The most common cause of thrombocytopenia is increased destruction of platelets. Platelets are eliminated from peripheral circulation faster than the bone marrow can produce new platelets.
Increased platelet destruction may be the result of immune or non-immune mechanisms. Immune platelet destruction begins when antibodies coat platelets. These sensitized platelets are then destroyed by macrophages, mostly from the spleen, but also from the liver. Disorders that are associated with immune mechanisms of destruction include:
- Idiopathic (or immune) thrombocytopenic purpura (ITP)
- Heparin-induced thrombocytopenia (HIT)
- Neonatal alloimmune thrombocytopenia (NAIT)
Increased destruction of platelets is not always caused by the immune system. Platelet destruction can occur as a result of abnormal platelet aggregation or endothelial cell injury. Both of these occurrences can cause fibrin to form in arterioles and capillaries. This leads to platelet activation and platelet utilization (consumption). Platelets are consumed during formation of thromboses. Conditions associated with nonimmune destruction and consumptive thrombocytopenia include:
- Thrombotic thrombocytopenic purpura (TTP)
- Hemolytic uremic syndrome (HUS)
- Disseminated intravascular coagulation (DIC)
All of these conditions are associated with significantly decreased platelet counts that may become life threatening. Restoration of platelet numbers is essential to promote normal clotting processes.
The image on the right is thrombocytopenia occurring in conjunction with DIC. Note the presence of schistocytes (indicated by the blue arrows) and polychromatophilic erythrocytes (indicated by the red arrows), suggesting TTP, HUS, or DIC. Abnormal coagulation tests distinguish DIC from these other two conditions.