional etiologies exist for chronic urticaria. A thorough medical evaluation is indicated to eliminate the possibility of treatable causes of urticaria, which include malignancies, connective tissue disorders, and chronic infections.

• Acute urticaria is commonly caused by a variety of infections, medications, food allergies, physical stimulants, chemicals, chronic inflammatory diseases, and insect bites, as follows⁷ :
  • Recent infection from a viral syndrome or an upper respiratory tract illness (39%)
  • Medications (eg, ACE inhibitors, aspirin, nonsteroidal anti-inflammatory drugs, sulfa-based drugs, penicillins, diuretics, opioids, polymyxin B)
  • Food and food additives (eg, nuts, fish, shellfish, eggs, chocolate, strawberries, salicylate, benzoates)
  • Parasitic infections (eg, Ascaris, Ancylostoma, Strongyloides, Echinococcus, Trichinella, Filaria)
  • Physical stimulants (eg, cold, pressure, aquagenic)
  • Chemicals (eg, latex, ammonium persulfate in hair chemicals)
  • Intravenous radiocontrast media
  • Arthropod bites
• New-onset fever and constitutional symptoms suggest chronic autoimmune disease.

Physical

Lesions of urticaria can be polymorphic and vary from several millimeters to large, continuous plaques.

• Plaques have smooth surfaces with polycyclic curved borders. Lesions do not have scales.
• Lesions show an intense erythema in the newest areas, with a trailing clearing region in older areas.
• Central clearing can cause a target configuration in expanding plaques. The advancing border shows a discrete edge followed by a faint, trailing, diffuse border.
• Lesions last less than 24 hours, and scars do not develop.

• Erythema multiforme can resemble urticaria.
  • Both processes can be a reaction to medication.
  • Early lesions of erythema multiforme may appear edematous, round, targetoid, and polycyclic as the lesion expands. However, in erythema multiforme, each lesion can be differentiated by the stationary nature and the progression to a dusky color with bulla formation.

Causes

A definitive inciting agent can be identified in 40-50% of cases of acute urticaria.

• In one study, causes were identified as an upper respiratory tract infection in 39.5% of the total cases, analgesics in 9%, and food intolerance in 0.9%.⁸
• Urticaria associated with the onset of autoimmune disorders or malignancy (eg, systemic lupus erythematosus, lymphoma) becomes chronic.
• Most cases of new-onset urticaria are idiopathic in nature.

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