Chronic Urticaria: Navigating the Evolving Treatment Landscape (Recording)

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Published: June 8, 2026

Revised: September 10th, 2026

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This webinar was recorded on July 7, 2026

Imagine waking up and not knowing whether today will bring a wave of relentless, unpredictable hives. For roughly 0.5% to 1% of the global population living with chronic urticaria (CU), that uncertainty is daily life. And according to Dr. Nicole Negbenebor, Assistant Professor in Mohs Surgery and Cutaneous Oncology and Director of the Skin of Color Clinic at the University of Iowa Hospitals and Clinics, the clinical community is finally catching up with the complexity this condition demands.

Beyond “Just Hives”

CU is not a nuisance condition. It is a genuine autoimmune disease with two distinct immunological pathways driving it. Type 1 autoimmunity, sometimes called autoallergy, involves IgE autoantibodies that cross-link on mast cells and basophils, triggering rapid degranulation and a cascade of histamine, leukotrienes, and cytokines. Type 2B autoimmunity, mediated by IgG antibodies targeting the IgE receptor itself, produces more severe, refractory disease with slower responses to anti-IgE therapies. Understanding which endotype a patient has is no longer academic. It directly shapes treatment strategy.

Biomarkers are beginning to clarify that picture. Elevated baseline total IgE strongly predicts a robust response to omalizumab. Conversely, very low IgE combined with elevated anti-TPO antibodies signals Type 2B disease, where omalizumab may underperform.

A Widening Treatment Arsenal

First-line management still centers on second-generation H1 antihistamines like cetirizine or fexofenadine, sometimes escalated to four times the standard daily dose during flares. Short courses of systemic steroids, strictly limited to three to five days, can manage acute rescue situations, but long-term steroid use remains contraindicated given the well-documented risks of bone loss, insulin resistance, and systemic toxicity.

For antihistamine-refractory patients, omalizumab has long been the gold standard biologic. Now, dupilumab, the anti-IL-4 receptor antibody already proven in atopic dermatitis and asthma, has earned approval for moderate to severe CU, simultaneously blocking IL-4 and IL-13 signaling to stabilize mast cells.

Perhaps the most exciting recent development is remibrutinib, an oral BTK inhibitor. By blocking Bruton’s tyrosine kinase intracellularly, it halts the degranulation cascade before it begins. For patients who genuinely cannot tolerate injectable biologics, this oral twice-daily option represents a meaningful clinical advance.

Emerging therapies targeting siglec-8 receptors, MRGPRX2, C5aR1, alarmins like TSLP and IL-33, and anti-KIT receptor antibodies suggest the pipeline is far from exhausted.

One underappreciated clinical challenge is accurate diagnosis in patients with darker skin tones. A Yale and Brown University-trained dermatologist whose work centers on skin of color advocacy and expanding access to care for underserved communities, Dr. Negbenebor brings particular authority to this point. Classic textbook presentations describe bright red wheals, but in patients with higher Fitzpatrick skin types, active urticaria may appear violaceous or hyperpigmented rather than erythematous. This leads to systematic underestimation of UAS7 scores and, consequently, undertreated disease. Her practical guidance is straightforward: palpate the active border. The edematous, raised quality of an active wheal is detectable by touch regardless of skin tone, and tactile assessment should complement visual evaluation in every patient encounter.

Shared Decision-Making as Clinical Strategy

All the pharmacological sophistication in the world means little without patient buy-in. Up to 40% of patients fail first-line therapy due to poor adherence, often rooted in fear of side effects or discomfort with self-injection. Helping patients understand realistic treatment timelines, setting clear control targets, and addressing injection anxiety with practical strategies like ice application and supervised teaching sessions can meaningfully improve outcomes.

The evolving landscape of chronic urticaria treatment is genuinely promising. The clinical imperative now is ensuring that every patient, regardless of skin tone, needle tolerance, or insurance status, has access to individualized, evidence-based care.

Our speaker:

Dr. Nicole Negbenebor is an Assistant Professor in Mohs Surgery and Cutaneous Oncology and Director of the Skin of Color Clinic, Director of Resident Surgery Education, and Director of the HS Clinic at the University of Iowa Hospitals & Clinics in Iowa City, Iowa. She completed her Mohs fellowship in the Department of Dermatology at the University of Iowa and attended Yale University for undergraduate studies. After earning her medical degree from Brown University, Dr. Negbenebor completed dermatology residency training at Brown University. Her work focuses on skin of color dermatology, advocacy, and expanding access to dermatologic care for underserved communities. She is also a co-founder of the Skin of Color Community Event Series, an initiative aimed at increasing access to dermatology for underserved populations.

Key Learning Topics

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