Transient pruritic edematous wheals from mast cell degranulation; acute (<6 wks) or chronic (≥6 wks).
Also known as: urticaria, hives, wheals, chronic spontaneous urticaria, CSU, angioedema
Overview
An inflammatory disorder of the dermis characterized by transient, pruritic, edematous wheals (hives), each lasting <24 hours, with normal-appearing skin between flares. Often accompanied by angioedema (deeper dermal/subcutaneous edema). Classified by duration: acute (<6 weeks) and chronic (≥6 weeks).
Epidemiology
Lifetime prevalence ~20% for acute urticaria. Chronic spontaneous urticaria (CSU) affects ~0.5-1% of adults; female predominance 2:1; peak ages 20-40.
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Question 1DermatologyMedium
A 28-year-old woman presents with a 3-day history of an intensely itchy, recurrent rash. She reports raised, pink, well-circumscribed plaques on her trunk and arms that last a few hours, fade completely, then recur in new locations, with each individual lesion resolving within 24 hours and leaving no bruising or skin discoloration. She has no fever, joint pain, mucosal lesions, or breathing difficulty. On examination, stroking her forearm with a tongue depressor produces a linear wheal, and the intervening skin appears entirely normal. Which of the following is the most likely diagnosis?
AContact dermatitis
BChronic urticaria
CAcute urticaria
DErythema multiforme
EUrticarial vasculitis
Reveal answer & full explanation
Correct answer: C — Acute urticaria
AContact dermatitis
BChronic urticaria
CAcute urticaria✓
DErythema multiforme
EUrticarial vasculitis
Why Acute urticaria is correct
Transient, migratory, intensely pruritic wheals in which each individual lesion lasts under 24 hours and resolves with completely normal skin in between is the classic, defining presentation of urticaria; a course under 6 weeks makes it acute.
The lesions fade without residual purpura, scarring, or pigment change, and the patient lacks systemic involvement (no fever, arthralgia, mucosal lesions, or airway symptoms).
A linear wheal produced by stroking the skin is dermographism, the most common physical (inducible) urticaria, further supporting mast cell-mediated hives.
Why the others are wrong
Urticarial vasculitis produces wheal-like lesions that persist beyond 24 hours, burn or hurt rather than itch, and leave residual purpura or hyperpigmentation, with leukocytoclastic vasculitis on biopsy; her fleeting, cleanly resolving lesions argue against it.
Erythema multiforme produces fixed target lesions with a dusky center, often with mucosal involvement and an HSV or drug trigger; the lesions last days rather than hours and do not migrate.
Contact dermatitis is an eczematous, often vesicular eruption confined to the site of allergen contact with a delayed, persistent course, not transient migratory wheals appearing across the trunk and arms.
Chronic urticaria — the recurring crops of hives and the dermographism are tempting, because symptomatic dermographism is a common chronic inducible urticaria, but chronic urticaria requires wheals recurring for more than 6 weeks; a 3-day course is acute urticaria no matter how often the lesions come and go.
Question 2DermatologyMedium
A 34-year-old woman has had daily itchy hives for the past 4 months. Individual wheals are raised, pink, and migratory, each fading within several hours and leaving completely normal skin behind. She has no fever, joint pain, or residual bruising, and no identifiable food or drug trigger. Past history includes Hashimoto thyroiditis, and TPO antibodies are elevated. A diagnosis of chronic spontaneous urticaria is made. Which of the following best explains the findings?
ABradykinin accumulation from deficient C1 esterase inhibitor activity
BClonal mast cell expansion from an activating KIT D816V mutation
CKeratinocyte apoptosis from cytotoxic T cells targeting HSV antigen
DIgG autoantibodies cross-link the high-affinity IgE receptor on mast cells
EImmune complex deposition driving leukocytoclastic vasculitis of dermal vessels
Reveal answer & full explanation
Correct answer: D — IgG autoantibodies cross-link the high-affinity IgE receptor on mast cells
ABradykinin accumulation from deficient C1 esterase inhibitor activity
BClonal mast cell expansion from an activating KIT D816V mutation
CKeratinocyte apoptosis from cytotoxic T cells targeting HSV antigen
DIgG autoantibodies cross-link the high-affinity IgE receptor on mast cells✓
EImmune complex deposition driving leukocytoclastic vasculitis of dermal vessels
Why IgG autoantibodies cross-link the high-affinity IgE receptor on mast cells is correct
Chronic spontaneous urticaria (CSU) is largely a non-IgE immunologic process: in roughly a third of patients, IgG autoantibodies target the alpha subunit of the high-affinity IgE receptor (FcεRI) or target IgE itself, cross-linking the receptor and driving mast cell and basophil degranulation.
