A 45-year-old woman with chronic immune thrombocytopenic purpura (platelets 18,000/µL) is started on high-dose intravenous immunoglobulin (IVIG). The platelet count rises to 65,000/µL within 48 hours. Which mechanism explains the rapid response to IVIG?

• A IVIG directly stimulates megakaryocyte proliferation and platelet production in the bone marrow
• B IVIG activates thrombopoietin receptors on hematopoietic stem cells
• C IVIG neutralizes antiplatelet autoantibodies by anti-idiotype antibodies, halting new antibody production
• D IVIG saturates Fcγ receptors on splenic macrophages, reducing IgG-coated platelet destruction ✓

Explanation

IVIG in ITP works primarily by saturating Fcγ receptors on splenic and hepatic macrophages, blocking phagocytosis of IgG-opsonized platelets. The effect is rapid (24 to 48 hours) but transient (weeks). IVIG does not stimulate thrombopoiesis, neutralize existing antibodies meaningfully, or bind TPO receptors. This mechanism explains why splenectomy remains a definitive option when medical therapy fails.

Reference: Harrison's Principles of Internal Medicine, 20th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.