eMedicine Specialties > Pediatrics: General Medicine > Allergy & Immunology
Urticaria
Updated: Jun 15, 2009
Introduction
Background
Urticaria is a vascular reaction of the skin marked by the transient appearance of smooth, slightly elevated patches (wheals) that are erythematous and are often attended by severe pruritus. The eruption rarely lasts longer than 2 days but may be recurrent. Chronic urticaria is defined as urticaria with recurrent episodes lasting longer than 6 weeks.
Acute urticaria is more common and affects 4.5-15% of children in the United Kingdom, whereas chronic urticaria is thought to affect 0.1-3% of children in the United Kingdom. Acute urticaria differs from chronic urticaria in that a cause is more frequently established (eg, acute infection, allergen ingestion). In either case, the presence of urticaria may significantly impair quality of life. Children commonly miss significant periods of school because of a lay perception that the condition is infectious or allergic and a fear that the child is unwell. Approximately 50-80% of children with chronic urticaria also have accompanying angioedema. (See Angioedema.)
Although urticaria results from transient extravasation of plasma into the dermis, angioedema is the subcutaneous extension of urticaria that results in deep swelling within subcutaneous sites. Papular urticaria in children is characterized by 10-mm to 20-mm wheals surrounding 2-mm to 4-mm red papules. Physical urticaria typically involves 10-mm to 20-mm red blotchy macules with a 0.1-mm wheal in the center.
The development of urticaria can be an isolated event without systemic reaction or it can be a prelude to the development of an anaphylactic reaction.The images below depict various presentations of urticaria.
Urticaria developed after bites from an imported fire ant.
Urticaria associated with acute group A beta-hemolytic streptococci infection.
Urticaria associated with a drug reaction.
Local urticaria on a patient with latex allergy who was touched with a latex glove.
Pressure urticaria (dermatographia) developed after strokes.
Pathophysiology
Histamine is the primary chemical mediator of transient urticaria. The mast cell is central in all forms of transient urticaria. Histamine may be directly released from cutaneous mast cells in response to certain allergens or medications. Specific immunoglobin E (IgE) antibodies bind to mast cell surfaces that recognize certain antigens (eg, penicillin, certain foods, insect venom), causing the release of histamine after binding with antigen. In infection, complement fragments (eg, C3a) may activate mast cells to release histamine. Eicosanoids may also induce mast cell mediator release, and other cytokines have been implicated in urticaria. Papular urticaria represents a delayed hypersensitivity reaction in which basophil infiltrates can be found around dermal blood vessels. In physical urticaria, neuropeptide and complement products, in addition to histamine, are suspected to cause skin lesions.
In children, physical factors such as pressure or cold exposure are the most commonly diagnosed precipitating factors for chronic urticaria; other factors account for less than 1% of cases. Interestingly, one study reported that 30% or more of children with chronic urticaria have an autoimmune etiology with positive autologous serum skin test (ASST) findings. Also, approximately 4% of children with chronic urticaria have positive antithyroid antibodies, although most patients with positive antithyroid antibodies remain euthyroid.
The etiological classification of chronic urticaria below may help shorten the course of work-up in those patients.
Etiological Classification of Chronic Urticaria
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Table
| Etiology | Mechanisms | Examples |
| Idiopathic (40-50% of cases) | Unknown | ... |
| Autoimmune | Immunoglobulin G (IgG) autoantibody to high-affinity IgE receptor or to IgE antibody | Possibly associated with autoimmune thyroiditis |
| Physical stimuli | Direct mast cell mediator release | Exercise, heat, cold, pressure, water exposure, sun exposure, delayed pressure, dermatographia |
| Drug induced | Reduced kinin metabolism; elevated leukotriene level | Angiotensin-converting enzyme (ACE) inhibitor, nonsteroidal anti-inflammatory drugs (NSAIDs) |
| Infection | Complement activation and immune complex formation | Parasites, Epstein-Barr virus, hepatitis B and C, viral exanthem |
| Allergic | IgE-mediated allergic contact | Latex, animals, grass, food |
| Non-IgE mediated mast cell degranulation | Non–receptor mediated | Opiates, adrenocorticotropic hormone (ACTH) |
| Vasculitis | Small vessel vasculitis; deposition of immunoglobulin or complement | Urticarial vasculitis |
| Food constituent (rare) | Unknown | Salicylates |
| Etiology | Mechanisms | Examples |
| Idiopathic (40-50% of cases) | Unknown | ... |
| Autoimmune | Immunoglobulin G (IgG) autoantibody to high-affinity IgE receptor or to IgE antibody | Possibly associated with autoimmune thyroiditis |
| Physical stimuli | Direct mast cell mediator release | Exercise, heat, cold, pressure, water exposure, sun exposure, delayed pressure, dermatographia |
| Drug induced | Reduced kinin metabolism; elevated leukotriene level | Angiotensin-converting enzyme (ACE) inhibitor, nonsteroidal anti-inflammatory drugs (NSAIDs) |
| Infection | Complement activation and immune complex formation | Parasites, Epstein-Barr virus, hepatitis B and C, viral exanthem |
| Allergic | IgE-mediated allergic contact | Latex, animals, grass, food |
| Non-IgE mediated mast cell degranulation | Non–receptor mediated | Opiates, adrenocorticotropic hormone (ACTH) |
| Vasculitis | Small vessel vasculitis; deposition of immunoglobulin or complement | Urticarial vasculitis |
| Food constituent (rare) | Unknown | Salicylates |
A diagnostic skin biopsy should be considered, especially in patients who present with features such as fever, painful lesions, arthralgia, elevated erythroid segmentation rate, or lesions that last 24 hours or longer or lesions that resolve with residual petechiae or purpura. Biopsy findings may reveal a leukoclastic angiitis rather than the non-necrotizing vasculopathy that is typical in chronic urticaria. Henoch-Schönlein purpura is the most common cause of acute urticarial vasculitis in children. The pathology may show immunoglobulin A (IgA) deposits in the vessels.
