Urticaria
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Urticaria (Hives)
Definition
Urticaria (hives) is one of the most common cutaneous reaction patterns, characterized by well-circumscribed, raised wheals with erythematous serpiginous borders and blanched centers. Individual lesions last <24 hours, are intensely pruritic, migrate around the body, and leave no bruising or scarring. Angioedema, which involves deeper dermis and subcutaneous tissues, co-exists in roughly 40% of cases. - Harrison's Principles of Internal Medicine 22E, p. 2849
Classification
| Category | Subtypes | Key Features |
|---|---|---|
| Acute urticaria | Allergic, infection-triggered, drug-induced | Duration <6 weeks; >2/3 of new cases |
| Chronic spontaneous urticaria (CSU) | Autoimmune (~45%), idiopathic | Duration ≥6 weeks, no identifiable trigger; peaks 3rd-4th decade |
| Chronic inducible urticaria | Physical subtypes (below) | Triggered by a specific physical stimulus |
Inducible (Physical) Subtypes
| Subtype | Trigger | Clinical Clue |
|---|---|---|
| Dermatographism | Firm stroking of skin | Linear wheals; 2-5% prevalence |
| Cold urticaria | Cold contact/temperature drop | Ice cube test positive; risk of anaphylaxis on swimming |
| Pressure urticaria | Sustained pressure (belts, straps) | Often accompanies CSU |
| Cholinergic urticaria | Sweating, exercise, hot bath | Tiny 1-4 mm wheals with wide flare; common in young |
| Solar urticaria | UV/visible radiation | Minutes after sun exposure |
| Aquagenic urticaria | Water (any temperature) | Distinguished from cold/heat urticaria by temperature independence |
| Vibratory urticaria | Vibratory stimuli | ADGRE2 mutation in familial form |
| Contact urticaria | Skin contact with substance | IgE-mediated or non-immunologic |
- Fitzpatrick's Dermatology, pp. 714-732
Epidemiology
- Lifetime prevalence ~8-20% of the general population
- CSU: prevalence ~0.8% in any given year; women affected ~2x more than men
- Peak age for CSU: 20-40 years (bimodal in children and adults)
- 50% of CSU patients have disease for ≥5 years
Pathophysiology
Urticaria arises from mast cell degranulation in the superficial dermis, releasing histamine, slow-reacting substance of anaphylaxis (leukotrienes), bradykinin, kallikrein, and other mediators. This causes localized vasodilation and increased vascular permeability.
Mechanisms:
- IgE-mediated (immunologic): Classic type I hypersensitivity - food allergens, drugs, insect stings
- Autoimmune: Up to 45% of CSU - IgG autoantibodies against IgE or the α-chain of FcεRI on mast cells; positive autologous serum skin test (ASST)
- Immune complex-mediated: Complement activation, as in urticarial vasculitis and serum sickness
- Non-immunologic direct mast cell release: Opioids, vancomycin, NSAIDs, contrast media, certain foods (strawberries, lobster - histamine release)
- Bradykinin-mediated: ACE inhibitor-induced angioedema, hereditary angioedema (HAE)
- Goldman-Cecil Medicine, p. 4301; Harrison's 22E, p. 2850
Common Triggers / Etiology
Acute urticaria:
- Drugs: Penicillin (most common antibiotic trigger), NSAIDs/aspirin (probably non-immunologic), opioids, ACE inhibitors
- Foods: Seafood, tree nuts, eggs, peanuts; strawberries/lobster (non-immunologic histamine release)
- Infections: Rhinovirus, rotavirus, hepatitis viruses, EBV/mono, coxsackievirus; also candida, dermatophytes, parasites
- Contact: Animal dander/saliva, latex, cosmetics, plants
Chronic urticaria:
-
Autoimmune (most common identifiable cause in CSU)
-
Thyroid disease (anti-thyroid peroxidase / anti-thyroglobulin antibodies, even when euthyroid)
-
Occult infection (H. pylori, dental abscess)
-
Stress and psychological factors (aggravating, not causal)
-
Malignancy (rare; hematologic malignancies have weak association)
-
Rosen's Emergency Medicine, p. 2413; Fitzpatrick's Dermatology, p. 5845
Clinical Features
Wheals (urticaria):
- Pink-to-red, raised, blanching plaques with surrounding erythema ("wheal and flare")
- Any body surface, intensely pruritic (stinging in cholinergic type)
- Individual lesions last <24 h; inducible urticarias <2 h
