Urticaria

rana.abou.fayad lindsey43881 laura20204 133 Users are discussing this topic

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Urticaria, otherwise known as hives, is an itchy red blotchy rash resulting from swelling of the superficial part of the skin. It can be localised or more widespread. Angio-oedema occurs when the deeper tissues, the lower dermis and subcutaneous tissues, are involved and become swollen.

The typical lesion is a central itchy white papule or plaque due to swelling of the surface of the skin (weal or wheal). This is surrounded by an erythematous flare. The lesions are variable in size and shape and may be associated with swelling of the soft tissues of the eyelids, lips and tongue (angio-oedema).

Individual lesions are typically transient. They come and go within a few minutes to hours and the patient may need to be questioned carefully to establish this. If they are unsure how long each lesion lasts, a line drawn around one lesion will demonstrate any change when inspected the following day. Individual weals may join to form large patches.

Urticaria

In terms of timescale, urticaria can be classified into:[1] 

  • Acute urticaria - where symptoms develop quickly but resolve speedily, often within 48 hours.
  • Chronic urticaria - where the rash persists for more than six weeks. Urticaria may also be episodic and recurrent.

NEW - log your activity

  • Notes Add notes to any clinical page and create a reflective diary
  • Track Automatically track and log every page you have viewed
  • Print Print and export a summary to use in your appraisal
Click to find out more »

Approximately 15% of people experience urticaria at some time in their lives. Acute urticaria is much more common than chronic urticaria. (Estimated lifetime incidence is 1 in 6 people compared to 1 in 1,000.) The prevalence rate for chronic urticaria has been estimated as 1-5 per 1,000. Acute urticaria is most common in children, and is more common in women than in men, particularly in the 30-60 age range. It is more common in individuals who suffer with atopy.

Urticaria is thought to be due to release of histamine and other mediators from mast cells in the skin; why this occurs is not always understood. These chemicals cause capillary leakage, which causes the swelling of the skin, and vasodilation causing the erythematous reaction.[2] There may be a trigger identified which causes this release, but often the cause is not identifiable, particularly in chronic urticaria. An autoimmune reaction is thought to be involved in many such cases.[1] 

Aetiological classifications vary and overlap. The British Association of Dermatologists (BAD) guidelines classify the aetiology of urticaria into idiopathic, immune or non-immune.[3][4] 

  • Idiopathic (up to 50% of cases. Cause unknown.)
  • Immunological:
    • Autoimmune (autoantibodies against Fc epsilon 5RI or IgE).
    • Allergic (IgE-mediated type I hypersensitivity reactions). Food allergies, certain reactions to medications, and reactions to bee or wasp stings.
    • Immune complex (urticarial vasculitis).
    • Complement-dependent (C1 esterase inhibitor deficiency). Usually the mechanism when infection is the cause.
  • Non-immunological:
    • Physical stimuli causing mast cell release: exercise, heat, cold, pressure, solar rays, dermatographism.
    • Direct mast cell-releasing agents (eg, opiates).
    • Aspirin, non-steroidal anti-inflammatory drugs (NSAIDs).
    • Angiotensin-converting enzyme (ACE) inhibitors (angio-oedema).

There is no consensus on the clinical classification of urticaria. There is much overlap between categories. Different European guidelines use different classification systems.[1][2][3][4][5] 

Most simply, urticaria can be classified as follows:

Ordinary urticaria
This is the most common type. It includes:

  • Acute urticaria - due to medication, food, stings, infections.
  • Chronic urticaria - often thought to be due to an autoimmune cause.

Physical urticaria
This is due to external physical stimuli. It includes contact urticaria, cold urticaria, cholinergic urticaria from sweating, heat and solar causes, vibratory urticaria, delayed pressure urticaria, and dermatographism.

Dermatographia urticaria

Vasculitic urticaria
A histological diagnosis. This is an autoimmune process where there is inflammation of the blood vessels. There may be joint and kidney involvement.

This is usually a clinical diagnosis from the history and appearance of the rash. It can be established once it has been shown that individual lesions only last a few hours. Sometimes an eczema may be difficult to distinguish if the history is vague.

The diagnosis is usually made clinically and on history, particularly in acute ordinary urticaria, and no investigations are needed.

In chronic or episodic cases where investigations are needed, these will be guided by history.

Tests may include:[5] 

  • FBC.
  • ESR or CRP.
  • Exclusion of suspected medication
  • Physical challenge. Cold provocation testing (ice cube), heat provocation test (warm water), pressure testing, UV light testing, exercise or hot bath provocation for cholinergic urticaria.
  • Elicit dermatographism.
  • Patch testing/prick testing for contact urticarias.
  • Thyroid autoantibodies if autoimmune mechanism is suspected.
  • Dietary challenges.
  • Tests for infectious diseases, including Helicobacter pylori, which may have a role in some cases - research in this area continues.
  • Skin biopsy (urticarial vasculitis).