An association between childhood chronic urticaria and thyroid autoimmunity has been postulated. Whether the association is causal is unclear because most children present with hyperthyroid symptoms or hypothyroid symptoms before or after the onset of chronic urticaria and because the urticarial symptoms do not always improve with thyroxin-replacement therapy. Nonetheless, ongoing thyroid function monitoring is encouraged in children with chronic urticaria and thyroid autoimmunity.
An association has been reported between chronic urticaria and celiac disease, which may improve if a gluten-free diet is followed.
An association of Helicobacter pylori and chronic idiopathic urticaria has been reported in India.1 All patients underwent endoscopy with antral biopsy for urease and histopathology to identify H pylori– associated gastritis. Infected patients were given H pylori eradication therapy. Eradication of bacterium was confirmed by fecal antigen assay. The response of H pylori eradication therapy in patients with chronic idiopathic urticaria was determined to be significant. H pylori should be included in diagnostic workup for patients with chronic idiopathic urticaria.
The immunologic characterization of chronic idiopathic urticaria, regarding the cytokine profile, has been reported.2 The study examined levels of circulating inflammatory cytokines, cytokine production in response to phytohemagglutinin, a T-cell mitogen, and cytokine mRNA expression by peripheral blood mononuclear cells in patients with chronic idiopathic urticaria. Authors concluded that immunologic dysregulation occurs in chronic idiopathic urticaria, revealing a systemic inflammatory profile associated with disturbed cytokine production by T cells, mainly related to increase of interleukin (IL)-17 and IL-10 production.
A study reported investigation of relationship between human leukocyte antigen (HLA) class I and class II antigens and immune pathogenesis of chronic urticaria in Turkey.3 The study revealed the association of HLA-B44, HLA-DRB1*01 and HLA-CRB*15 alleles with idiopathic chronic urticaria, indicating a genetic component should be considered in the pathogenesis.
One study highlighted the possibility that food additive intolerance may lead to urticaria-angioedema syndrome.4 The exact mechanism remains unclear. However, both IgE-mediated and non-IgE mediated mechanisms may be involved.
In Spain, fish protein was reportedly the third leading cause of urticaria in children, next to ingestion of eggs or cow's milk.5 Most of the reactions were IgE-mediated reactions due to ingestion or contact with fish. They emphasized that inhalation of cooking vapor is also important cause of allergic symptoms, including urticaria.
A retrospective study included 953 children admitted to the emergency department with a first attack of acute urticaria;6 4.3% of the children were adolescents and the remainder were younger. The etiologies listed included infection (48.4%), medications (11.5%), foods (23.5%), inhalents (1.7%), insect bites (1.5%), and contact materials (0.2%). The idiopathic etiology rate was 13.2%. Interestingly, only 44% of patients had skin lesions, whereas the rest had associated symptoms of other systems, the most common of which was respiratory symptoms. The geographic difference may explain the differences with other studies.
Frequency
United States
Urticaria is common in infancy and childhood, although the exact frequency is unknown. Urticaria affects 15-25% of the US population. Several large studies indicate that 3% of preschool-aged children and 2% of older children are affected. Chronic idiopathic urticaria, in which lesions of an unknown etiology last longer than 6 weeks, is estimated to occur in as much as 3% of the population.