Released histamine, leukotrienes, and prostaglandins cause vasodilation, increased capillary permeability, and plasma extravasation into the dermis, producing transient pruritic wheals with normal skin between flares.
The association with autoimmune thyroid disease (Hashimoto, elevated TPO antibodies) and the absence of an external IgE trigger fit this autoimmune CSU mechanism. Per EAACI/AAAAI guidance, management starts with second-generation H1 antihistamines, up-titrated to as much as 4x dose, with omalizumab (anti-IgE) as the preferred add-on.
Why the others are wrong
Immune complex deposition driving leukocytoclastic vasculitis of dermal vessels — urticarial vasculitis produces lesions that last more than 24 hours, burn rather than itch, and leave residual purpura/pigmentation; here each wheal fades within hours and leaves normal skin.
Clonal mast cell expansion from an activating KIT D816V mutation — this is the driver of systemic mastocytosis in most adults, whose skin lesions are fixed red-brown macules and papules that persist for years and urticate when stroked (Darier sign); it does not produce migratory wheals that fade within hours and leave completely normal skin.
Bradykinin accumulation from deficient C1 esterase inhibitor activity — this is the mechanism of hereditary angioedema, which causes angioedema WITHOUT urticaria/wheals and is unresponsive to antihistamines; this patient has classic itchy wheals.
Keratinocyte apoptosis from cytotoxic T cells targeting HSV antigen — the mechanism of erythema multiforme, a classic urticaria look-alike, but its targetoid lesions are fixed in place for a week or more, often with a dusky or blistered center, rather than migrating and fading within hours to leave completely normal skin as these wheals do.
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Acute: viral infections (most common in children), foods (peanuts, tree nuts, shellfish, eggs, dairy, soy), medications (NSAIDs, antibiotics, opioids, contrast media), insect stings, latex
Chronic spontaneous: autoimmune disease (thyroid disease in 25%, ANA positive in ~30%, autoimmune antibodies against FcεRI or IgE), atopic disease, stress
Mast cell and basophil degranulation releases histamine, leukotrienes, prostaglandins, cytokines → vasodilation, increased capillary permeability, plasma extravasation into dermis (wheal) or deeper tissue (angioedema). Triggers: IgE-mediated (food/drug allergy), non-IgE immunologic (autoantibodies in CSU), direct mast cell activators (opioids, contrast), complement-mediated (urticarial vasculitis, hereditary angioedema), pseudoallergic (NSAIDs via COX-1 inhibition).
Clinical presentation
Symptoms
Intense pruritus (rarely burning or stinging)
Sudden onset of wheals lasting minutes to <24 hours each, fluctuating in location
Angioedema: face (lips, eyelids), hands, feet, genitalia, larynx — may compromise airway
Systemic symptoms (anaphylaxis): dyspnea, wheezing, syncope, GI distress — IM EPINEPHRINE
Signs / physical exam
Wheals: well-circumscribed raised pink or pale-centered plaques with surrounding flare; size mm to >10 cm; round, oval, polycyclic, annular; resolve without scarring or pigment change
Dermographism: linear wheal where skin is stroked — most common physical urticaria
Cholinergic urticaria: small (1-3 mm) wheals with surrounding flare after exercise, hot showers, emotional stress
Cold urticaria: wheal/angioedema in areas of cold contact; positive ice cube test
Angioedema: deeper, often asymmetric, non-pitting swelling of face, lips, tongue, extremities; LESS pruritic, more burning/painful
Classic findings
Transient migratory pruritic wheals lasting <24 hours each, with completely normal skin between.
Differential diagnosis
Urticarial vasculitis — Individual lesions >24 hours, painful/burning rather than itchy, residual purpura/pigmentation; biopsy = leukocytoclastic vasculitis; check complement, ANA, SSA, hep C
Erythema multiforme — Target lesions, dusky center, fixed >24 hours, mucosal involvement; HSV or drug trigger
Mastocytosis / mastocytoma — Persistent reddish-brown macules/papules with Darier sign (urticate on stroking); elevated tryptase
Hereditary angioedema (HAE) — Angioedema WITHOUT urticaria, family history, recurrent abdominal pain attacks, low C4 and C1-INH levels
ACE-inhibitor angioedema — Angioedema without urticaria, often facial/tongue, days to years after starting ACEi
Atopic dermatitis — Chronic eczematous lesions, lichenification, flexural; not transient
Contact urticaria — Wheals at site of contact with latex, food, plants; immediate or delayed
Diagnostic workup
Diagnostic criteria
Clinical: characteristic wheals lasting <24 hours each, total episode duration determines acute vs chronic; angioedema without urticaria requires HAE/ACEi workup.
