Treatment guidelines recommend that patients receive treatment if they have any of the following:
- Significant bleeding risk
- <20 × 109/L platelets and moderate bleeding
- <10 × 109/L platelets with no bleeding symptoms
Corticosteroids are effective treatments for 50–80% of individuals with acute or chronic ITP. Even with a reduction or discontinuation of corticosteroid treatment, remission can be maintained.
Anti-D immunoglobulin, administered intravenously, may be an effective treatment for Rh-positive children or adults diagnosed with acute or chronic ITP. Anti-D immunoglobulin forms red blood cell complexes that block the destruction of platelets. Although the mechanism of anti-D treatment is not yet fully discovered, the most likely scenario is that competitive inhibition and blockade of the mononuclear phagocytic system occurs by sensitized red blood cells within the spleen. Stated another way, anti-D treatment may down-regulate splenic macrophages and prevent increased platelet sequestration. This treatment cannot be used for patients who have undergone a splenectomy.
When a patient is refractory to the above treatments, other treatment possibilities include thrombopoietic drugs to stimulate the megakaryoblast or Rituximab. This treatment targets CD 20-positive B-cells and reduces platelet autoantibody production.
Splenectomy may be a last resort treatment for chronic ITP sufferers if their platelet counts are below 30 × 109/ L or if symptoms warrant it. In ITP, antibodies develop that coat the platelets. The spleen produces macrophages whose Fc receptors recognize and destroy these antibody-coated platelets. Removing the spleen would decrease platelet destruction, but it is a last resort since the immunologic function of the spleen would also be lost.