Why is IVIg given in thrombocytopenia?

October 12, 2025 •

4 min read

The annual incidence of immune thrombocytopenia (ITP) in adults is estimated to be 1 to 6 cases per 100,000 people. A primary clinical question is, why is IVIg given in thrombocytopenia? This therapy is essential for rapidly boosting platelet counts in critical situations.

Quick Summary

Intravenous Immunoglobulin (IVIg) is administered for immune thrombocytopenia to quickly elevate low platelet counts. It primarily works by blocking macrophage receptors, thereby preventing the destruction of antibody-coated platelets and offering a rapid therapeutic benefit.

Key Points

Primary Mechanism: IVIg works mainly by blocking Fc receptors on macrophages, which prevents them from engulfing and destroying antibody-coated platelets.
Rapid Response: It is favored in clinical practice because it can raise platelet counts very quickly, typically within 24 to 48 hours of administration.
Emergency Use: IVIg is a critical therapy in emergency situations, such as for patients with active, severe bleeding or those needing an urgent surgical procedure.
Temporary Solution: The platelet-boosting effects of IVIg are not permanent, with counts often declining again after three to four weeks.
Clinical Efficacy: Studies show that IVIg is effective in 70–80% of patients with ITP, making it a reliable treatment for acute management.
Cost and Availability: IVIg is an expensive therapy derived from human plasma, which can be subject to supply shortages, influencing its use in clinical guidelines.

Understanding Thrombocytopenia and IVIg

Immune Thrombocytopenia (ITP), formerly known as idiopathic thrombocytopenic purpura, is an autoimmune disorder where the immune system mistakenly attacks and destroys the body's own platelets. Platelets are essential for blood clotting, and a low count (thrombocytopenia) can lead to a high risk of bleeding. The annual incidence in adults is estimated at 1 to 6 per 100,000, with prevalence around 12 per 100,000. While many cases in children resolve, ITP is more often a chronic condition in adults.

Intravenous Immunoglobulin (IVIg) is a blood product made from the pooled plasma of thousands of healthy donors. It is rich in IgG antibodies and is used to treat a variety of autoimmune and inflammatory diseases. In the context of ITP, it serves as a crucial intervention to rapidly increase platelet counts, especially in emergencies.

The Primary Mechanism: Fc Receptor Blockade

The most widely accepted reason why IVIg is given in thrombocytopenia relates to its ability to overwhelm the mononuclear phagocyte system, particularly in the spleen. In ITP, autoantibodies coat the surface of platelets. These antibody-coated platelets are then recognized by macrophages (a type of white blood cell) via their Fc receptors. This recognition leads to the engulfing and destruction of the platelets, causing the platelet count to drop.

When IVIg is administered, the volume of donated antibodies can saturate these Fc receptors on the macrophages. With their receptors blocked, the macrophages are unable to bind to and destroy the antibody-coated platelets. This allows the platelets to survive longer in circulation, leading to a rapid increase in the overall platelet count, often seen within a day or two.

Other Potential Mechanisms of Action

While Fc receptor blockade is the primary mechanism, research suggests other ways IVIg may help modulate the immune system in ITP:

Anti-idiotypic Antibodies: IVIg may contain antibodies that can neutralize the specific autoantibodies responsible for attacking the platelets.
Complement Inhibition: It can prevent the complement system, another part of the immune response, from contributing to platelet destruction.
Modulation of Immune Cells: IVIg can influence the function and production of various immune cells, including B cells and T cells, leading to a broader suppression of the autoimmune response.

Clinical Use and Efficacy

IVIg is particularly valuable in specific clinical scenarios where a fast and significant increase in platelet count is necessary. According to guidelines from the American Society of Hematology (ASH) and other international bodies, IVIg is often reserved for:

Active or Severe Bleeding: When a patient with ITP is experiencing a critical bleed.
Pre-Surgical Preparation: To raise platelet counts to a safe level before an urgent or major surgery.
Corticosteroid Intolerance/Failure: For patients who do not respond to or cannot tolerate first-line treatments like corticosteroids.

The efficacy of IVIg is well-documented, with response rates in 70-80% of ITP patients. The platelet count typically begins to rise within 1-3 days. However, this effect is temporary. The remission from a single course of IVIg usually lasts for only three to four weeks, after which the platelet count may fall again, necessitating further treatment.

Administration and Side Effects

IVIg is administered intravenously over several hours. While generally considered safe, IVIg therapy is associated with potential side effects. Common side effects are often mild and infusion-related, including:

Headache (up to 50%)
Fever and chills
Nausea and vomiting
Fatigue and muscle pain

Rarer but more serious adverse effects can include aseptic meningitis, kidney impairment, thrombotic (clotting) events, and hemolytic anemia. Premedication with certain medications can help reduce the incidence of mild reactions.

Comparison of ITP Treatments

IVIg is one of several options for treating ITP. Corticosteroids are often the first-line therapy due to their effectiveness and lower cost, while newer agents like Thrombopoietin Receptor Agonists (TPO-RAs) stimulate platelet production.


Feature	IVIg	Corticosteroids (e.g., Prednisone)	TPO-Receptor Agonists (e.g., Romiplostim)
Mechanism	Blocks macrophage Fc receptors, preventing platelet destruction	Broad immunosuppression, reduces autoantibody production	Stimulates bone marrow to produce more platelets
Onset of Action	Rapid (1–3 days)	Slower (3–14 days)	Gradual (7–14 days)
Duration of Effect	Temporary (2–4 weeks)	Variable; requires tapering	Requires ongoing administration
Common Side Effects	Headache, fever, chills, nausea	Insomnia, mood changes, weight gain, high blood sugar	Headache, myalgia
Primary Use Case	Emergency situations, rapid platelet increase	First-line treatment for newly diagnosed ITP	Second-line for chronic ITP, steroid-dependent patients

Conclusion

In conclusion, IVIg is given in thrombocytopenia, specifically immune-mediated forms like ITP, for its reliable and rapid ability to increase platelet counts. By primarily blocking the Fc receptors on macrophages, it provides a crucial bridge in emergency situations, preventing life-threatening bleeding and allowing time for other long-term therapies to take effect. While its high cost and temporary nature relegate it to specific scenarios, its role as a fast-acting rescue therapy remains indispensable in the management of severe ITP.

For more information from an authoritative source, visit the Platelet Disorder Support Association (PDSA).

Frequently Asked Questions

IVIg typically leads to a rapid increase in platelet counts, often within 24 to 48 hours, with some studies noting responses in 1 to 3 days.

No, IVIg is not a cure for Immune Thrombocytopenia (ITP). It provides a temporary increase in platelet counts that typically lasts for about 3 to 4 weeks before another treatment may be needed.

The most common side effects are usually mild and include headache, fever, chills, nausea, fatigue, and muscle pain. Slowing the infusion rate can often alleviate these symptoms.

IVIg is given as an intravenous (IV) infusion over several hours.

IVIg is preferred over corticosteroids when a very rapid increase in platelet count is required, such as in cases of severe bleeding or before emergency surgery. It's also used for patients who don't respond to or cannot tolerate corticosteroids.

IVIg is expensive due to the complex manufacturing process, which involves pooling and processing plasma from thousands of human donors. The cost per gram can range from $100 to $350, leading to high overall treatment costs.

IVIg works by preventing the destruction of existing platelets, providing a rapid but temporary effect. TPO-RAs work by stimulating the bone marrow to produce new platelets, leading to a more sustained but slower increase in platelet count.