Chronic Spontaneous Urticaria Is More Than IgE: New Pathways Drive Targeted Care

As discussions at the American Academy of Dermatology annual meeting emphasized advances in chronic spontaneous urticaria (CSU), evolving research is challenging the long-held view of the disease as primarily driven by immunoglobulin E (IgE).

In this exclusive MedPage Today video, Gil Yosipovitch, MD, of the University of Miami Miller School of Medicine, discusses how a broader understanding of CSU biology is enabling more precise, targeted treatment approaches.

Following is a transcript of his remarks:

Clearly, a lot of our understanding before was that the mast cells are secreting histamine and that histamine is the major mediator, but we now know that there are many factors involved in proteases and other pathways like leukotrienes and cytokines that induce the activity that causes chronic urticaria.

So these drugs address really better the aspect of this disease that is not just mediated by histamine and therefore major advances in better treatment and more precision and targeted treatment is available.

We know now also with IgE, we have known for a long time now with IgE levels, patients with low IgE levels, who are not responding well to omalizumab [Xolair], it targets the IgE and therefore now these drugs are better suited for patients who have low IgE levels and it can go on and on.

What I would say is that also we are facing now drug trials to compare efficacy and in particularly the rapid effect of remibrutinib [Rhapsido] versus dupilumab [Dupixent]. So we will know even better which drug may fit patients of different types of chronic spontaneous urticaria because they’re kind of different presentations of disease and it’s not totally homogeneous.