Chronic Urticaria: Symptoms, Causes & Treatment

Chronic urticaria (CU) is defined as the recurrence of wheals (hives), angioedema, or both for more than six weeks, occurring on most days. Individual lesions are pruritic, red, and blanching; they characteristically appear and resolve within 24 hours without scarring. Angioedema accompanies wheals in 40–50% of cases. CU affects approximately 1% of the global population, predominantly women aged 20–40, and has a profound impact on sleep, quality of life, and work productivity — often comparable to moderate-to-severe asthma.

CU is classified as chronic inducible urticaria (CIndU) — triggered by specific physical stimuli (cold, pressure, heat, vibration, UV light) — or the more common chronic spontaneous urticaria (CSU), occurring without an identifiable trigger (>70% of cases). In CSU, no cause is found in ~80% of patients; autoimmune mechanisms (IgG autoantibodies against IgE or the high-affinity IgE receptor FcεRI on mast cells) explain 20–45% of cases, establishing CSU as an autoimmune disease in a substantial subset. Rarely, CSU is associated with chronic infections (H. pylori, hepatitis), thyroid autoimmunity, or drug hypersensitivity.

Mast cell degranulation — triggered by IgE crosslinking or direct IgG autoantibody activation — releases histamine, prostaglandins, leukotrienes, and cytokines that produce the characteristic wheal-and-flare response. Second-generation H1 antihistamines are first-line treatment; omalizumab (anti-IgE monoclonal antibody) is highly effective in antihistamine-refractory CSU and has transformed management of severe cases.

• Recurring erythematous pruritic wheals of variable size and shape, appearing and resolving within 24 hours
• Intense pruritus — often nocturnal, disrupting sleep
• Angioedema in 40–50%: sudden deep swelling of lips, eyelids, tongue, or larynx
• Symptom exacerbation by stress, heat, alcohol, and NSAIDs
• No scarring or bruising after wheals resolve — distinguishes from urticarial vasculitis

• Idiopathic in ~80% of CSU — no identifiable cause found after thorough investigation
• Autoimmune IgG antibodies against IgE or FcεRI mast cell receptor — present in 20–45% of CSU
• Physical stimuli (CIndU): cold, pressure, dermographism, heat, exercise, vibration, UV radiation
• Chronic infections: H. pylori (modest association), hepatitis B/C, parasites
• Autoimmune thyroid disease, systemic lupus, or other autoimmune conditions as comorbidities
• Drug-induced: aspirin/NSAIDs, ACE inhibitors, opioids worsening pre-existing CU

Diagnosis is clinical: recurrent wheals or angioedema for >6 weeks with exclusion of urticarial vasculitis (lesions lasting >24 hours or leaving bruising) by skin biopsy. Basic workup: CBC, CRP/ESR, thyroid function (TSH, anti-TPO), H. pylori testing. Physical challenge tests for CIndU (ice-cube test for cold urticaria, dermographometer for symptomatic dermographism). Autologous serum skin test or basophil activation test for autoimmune CSU. Allergy skin testing has low yield in CSU and is not routinely recommended.

First-line: second-generation H1 antihistamines (cetirizine, loratadine, fexofenadine, bilastine) — up to 4× standard dose for inadequate control (licensed in guidelines). Second-line: omalizumab 300 mg SC every 4 weeks — significantly effective in >80% of antihistamine-refractory CSU patients; approved for this indication. Third-line: cyclosporine for severe refractory cases. Avoid triggers, NSAIDs, and alcohol. Short systemic corticosteroid courses (3–5 days) for acute severe flares only — not for maintenance. Novel agents: ligelizumab (anti-IgE) and anti-Siglec-8 are in clinical trials.

• Laryngeal angioedema — rare but potentially life-threatening; epinephrine should be prescribed for patients with angioedema
• Depression and anxiety from chronic unpredictable disease course
• Significant quality-of-life impairment affecting work, sleep, and relationships

• Identify and avoid personal triggers: aspirin/NSAIDs, alcohol, physical stimuli, emotional stress
• Consistent daily antihistamine dosing (not on-demand) to maintain baseline symptom control
• Treatment of any identified comorbid conditions (H. pylori eradication, thyroid management)
• Carry epinephrine auto-injector if angioedema is present