- Crops of new lesions appear as old ones fade
Angioedema:
- Deeper, asymmetric, non-pitting swelling; more painful than pruritic
- Favors periorbital and perioral regions, tongue, larynx, GI tract
- Laryngeal angioedema is life-threatening
- Takes hours-to-days to resolve
This is what dermatographism looks like on provocation:
Investigations
For acute urticaria, extensive workup is rarely needed. For chronic urticaria, guided investigation is appropriate:
| Test | Indication |
|---|---|
| CBC, ESR/CRP | Baseline; eosinophilia, infection screen |
| Anti-thyroid antibodies (anti-TPO, anti-TG) | Autoimmune thyroid disease association |
| ASST (autologous serum skin test) | Screen for functional IgG autoantibodies (sensitivity ~60-70%) |
| Basophil histamine release assay | More specific for anti-FcεRI/anti-IgE autoantibodies |
| Skin biopsy + DIF | Rule out urticarial vasculitis (if lesions last >24h, leave bruising, or systemic features) |
| C3, C4, CH50 | Suspected urticarial vasculitis or HAE |
| Serum IgE, specific IgE RAST | If allergic trigger suspected |
| Provocation tests | For each inducible subtype (ice cube test, dermographometer, etc.) |
- Fitzpatrick's Dermatology, p. 5996
Differential Diagnosis
- Urticarial vasculitis (lesions last >24h, leave purpura/bruise)
- Bullous pemphigoid (urticarial phase)
- Erythema multiforme
- Contact dermatitis
- Mastocytosis / urticaria pigmentosa
- Angioedema from ACE inhibitors / HAE (bradykinin-mediated - does NOT respond to antihistamines)
- Adult-onset Still disease
- Schnitzler syndrome
- Polymorphic eruption of pregnancy
Treatment
General Principles
- Identify and eliminate triggers
- Avoid NSAIDs and aspirin (can worsen most urticaria types)
- Note: bradykinin-mediated angioedema (HAE, ACE inhibitor) does NOT respond to antihistamines or steroids - requires specific therapy (C1-INH, icatibant, ecallantide)
EAACI/AAAAI Stepwise Algorithm for Chronic Urticaria
| Step | Treatment |
|---|---|
| Step 1 | Second-generation H1-antihistamine (sgAH) monotherapy (cetirizine, loratadine, fexofenadine, bilastine) + trigger avoidance |
| Step 2 (if inadequate at 2-4 weeks) | Up-dose sgAH up to 4x standard dose; add H2 antagonist; add leukotriene receptor antagonist; add first-generation AH at bedtime |
| Step 3 | Add potent antihistamine (hydroxyzine or doxepin) as tolerated |
| Step 4 | Add omalizumab (anti-IgE biologic, 300 mg SC monthly) or cyclosporin |
Omalizumab is highly effective for antihistamine-refractory CSU. A 2025 systematic review and meta-analysis confirms its safety and efficacy in pediatric CSU as well (PMID 40545961).
A 2024 systematic review (PMID 38420865) of acute urticaria treatment confirms the priority of antihistamines with epinephrine reserved for anaphylactic presentations.
Systemic corticosteroids: Generally avoided long-term for idiopathic urticaria due to toxicity. Indicated short-term for severe exacerbations, pressure urticaria, urticarial vasculitis, or debilitating disease refractory to antihistamines.
Refractory/specialty cases:
-
Urticarial vasculitis: hydroxychloroquine, dapsone, colchicine ± steroids
-
HAE: acute attacks - icatibant (bradykinin-2 receptor antagonist), ecallantide (kallikrein inhibitor), purified C1-INH or fresh frozen plasma; prophylaxis - lanadelumab, C1-INH, attenuated androgens
-
Other refractory options: methotrexate, tacrolimus, IV immunoglobulin, plasmapheresis, narrow-band UVB
-
Fitzpatrick's Dermatology, p. 732; Harrison's 22E, pp. 2851-2854; Goldman-Cecil Medicine, p. 4302
Key Points to Remember
- Urticaria = superficial dermis; angioedema = deep dermis/subcutaneous; ~40% have both
- Chronic = ≥6 weeks; CSU is most common chronic form and is often autoimmune
- Individual wheals lasting >24h, with bruising or systemic signs → biopsy to rule out urticarial vasculitis
- ACE inhibitor / HAE angioedema is bradykinin-mediated → antihistamines and epinephrine are ineffective → needs C1-INH or icatibant
- Stepwise treatment: sgAH → up-dose → add omalizumab → add cyclosporin
- NSAIDs worsen urticaria in most patients and should be avoided
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