Urticaria (Hives) — Symptoms, Causes & Treatment | MyMedicPlus

Urticaria (hives) is one of the most common dermatological conditions, characterised by the sudden appearance of transient, intensely pruritic wheals (raised, blanching, erythematous skin plaques) and/or angioedema (deeper soft tissue swelling). Individual urticarial lesions last less than 24 hours at any single site and migrate across the body, distinguishing them from other inflammatory dermatoses such as eczema. Urticaria is classified by duration: acute (below 6 weeks — often allergic or infective), and chronic (above 6 weeks — spontaneous or inducible). Chronic spontaneous urticaria (CSU) affects approximately 1% of the population, frequently without identifiable external triggers, and significantly impairs quality of life. Physical urticaria subtypes — dermographism, cold, cholinergic, and pressure — are triggered by specific physical stimuli. Angioedema accompanies urticaria in 40% of CSU cases; laryngeal angioedema is a life-threatening emergency requiring immediate intramuscular epinephrine.

Acute urticaria: IgE-mediated allergic reactions (foods — nuts, shellfish, eggs; drugs — NSAIDs, penicillin; insect stings), non-allergic drug reactions (opioids, radio-contrast), infections (viral — common cold, EBV, COVID-19; bacterial; parasitic). Chronic spontaneous urticaria (CSU): autoimmune (IgG anti-FcεRI or anti-IgE autoantibodies activating mast cells and basophils — in approximately 40%); thyroid autoimmunity (Hashimoto's — anti-TPO antibodies — in 10%); H. pylori infection; psychological stress. NSAIDs (via prostaglandin pathway disruption) and ACE inhibitors (via bradykinin excess) exacerbate CSU. Physical urticaria subtypes: dermographism (urticaria factitia — linear whealing from light skin stroking — the most common physical subtype, affecting 4-5% of the population); cold urticaria (cold water, food, or air contact — cold immersion test); cholinergic urticaria (heat, exercise, emotional stress — characteristically small 1-3 mm papular wheals); solar urticaria (UV exposure); pressure urticaria (delayed 4-8 hours after sustained skin pressure from heavy clothing or belts). Exercise-induced anaphylaxis: urticaria plus systemic anaphylaxis triggered by exercise — sometimes requiring cofactors such as aspirin or wheat ingestion.

Wheals (urticarial plaques): raised, erythematous, pruritic skin plaques with central pallor surrounded by an erythematous flare; blanch completely on pressure (distinguishing them from purpura or petechiae); characteristically transient — each individual wheal lasts less than 24 hours (typically 1-6 hours) and resolves without residual marking, bruising, or skin change; new wheals appear as old ones fade, giving a migrating quality. Intense pruritus (itching) is the cardinal symptom — often worst in the evening and at night from physiological histamine release, causing severe sleep disruption and insomnia. The wheals range from small papular lesions (1-3 mm — characteristic of cholinergic urticaria triggered by heat, exercise, or emotional stress) to large coalescing plaques covering the entire trunk, limbs, and face. Angioedema (concurrent in 40-50% of chronic spontaneous urticaria patients): asymmetric, non-pitting, deep dermal and submucosal swelling affecting the lips, eyelids, tongue, soft palate, genitalia, and extremities; typically not pruritic but often painful, burning, or tight; resolves over 24-72 hours; most dangerous when affecting the tongue, larynx, or pharynx where it can cause life-threatening airway obstruction. Dermographism (urticaria factitia — the most common physical urticaria, affecting 4-5% of the general population): immediate raised, linear, erythematous whealing within 2-3 minutes of light mechanical stroking of the skin; demonstrated clinically by running the blunt end of a spatula along the forearm. Pressure urticaria: delayed deep, aching, oedematous swelling at sites of sustained skin pressure (waistbands, bra straps, shoe straps) appearing 4-8 hours after the pressure is applied.

Acute urticaria: primarily a clinical diagnosis based on characteristic transient wheals; investigation focuses on identifying the trigger — allergy testing (skin prick tests or serum-specific IgE panel for suspected food allergens [peanut, tree nuts, shellfish, milk, egg, wheat] or drug allergens [penicillin, NSAIDs, aspirin]); blood tests and throat swab for infection if clinically relevant; baseline tryptase within 1-2 hours of an acute anaphylactic reaction. Chronic urticaria lasting more than 6 weeks requires systematic investigation: full blood count (eosinophilia above 0.5 x10^9/L suggests parasitic infection or eosinophilic granulomatosis with polyangiitis); ESR and CRP (elevated in urticarial vasculitis, systemic lupus, or systemic inflammatory disease); thyroid function (TSH) and anti-TPO antibodies (thyroid autoimmunity is present in 10% of CSU patients); antinuclear antibody and anti-double-stranded DNA (if vasculitic features — livedo, joint pain, prolonged individual wheals lasting more than 24 hours suggesting urticarial vasculitis); H. pylori antigen stool test (eradication resolves or significantly improves refractory CSU in 30-40% of H. pylori-positive patients); urinalysis (haematuria and proteinuria in urticarial vasculitis or IgA nephropathy). Total serum IgE (elevated in atopic individuals — supports but does not diagnose IgE-mediated disease); serum tryptase (elevated above 11.4 mcg/L suggests systemic mastocytosis requiring bone marrow biopsy). Physical urticaria provocation tests: ice cube or cold saline-filled glove (cold urticaria — positive if wheal forms within 10 minutes of removal); standardised dermatographometer at 4900 g/cm² (dermographism); exercise or hot bath challenge (cholinergic urticaria). Urticaria Activity Score 7 (UAS7 — a 7-day patient-completed diary scoring wheals and pruritus on 0-3 scales; maximum score 42) is the validated tool for monitoring CSU severity and treatment response, guiding step-up decisions.

