In this video blog, Dr. Jason Hawkes summarizes his lecture in the panel discussion, Discussions in CSU , on November 8, 2024, 5th Annual Elevate-Derm West Conference at the Westin Kierland Resort in Scottsdale, AZ.

In this video

Dr. Hawkes starts by dividing urticaria at the six-week mark: patients with hives for only a couple of weeks are acute, while those with months of disease are chronic. Within the chronic group, about 20% have chronic inducible (physical) urticaria driven by a specific trigger — heat, pressure, cold, or UV light — and the other 80% have chronic spontaneous (formerly "idiopathic") urticaria with no trigger at all. Acute cases, most often in kids under five, are usually idiopathic and typically resolve within a week or two. On workup, he pushes back on the reflex to order thyroid panels, CBC, CMP, and sed rate: citing a British Association of Dermatologists study, far less than 1% of true chronic patients had an identifiable cause, so he reserves testing for symptom-driven or clinically suspected conditions (autoimmune thyroiditis being by far the most common association, up to ~50%) and spends his time educating patients that the labs rarely explain their disease.

On treatment, Dr. Hawkes calls antihistamines first line — cheap, fast, effective, and low-risk — and stresses pushing second-generation H1 blockers up to four times the dose before calling someone a non-responder. He favors the international guideline approach of moving non-responders to omalizumab rather than layering on leukotriene antagonists or cimetidine, which he says "hasn't really been all that effective in my hands." Broad-acting agents like cyclosporine and methotrexate work but carry renal and hepatic strings and can't be used indefinitely — a problem because most patients still have disease at 10 years. He argues dermatology has been slow to embrace omalizumab (patients chasing a cause through allergy, in-clinic waiting periods, and a black box warning that actually came from asthma patients, not urticaria) and points to two late-stage options ahead: dupilumab, targeting type 2 inflammation, and remibrutinib, an oral, highly selective BTK inhibitor that is fast, effective, and works for both urticaria and angioedema.

  • Use six weeks to split acute from chronic; within chronic, ~20% are inducible (trigger-based) and ~80% are spontaneous with no trigger.
  • Skip the reflex lab barrage — less than 1% of chronic patients have an identifiable cause, so test only when symptoms or clinical suspicion warrant it.
  • Antihistamines are first line; escalate a second-generation H1 up to four times the dose before deeming a patient a non-responder.
  • Move non-responders to omalizumab — one of the broadest, most robust trial programs — before reaching for broad-acting agents like cyclosporine or methotrexate.
  • Prepare patients from day one that CSU is chronic — most still have disease years out — and that the black box warning tied to omalizumab came from asthma patients, not urticaria.
  • Watch for dupilumab and the oral BTK inhibitor remibrutinib as emerging, injection-optional options with reassuring safety data.