The bone marrow is capable of increasing the production of platelets up to 6 to 8 times normal, if necessary. However, platelet production in many ITP patients is less than would be expected, in view of the ongoing platelet destruction. This suggests that the autoantibody, in some patients, may inhibit platelet production or destroy platelets in the bone marrow before they can be released into the blood. Platelet survival in the bloodstream. Once released from the bone marrow, platelets normally circulate in the blood for 8-10 days.
Platelet destruction occurs mainly in the spleen and to some extent in the liver and bone marrow.
This is one reason that patients with ITP respond to removal of the spleen. Studies in the 1950's showed that transfusion of blood or plasma from a patient with chronic ITP into a normal volunteer subject caused thrombocytopenia. Subsequent studies showed that the substance, in the blood of ITP patients, that destroys platelets is an autoantibody. Since these glycoprotein complexes are also present on the megakaryocyte, the autoantibody in chronic ITP may also affect platelet production. Sites of antibody production.