Allergen avoidance (acute allergic urticaria). Step 1: Non-sedating second-generation H1 antihistamines (cetirizine 10 mg, fexofenadine 180 mg, bilastine 20 mg, loratadine 10 mg) — first-line for all urticaria. Step 2: Updose antihistamine x4 standard dose if no response at 2 weeks. Step 3: Omalizumab (anti-IgE monoclonal antibody, Xolair) 300 mg monthly SC injection — highly effective for refractory CSU (CRR 35-40%); NICE-approved. Step 4: Cyclosporine A for refractory cases. Short-course prednisolone for severe acute flares (5-7 days). Epinephrine (0.3-0.5 mg IM) for anaphylaxis. Regular monitoring of treatment response, early detection of side effects, and ongoing assessment of disease progression are essential components of optimising patient outcomes over the long term. Treatment plans should be proactively reviewed and appropriately adjusted based on clinical response, patient-reported tolerability, changing patient circumstances, and continuously evolving evidence-based clinical guidelines. Meaningful shared decision-making between patients and their healthcare team, incorporating patient values and treatment preferences, consistently improves both treatment adherence and long-term outcomes.

Anaphylaxis (life-threatening systemic hypersensitivity — urticaria with hypotension, tachycardia, bronchospasm, and angioedema simultaneously; requires immediate intramuscular epinephrine 0.5 mg (0.3 mg from EpiPen) and emergency services; approximately 1-2% of acute urticaria presentations involve anaphylaxis). Laryngeal angioedema (oedema of the larynx causing stridor and acute airway obstruction — requires immediate epinephrine, IV hydrocortisone, IV chlorphenamine, and emergency anaesthetic assessment; potentially fatal without prompt airway management). Hereditary angioedema (HAE — bradykinin-mediated angioedema without urticarial wheals, caused by C1-inhibitor deficiency; completely unresponsive to antihistamines or corticosteroids and must not be treated as histaminergic urticaria; requires specific treatment with C1-inhibitor concentrate, icatibant, or lanadelumab for prevention). Psychosocial complications (chronic urticaria causes sleep disturbance in 60-70% of patients; clinically significant depression and anxiety are significantly more prevalent; DLQI impairment comparable to ischaemic heart disease — justifying escalation to omalizumab for refractory CSU; chronic urticaria resolves spontaneously in 80% within 5 years but causes major quality of life burden in the interim).

Identify and avoid confirmed triggers: a supervised allergen elimination diet (removing the suspect food for 4-6 weeks, then reintroducing under controlled conditions) guided by a specialist dietitian reduces acute urticaria recurrence in confirmed food allergy; wear a medical alert bracelet if previous anaphylaxis; carry two epinephrine auto-injectors (EpiPen 300 mcg for adults, EpiPen Jr 150 mcg for children weighing below 30 kg) and ensure the patient and family members are trained in their use. Avoid known pharmacological triggers: NSAIDs (aspirin, ibuprofen, naproxen — inhibit COX enzymes, shifting arachidonic acid metabolism toward leukotriene production and directly triggering mast cell degranulation in susceptible individuals; use paracetamol as the alternative analgesic); ACE inhibitors (cause bradykinin accumulation — exacerbate urticaria and cause angioedema; switch to ARB if an inhibitor of the renin-angiotensin system is required). Treat identified comorbidities: H. pylori eradication (standard triple therapy: proton pump inhibitor plus clarithromycin plus amoxicillin for 7-14 days) resolves or significantly improves refractory CSU in approximately 30-40% of H. pylori-positive patients; thyroid autoimmunity treatment may improve urticaria in patients with coexistent Hashimoto's thyroiditis and high anti-TPO antibody titres. Complete a UAS7 diary daily to track wheal count and pruritus severity — guides treatment step-up from antihistamines to omalizumab (300 mg monthly for CSU not controlled on maximally dosed non-sedating antihistamines). Omalizumab responders should continue for at least 12 months before attempting gradual dose reduction or cessation; spontaneous remission in 80% within 5 years.

Call emergency services (999/112/911) immediately if urticaria is associated with: swelling of the lips, tongue, throat, or airway (angioedema — risk of airway obstruction); difficulty breathing or wheezing; dizziness, collapse, or feeling faint (anaphylaxis). If you have had previous anaphylaxis, always carry two adrenaline auto-injectors (EpiPens) and use one at the first sign of throat swelling or breathlessness, then call emergency services. See your GP if urticaria: lasts more than 6 weeks (chronic urticaria); occurs daily or near-daily and is significantly affecting quality of life; is associated with fever, joint pain, or bruise-like lesions that do not blanch (possible urticarial vasculitis — requires investigation). Seek dermatology or allergy specialist referral if second-generation antihistamines at licensed doses fail to control symptoms — omalizumab (licensed for antihistamine-refractory chronic spontaneous urticaria) should be considered. Do not delay seeking review — chronic urticaria is highly treatable with modern therapies.