Labs
Acute urticaria: usually no workup needed unless trigger unclear — careful history identifies most triggers (foods, drugs, infections)
Chronic spontaneous urticaria: limited testing — CBC with differential and CRP/ESR in all patients; in specialist care, total IgE and IgG anti-TPO per the international guideline (low total IgE with high anti-TPO suggests autoimmune CSU and a poorer omalizumab response); the US practice parameter also allows TSH
If suspicion of urticarial vasculitis: skin biopsy, C3/C4, ANA, RF, hepatitis B/C, complement profile
If suspicion of hereditary angioedema: C4 (low during AND between attacks), C1-INH level and function, C1q
Autologous serum skin test or basophil activation test for autoimmune CSU (research/specialty)
Specific IgE / skin prick testing only for clinically suspected food/drug allergy with consistent history
Imaging
Not indicated
Diagnostic algorithm
flowchart TD
A[Itchy wheal,<br/>each lasting <24 h] --> B{Duration of episode}
B -->|<6 weeks| C[Acute urticaria]
B -->|≥6 weeks| D[Chronic urticaria]
C --> E[Identify trigger:<br/>infection, food, drug]
D --> F[Limited workup: CBC, CRP, TSH, TPO Ab]
E --> G[2nd-gen H1 antihistamine<br/>± short prednisone course]
F --> G
G --> H{Controlled in 2-4 wks?}
H -->|No| I[Up-titrate H1 antihistamine<br/>to 4x dose]
I --> J{Controlled?}
J -->|No| K[Add omalizumab<br/>or cyclosporine]
A --> L{Wheal lasts<br/>>24 h, painful,<br/>leaves purpura?}
L -->|Yes| M[Urticarial vasculitis<br/>Biopsy + autoimmune workup]
A --> N{Angioedema<br/>without wheals?}
N -->|Yes| O[Check C4, C1-INH<br/>ACEi history → Hereditary AE or ACEi reaction]
Urticaria evaluation and step-care management algorithm.
Solar urticaria — sun avoidance, broad-spectrum SPF 50+, antihistamines, phototherapy desensitization
Hereditary angioedema
Acute: IV C1 esterase inhibitor concentrate, ecallantide, icatibant
Prophylaxis: lanadelumab, berotralstat, attenuated androgens (danazol; rarely used now)
NOT responsive to antihistamines, epinephrine, or steroids
ACEi-induced angioedema
Discontinue ACE inhibitor permanently (angioedema recurs on an ARB in a minority, roughly 2-10%; an ARB may be used cautiously if needed)
Supportive care; refractory cases may respond to icatibant
Second-line / adjunct
Avoid first-generation sedating antihistamines (diphenhydramine, hydroxyzine) as routine therapy — sedation, anticholinergic effects, and short half-life make them inferior to second-generation agents
H2 antagonist (famotidine) addition has modest benefit
Leukotriene receptor antagonist (montelukast) sometimes added, especially for NSAID-sensitive patients
Counsel: most chronic urticaria resolves within 1-5 years
Complications
Anaphylaxis with airway compromise — life-threatening
Sleep disturbance, decreased quality of life, depression, work/school impairment
Adverse effects from chronic systemic corticosteroids (avoid if possible)
Misdiagnosis as drug allergy → unnecessary medication restriction
PANCE pearls
Individual wheals lasting >24 hours, painful rather than itchy, with residual purpura = urticarial vasculitis — biopsy.
Angioedema WITHOUT urticaria → think hereditary angioedema or ACE inhibitor reaction; antihistamines and steroids do NOT work.
Up-titration of second-generation H1 antihistamines to 4x dose is safe, evidence-based, and recommended BEFORE adding other agents.
Omalizumab is the most effective add-on for chronic spontaneous urticaria refractory to high-dose antihistamines.
Acute urticaria + respiratory or hemodynamic symptoms = anaphylaxis = IM epinephrine FIRST, not antihistamines.
References
International Urticaria Guideline 2026 (GA²LEN/EDF/APAAACI/AAD) — The International Guideline for the Definition, Classification, Diagnosis and Management of Urticaria (Zuberbier et al., Allergy 2026;81(8):2582-2632)
AAAAI/ACAAI 2014 — The Diagnosis and Management of Acute and Chronic Urticaria: 2014 Update (Bernstein et al., J Allergy Clin Immunol 2014;133(5):1270-1277)
WAO 2020 — World Allergy Organization Anaphylaxis Guidance 2020 (Cardona et al., World Allergy Organ J 2020)
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