Optimizing Care for Patients with Urticaria

In an interview with Dermatology Times, Jason Hawkes, MD, MS, a medical dermatologist and principal investigator at the Oregon Medical Research Center, highlighted significant unmet needs in the management of chronic urticaria. Historically, these patients have often been managed by allergists, who frequently employ extensive testing protocols. Hawkes emphasizes the importance of critically evaluating the evidence behind these tests, especially when considering their prognostic value and impact on patient care.

A common practice in the evaluation of patients with chronic urticaria involves a series of laboratory tests, including assessments of thyroid function, iron levels, inflammatory markers (eg, ESR, CRP), and blood counts. The rationale behind this testing stems from the recognition that patients with chronic urticaria are at an increased risk for other autoimmune conditions, such as autoimmune thyroiditis. However, Hawkes points out that while conditions like hypothyroidism are common comorbidities, they do not cause urticaria. Instead, urticaria often precedes the onset of these conditions, underscoring the importance of understanding their correlation rather than causation.

Hawkes says studies, particularly those conducted in Europe, have shown that less than 1% of patients with chronic urticaria have an underlying diagnosis identified through such workups. These findings challenge the utility of blanket laboratory testing, especially when it fails to guide therapeutic decisions or predict patient outcomes. From a cost-effectiveness perspective, these tests may not represent the best use of healthcare resources and can impose financial burdens on patients.

An exception to this general critique is the measurement of immunoglobulin E (IgE) levels. Elevated IgE levels have been associated with a better response to anti-IgE therapy, such as omalizumab. However, the predictive value of IgE levels is not absolute; patients with high IgE levels may not respond to therapy, while those with low levels can exhibit significant improvement. This inconsistency highlights the need for more reliable biomarkers that can predict therapeutic responses across different treatment options.

The complexity of chronic urticaria extends beyond IgE-mediated pathways. Hawkes discussed the role of type 2b autoimmunity, where antibodies such as IgG or IgA, rather than IgE, can activate mast cells and drive disease. This understanding opens new avenues for therapeutic targets, including anti-C-kit therapies, which aim to deplete mast cells. By reducing mast cell populations, these therapies could potentially mitigate disease activity regardless of the underlying mechanism.

Hawkes also emphasizes the importance of subclassifying patients with chronic urticaria to better understand their disease and tailor treatments. For instance, some patients predominantly experience angioedema, while others have more significant wheal formation. Understanding these subtypes could provide insights into why certain patients respond differently to therapies. Additionally, the field is beginning to explore the reasons behind varying responses in patients with chronic spontaneous urticaria versus chronic inducible urticaria.

Looking ahead, Hawkes envisions a shift in dermatology toward evidence-based testing that directly informs clinical management. By focusing on meaningful biomarkers and patient subtypes, the specialty aims to develop more consistent and effective therapies. This approach has the potential to optimize patient outcomes and reduce unnecessary healthcare expenditures. As research advances, the goal is to refine diagnostic and therapeutic strategies, ensuring that they align with the individual needs of patients with chronic urticaria.