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Disease modification in chronic spontaneous urticaria.

Marcus Maurer1,2, Pavel Kolkhir1,2, Manuel P Pereira1,2

  • 1Urticaria Center of Reference and Excellence (UCARE), Institute of Allergology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Allergy
|July 24, 2024
PubMed
Summary

Disease-modifying treatments (DMTs) for chronic spontaneous urticaria (CSU) aim to alter the disease course by targeting underlying mechanisms, not just symptoms. Effective DMTs should delay progression and achieve long-term remission.

Keywords:
chronic spontaneous urticariadisease modificationdisease‐driving signalsdisease‐modifying treatmentstherapy‐free clinical remission

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Area of Science:

  • Immunology
  • Dermatology
  • Pharmacology

Background:

  • Chronic spontaneous urticaria (CSU) is an inflammatory skin condition with limited treatment options focusing on symptom management.
  • Current therapies do not address the underlying disease progression or pathophysiology.
  • There is a critical need for treatments targeting upstream pathways to modify CSU disease course.

Purpose of the Study:

  • To define "disease modification" in the context of CSU treatment interventions.
  • To establish criteria for disease-modifying treatments (DMTs) in CSU.
  • To identify potential therapeutic targets for CSU beyond symptom relief.

Main Methods:

  • Conceptual framework development for disease modification in CSU.
  • Definition of criteria for DMTs, including prevention of progression, long-term remission, and mechanism-based action.
  • Review of potential therapeutic targets and biomarkers for CSU.

Main Results:

  • Disease modification in CSU is defined as a favorable, enduring change in pathophysiology and disease course.
  • DMT criteria include delaying progression, inducing therapy-free remission, and affecting underlying mechanisms.
  • Potential DMTs may target Bruton's Tyrosine Kinase, IL-4/IL-13, IgE autoantibodies, cytokine profiles, gut microbiome, and barrier function.

Conclusions:

  • Disease-modifying treatments offer a new paradigm for CSU management, moving beyond symptomatic relief.
  • Future therapies should aim to halt disease progression and achieve sustained remission by targeting immune pathways.
  • Developing DMTs for CSU could prevent associated comorbidities and improve long-term patient outcomes.