Mortality/Morbidity
Patients may experience recurrence of rash. Urticaria can be an isolated event. Without recurrence, the prognosis is good. Urticaria may be a clinical feature of anaphylaxis. In that case, the mortality rate is significant.
Race
Urticaria has no known racial predilection.
Sex
In children, both sexes are affected with equal frequency. Chronic urticaria tends to occur in females, especially adults.
Age
Several large studies indicate that 3% of preschool-aged children and 2% of older children are affected. Acute urticaria usually occurs in children, whereas chronic idiopathic urticaria is more common in adults.
Clinical
History
Some effort should be made to determine whether the lesions have an allergic (immunoglobulin E [IgE]) or nonallergic (non-IgE) basis. In addition, the urticaria should be classified as acute (duration <6 wk) or chronic (duration >6 wk).
- Common nonallergic, acute, or transient urticaria often follows infection with streptococci; infectious mononucleosis; hepatitis A, B, and C; adenovirus; enterovirus; or parasites.
- In nonallergic chronic urticaria, carefully obtain the history of any chronic medical conditions to assess the presence of systemic diseases such as parasitic disorders, hepatic disorders (history of blood transfusion), endocrine disorders (especially hypothyroidism [Hashimoto thyroiditis] with the presence of autoantibodies to thyroid tissue [antithyroglobulin antibody or antiperoxidase antibody]), collagen vascular diseases or rheumatological disorders (eg, rheumatoid arthritis, systemic lupus erythematosus [SLE], dermatomyositis, Behçet disease), or inflammatory bowel diseases.
- Any recent, chronic, or recurrent viral infections should be determined, especially those due to herpes simplex virus or Epstein-Barr virus. Also, look for focal but persistent bacterial infection (eg, dental abscess, sinusitis) or miscellaneous conditions such as aphthous stomatitis or occult malignancy.
- Acute allergic urticaria can be caused by a sting from creatures such as bees, wasps, and scorpions or can be caused by bites from insects and spiders. Jellyfish venom may also cause urticaria.
- The ingestion of various medications (especially antibiotics) or foods (eg, tree nuts, peanuts, eggs, shellfish, strawberries, tomatoes) 2 hours before the onset of a rash is a probable allergic cause. Therefore, determine whether the rash is associated with any foods (new or old) or medicines. Ask specifically for the ingestion of any aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) in over-the-counter medications.
- Urticaria may be the first manifestation of latex allergy at the site of skin contact in individuals who are allergic to latex protein. Two high-risk populations for latex allergy are children with a history of multiple surgeries (especially those with spina bifida or those who have had multiple surgeries in the past) and children exposed to frequent latex tubing or gloves in the past, such as those undergoing chronic renal dialysis.
- Less than 5% of patients have documented IgE-mediated allergic urticaria compared with about 15% of children who may have physical urticaria. Most patients fall into an idiopathic group.
- Physical urticaria is not associated with underlying medical conditions but is related to physical triggers. Triggers include exposure to heat, cold, sunlight, water, pressure, or vibration. Cold urticaria has recently been associated with anaphylaxis. History of swimming in cold water, touching of cold objects, or exposure to cold weather should be obtained in those cases.
- Cholinergic urticaria often follows exercise or strenuous work.
- Papular urticaria is usually the result of an encounter with fleas or mites and is most often observed in toddlers.
- Stress or psychogenic urticaria has been casually coined or speculated in clinical settings to explain patients who have non–IgE-mediated urticaria, but no prospective study has been performed to confirm a cause-and-effect relationship.
- Hereditary angioedema is an autosomal dominant condition related to a deficiency of C1 inhibitor that is associated with repeated episodes of swelling of the face, larynx, extremities, and abdominal pain. Onset usually follows trauma, surgery, dental manipulation, or accidents. This condition can be differentiated from angioedema in that urticaria does not occur, the lesions are not pruritic, and the lesions are nonresponsive to antihistamines and epinephrine. An acquired form of this disorder may also be observed, sometimes in association with an underlying lymphoma.
- Finally, determine whether any features suggest anaphylaxis (eg, hypotension, respiratory problems, GI discomfort).
- Recently, a study indicated that children with chronic urticaria have a significantly higher prevalence of celiac disease than control children.7 Furthermore, the study showed that a gluten-free diet in those patients resulted in remission of chronic urticaria. Thus, celiac disease may cause chronic urticaria.
- Chronic urticaria has been reported in children who had a familial cold autoinflammatory syndrome.8 Many were confirmed by presence of a novel CIAS1 mutation and were refractory to symptomatic treatment. Many patients responded to the treatment of the IL-1-receptor antagonist. Obviously, this is a very rare syndrome, and inflammatory conditions can be effectively controlled by attenuating the actions of IL-1ß.
