Mechanisms of platelet recovery in ITP associated with therapy.
Immune thrombocytopenia (ITP) is an autoimmune disease primarily characterized by increased clearance of auto-antibody-sensitized platelets by Fc-receptor-bearing macrophages in the spleen and liver. It has been classically accepted that antibody-mediated platelet destruction is Fc dependent. Recent studies, however, may also indicate the involvement of Fc-independent pathways of platelet destruction. Current treatment options work by immunosuppression (e.g., corticosteroids), immunomodulation (e.g., IVIg and anti-D), or removal of the platelet destruction site (splenectomy) in ITP. This review will discuss the mechanisms of action of these and other treatments for ITP.
Pang
Sophie J Y
SJ
The Canadian Blood Services, Toronto, ON, Canada.
Lazarus
Alan H
AH
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D016824:Antigens, Human Platelet / Q000276:immunology; D001323:Autoantibodies; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use*; D056747:Immunomodulation; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000276:immunology / Q000628:therapy; D011961:Receptors, Fc / Q000276:immunology*; D020127:Recovery of Function; D013154:Spleen / Q000276:immunology; D013156:Splenectomy; D016896:Treatment Outcome
D000305:Adrenal Cortex Hormones; D016824:Antigens, Human Platelet; D001323:Autoantibodies; D016756:Immunoglobulins, Intravenous; D007166:Immunosuppressive Agents; D011961:Receptors, Fc