Urticaria

Common condition characterised by transient, pruritic, erythematous wheals (hives) caused by mast cell degranulation and histamine release. Classified as acute (<6 weeks) or chronic (≥6 weeks). Acute urticaria is usually triggered by infection, drugs, or food. Chronic spontaneous urticaria (CSU) is often autoimmune. Non-sedating antihistamines are first-line treatment.

Key Facts

Individual wheals resolve within 24 hours (if >24 hours, consider urticarial vasculitis — biopsy) Acute urticaria (<6 weeks): triggers include infection (viral — most common in children), drugs (NSAIDs, antibiotics), food, insect stings Chronic spontaneous urticaria (CSU, ≥6 weeks): autoimmune in ~50% (anti-FcεRI or anti-IgE autoantibodies); rarely allergic First-line: non-sedating antihistamine (cetirizine 10mg OD or fexofenadine 180mg OD); up-dose to 4× licensed dose if needed Omalizumab (anti-IgE): third-line for CSU refractory to high-dose antihistamines — NICE TA339 Urticarial vasculitis: wheals lasting >24 hours, painful (not just itchy), purpuric; may leave bruising; check complement — hypocomplementaemic form associated with SLE AVOID: identifying 'allergy' triggers in CSU — extensive allergy testing is NOT recommended (most CSU is autoimmune, not allergic) Physical urticarias: dermatographism, cold urticaria, cholinergic (exercise/heat), pressure urticaria — treat with antihistamines

Overview

Key Facts

Urticaria is extremely common, affecting ~15–20% of the population at some point. The key clinical distinction is acute vs chronic, as this determines investigation and management approach.

Epidemiology

  • Lifetime prevalence: ~15–20%
  • Acute urticaria: very common, especially in children
  • CSU: prevalence ~0.5–1%; female:male 2:1; peak age 20–40 years
  • CSU duration: median 2–5 years; ~50% resolve within 5 years

Aetiology

Acute: viral infection (commonest cause in children), drugs (NSAIDs, antibiotics, opioids), food (nuts, shellfish, egg), insect stings, latex Chronic spontaneous: autoimmune (~50%; autoantibodies to FcεRI or IgE), idiopathic (~50%); NOT food allergy Physical: dermatographism (most common physical urticaria), cold, cholinergic, pressure, solar, aquagenic

Pathophysiology

  • Mast cell degranulation → histamine, leukotrienes, prostaglandins → vasodilation, increased vascular permeability → wheal formation
  • Autoimmune CSU: IgG autoantibodies to high-affinity IgE receptor (FcεRI) on mast cells → chronic activation
  • Physical urticarias: specific physical stimulus triggers mast cell degranulation

Clinical Presentation

Typical Wheals

  • Raised, erythematous, pruritic
  • Variable size (mm to cm)
  • Individual wheals resolve within 24 hours leaving normal skin
  • Flare-and-wheal response

Angioedema

  • Deep tissue swelling (lips, eyelids, tongue, hands, feet, genitalia)
  • May accompany urticaria (~40% of CSU patients)
  • Lasts 24–72 hours

Physical Urticarias

  • Dermatographism: linear wheals from stroking/scratching skin
  • Cold urticaria: wheals after cold exposure; risk of anaphylaxis in cold water
  • Cholinergic: small 2–3mm wheals after exercise, heat, emotional stress

Red Flags

  • Anaphylaxis (urticaria + hypotension, bronchospasm, airway compromise)
  • Wheals lasting >24 hours (urticarial vasculitis)
  • Angioedema without urticaria (consider hereditary angioedema — C1-INH deficiency)
  • Wheals that leave bruising/purpura

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Urticarial vasculitisWheals >24h, painful, leave bruisingSkin biopsy, complement
AnaphylaxisUrticaria + cardiovascular/respiratory compromiseClinical emergency
Hereditary angioedemaAngioedema WITHOUT urticaria, family historyC4, C1-INH level and function
Erythema multiformeTarget lesions, fixed, may have mucosal involvementClinical, biopsy
Contact urticariaWheals at contact site (e.g. latex)Clinical history, SPT

Diagnosis / Investigation

Acute Urticaria

  • Usually NO investigations needed — clinical diagnosis
  • Consider allergy testing (specific IgE, skin prick test) if clear trigger suspected and future avoidance needed

Chronic Spontaneous Urticaria

  • FBC + differential: eosinophilia (parasites), basopenia
  • CRP/ESR: raised in urticarial vasculitis, autoinflammatory
  • TFTs: thyroid autoimmunity associated with CSU (~10%)
  • Total IgE: may help predict omalizumab response
  • Autologous serum skin test (ASST): research tool for autoimmune CSU
  • Extensive allergy testing NOT recommended in CSU

If Urticarial Vasculitis Suspected

  • Skin biopsy: leucocytoclastic vasculitis
  • Complement (C3, C4): low in hypocomplementaemic urticarial vasculitis (association with SLE)
  • ANA, anti-dsDNA: if SLE suspected

Management

Acute Urticaria

  • Identify and avoid trigger if clear
  • Non-sedating antihistamine: cetirizine 10mg OD, loratadine 10mg OD, or fexofenadine 180mg OD
  • Short course oral prednisolone: 30–40mg for 3–5 days for severe acute urticaria/angioedema
  • Adrenaline IM: if anaphylaxis

Chronic Spontaneous Urticaria (Stepwise — EAACI/BAD)

Step 1: Standard-dose non-sedating antihistamine (e.g. cetirizine 10mg OD) Step 2: Up-dose to 4× licensed dose (e.g. cetirizine 10mg QDS) — first escalation Step 3: Add omalizumab 300mg SC every 4 weeks (anti-IgE monoclonal — NICE TA339) Step 4: Add ciclosporin 3–5mg/kg/day (off-label; specialist only)

  • Avoid: oral corticosteroids long-term; sedating antihistamines as maintenance
  • LTRA (montelukast): weak evidence; can be tried as add-on

Physical Urticarias

  • Non-sedating antihistamines (may need higher doses)
  • Avoidance of specific trigger where possible
  • Cold urticaria: desensitisation protocols (specialist)

Referral Criteria

  • Dermatology/allergy: CSU not controlled with standard antihistamines
  • Immunology: suspected hereditary angioedema
  • Urgent: anaphylaxis, wheals >24h (biopsy for urticarial vasculitis)

Prognosis

  • Acute urticaria: self-limiting in most cases (days to weeks)
  • CSU: median duration 2–5 years; ~50% resolve within 5 years; ~20% persist >10 years
  • Omalizumab: ~65–70% achieve good control (UAS7 ≤6)
  • Autoimmune CSU: may have longer duration
  • Physical urticarias: often persistent but manageable with antihistamines
  • QoL: significant impact; comparable to coronary artery disease in some studies

Other Relevant Information

CSU Treatment Stepladder

StepTreatment
1Standard-dose antihistamine
2Up-dose antihistamine to 4×
3Add omalizumab (anti-IgE)
4Add ciclosporin

Urticaria Activity Score (UAS7)

ScoreSeverity
0–6Well-controlled
7–15Mild
16–27Moderate
28–42Severe