Physical
- The onset of eruption is usually sudden, and the eruption is usually pruritic and characterized by red, raised, 2-mm to 15-mm, flat-topped wheals scattered over the body (see image below).
Urticaria developed after bites from an imported fire ant.
- Edema can be observed by slightly stretching the skin to demonstrate whitish centers. Occasionally, large annular urticarial lesions as large as 30 cm in diameter with polycystic borders are observed.
- Determine the presence of dermographism by scratching the skin with the end of a tongue blade or key and observe for 5-15 minutes for whealing and edema (see image below).
Pressure urticaria (dermatographia) developed after strokes.
- Wheals commonly last 20 minutes to 3 hours, disappear, and then reappear in other skin areas. An entire episode of urticaria often lasts 24-48 hours; rarely, it lasts 3 weeks.
- Angioedema appears as swellings of the tissues, with indistinct borders around the eyelids and lips. Swellings may also appear on the face, trunk, genitalia, and extremities. The face, hands, and feet are involved in 85% of patients. As many as 50% of children who have urticaria exhibit angioedema with swelling of the hands and feet. Hereditary angioedema (C1 inhibitor deficiency) accounts for only 0.4% of cases of angioedema but is associated with a high mortality rate.
- In patients with mastocytosis, brownish pigmentation can be observed after wheals recede.
- Urticaria may be part of an anaphylactic reaction. Check for hypotension, stridor or wheezing, swallowing problems, abdominal pain, and joint involvement (swelling or pain).
Causes
- IgE-mediated mast cell activation may be caused by the following:
- Drugs such as penicillins, cephalosporins, sulfa drugs, salicylates, NSAIDs, barbiturates, amphetamines, atropine, hydralazine, insulin, blood, and blood products
- Foods such as tree nuts, peanuts, eggs, shellfish, and tomatoes (The involvement of food additives or preservatives is controversial.)
- Insect venom
- Latex protein exposure
- Non–IgE-mediated mast cell activation may be caused by the following:
- Drugs such as morphine and other opiates, meperidine, polymyxin B, and acetylsalicylic acid can cause release of mediators by other mechanisms.
- Certain foods or beverages, such as aged cheeses or red wine, can contain histidine, which is similar to histamine. However, the evidence in the medical literature that they cause urticaria is rare.
- Radiocontrast media can directly induce mast cell mediator release.
- Medical conditions implicated by unknown pathogenesis include the following:
- Infectious agents such as group A beta-hemolytic streptococci; Epstein-Barr virus; hepatitis A, B, and C; adenovirus; and herpes simplex virus have been implicated. Other infectious processes such as chronic sinusitis, cutaneous fungal infections, and chronic gastroenteritis by enterovirus, H pylori, or other parasites have also been implicated.
- Hormonal causes via endocrine tumors or ovarian pathology are rare. Thyroid dysfunction (hypothyroidism and hyperthyroidism) is more common. Patients with chronic urticaria can have positive anti-thyroid antibodies in euthyroid condition.
- Physical causes (physical urticaria) can be numerous and include cold, pressure, vibration, sunlight, water, dermographism, and exercise.
- Cholinergic urticaria is a subset of physical urticaria. It can be triggered by heat, exercise, or emotional stress and is thought to be mediated by acetylcholine.
- Neuropeptides and neurokinins are thought to mediate development of urticaria in stress or physical urticaria.
- The mechanisms of any of the above disorders may involve release of either cytokine or complement fragments.
- Autoantibody (IgG in isotype) against α chain of FcεR1α and IgE antibody have been found in some patients with chronic urticaria (both in adults and in children).
- C1 esterase inhibitor deficiency plays a role in hereditary angioedema.
- In most cases (≤75-80%) of chronic urticaria, no specific cause is identified; these cases are labeled chronic idiopathic urticaria.
More on Urticaria |
 Overview: Urticaria |
| Differential Diagnoses & Workup: Urticaria |
| Treatment & Medication: Urticaria |
| Follow-up: Urticaria |
| Multimedia: Urticaria |
| References |
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Further Reading
Keywords
urticaria, hives, anaphylactoid reaction, angioedema, pruritus, chronic urticaria, acute urticaria, papular urticaria, physical urticaria, histamine, transient urticaria, arthralgia, Henoch-Schönlein purpura, thyroid autoimmunity, celiac disease, hypothyroidism, hyperthyroidism, Hashimoto thyroiditis, collagen vascular diseases, rheumatoid arthritis, systemic lupus erythematosus, SLE, dermatomyositis, Behçet disease, inflammatory bowel disease, dental abscess, sinusitis, aphthous stomatitis, cholinergic urticaria, hereditary angioedema, edema
