A 34-year-old woman with chronic spontaneous urticaria remains symptomatic despite fourfold up-dosed cetirizine and a 6-month course of omalizumab. Which mechanism best explains the action of omalizumab?
- A Competitive antagonist at the H1 receptor with additional mast cell stabilising activity
- B Anti-C5 monoclonal antibody blocking terminal complement activation
- C Monoclonal antibody that binds free serum IgE and downregulates Fc epsilon RI expression on mast cells ✓
- D Anti-IgE receptor antibody that blocks IgE binding to basophil Fc receptors only
Explanation
Omalizumab is a humanised anti-IgE monoclonal antibody. It binds the A-epsilon-3 domain of free IgE, lowering free IgE levels, and this in turn downregulates high-affinity IgE receptors (Fc epsilon RI) on mast cells and basophils, reducing their responsiveness to allergen and autoantigen. It is not directed against complement (eculizumab targets A5) and it does not act on the H1 receptor. It is licensed for CSU unresponsive to H1 antihistamines.
Reference: Fitzpatrick's Dermatology, 9th ed.
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Written and medically reviewed by the StethoPrep medical team.