Where possible, identify and treat the cause. Nonspecific aggravating factors should be minimised, such as overheating, stress, alcohol, caffeine and drugs likely to cause urticaria (eg, aspirin, codeine).

  • Antihistamines:
    • Non-sedating H1 antihistamines are the mainstay of treatment. There are no meta-analyses comparing the different antihistamines for the treatment of acute urticaria, so choice is a matter of personal preference and local prescribing policy. It is common practice to offer the patient at least two choices of non-sedating H1 antihistamine in view of differences in tolerability and response. Alternatives include:[3]
      • Acrivastine
      • Cetirizine hydrochloride
      • Desloratadine
      • Fexofenadine hydrochloride
      • Levocetirizine hydrochloride
      • Loratadine
      • Mizolastine
      • Rupatadine
      H1 antihistamines may be increased beyond their licensed dose but this approach is usually initiated by a specialist. European guidelines allow up to four times the standard dose of antihistamines.[6] 

      Urticarial reactions to H1 antihistamines have occasionally been reported and this should be borne in mind when a patient treated with these drugs gets worse.[7] 
    • Sedating antihistamines such as chlorphenamine may be helpful in patients whose itching causes sleep disturbance but they are otherwise to be avoided due to their increased adverse effects (eg, headache, psychomotor impairment and antimuscarinic effects).[3] 
    • In children under the age of 6 months, non-sedative antihistamines are not licensed.
    • There are no systematic studies of safety in pregnancy, and chlorphenamine is often the first choice of antihistamine.[6] 
    • The addition of an H2 antihistamine (eg, cimetidine or ranitidine) may provide additional benefit in some cases. These have been used off licence for this but current evidence of efficacy is limited.[8] 
  • Menthol 1% in aqueous cream or calamine lotion help to soothe itch, although the residue can cause itching in some patients.
  • Oral steroids may help to shorten the duration of acute urticaria. 40 mg of prednisolone for three days is recommended for severe cases, although lower doses may be effective.[1] Long-term oral steroids are not indicated in chronic urticaria.
  • Options sometimes used in secondary care include:
    • Antileukotrienes (eg, montelukast), which may provide additional benefit in some selected patients when combined with an H1 antihistamine; there is little evidence that they are effective as monotherapy.
    • Phototherapy.
    • Ciclosporin.[6] 
    • Omalizumab, an anti-IgE antibody, which has been shown to be effective in selected cases.[9] 
  • If symptoms are not well controlled.
  • If antihistamines are needed continuously to control symptoms for more than six weeks.
  • If urticaria is painful and persistent, suspect vasculitic urticaria and refer for biopsy and histological diagnosis.
  • Urgent hospital admission is indicated if acute urticaria rapidly develops into angioneurotic oedema or anaphylactic shock.

This is variable. Most cases of idiopathic urticaria resolve over a period of six months but a minority can persist for many years. Chronic urticaria patients with angio-oedema and weals seem to have a worse prognosis than those presenting with weals alone.[3] 

Further reading & references

  1. Urticaria; NICE CKS, December 2011
  2. Urticaria; DermNet NZ
  3. Evaluation and management of urticaria in adults and children; British Association of Dermatologists (2007)
  4. Management of chronic urticaria and angio-oedema; British Society for Allergy and Clinical Immunology (2007)
  5. Zuberbier T, Asero R, Bindslev-Jensen C, et al; EAACI/GA(2)LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria. Allergy. 2009 Oct;64(10):1417-26. doi: 10.1111/j.1398-9995.2009.02179.x.
  6. Zuberbier T, Asero R, Bindslev-Jensen C, et al; EAACI/GA(2)LEN/EDF/WAO guideline: management of urticaria. Allergy. 2009 Oct;64(10):1427-43. doi: 10.1111/j.1398-9995.2009.02178.x.
  7. Inomata N, Tatewaki S, Ikezawa Z; Multiple H1-antihistamine-induced urticaria. J Dermatol. 2009 Apr;36(4):224-7.
  8. Fedorowicz Z, van Zuuren EJ, Hu N; Histamine H2-receptor antagonists for urticaria. Cochrane Database Syst Rev. 2012 Mar 14;3:CD008596. doi: 10.1002/14651858.CD008596.pub2.
  9. Maurer M, Rosen K, Hsieh HJ, et al; Omalizumab for the treatment of chronic idiopathic or spontaneous urticaria. N Engl J Med. 2013 Mar 7;368(10):924-35. doi: 10.1056/NEJMoa1215372. Epub 2013 Feb 24.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Helen Huins
Document ID:
2907 (v26)
Last Checked:
13/01/2014
Next Review:
12/01/2019