Summary
Effects of splenectomy on platelet kinetics and production of anti-platelet antibodies
were studied in male (NZW × BXSB) F1 (W/B F1) mice, which are known as the animal model of immune thrombocytopenic purpura (ITP).
Studies on organ localization of radiolabeled platelets revealed that splenic uptake
significantly increases in W/B F1 mice in comparison with that of normal controls. W/B Fj mice showed a significant
increase in platelet counts and, in contrast with sham-operated controls, high levels
of platelet counts were maintained up to 6 weeks after splenectomy. Platelet lifespans
(PLSs) did not reach normal levels, although prolonged PLSs were observed. In addition,
platelet-associated antibody (PAA) values showed a tendency towards transient decrease,
but there was no change in platelet-bindable serum antibodies (PBAs). These findings
indicate that the suppression of anti-platelet antibody production is essential to
the treatment of ITP; splenectomy may not be effective in treating severely affected
ITP patients because, although the spleen is one of the major sites of platelet sequestration
and antibody production, reticulo-endothelial systems (RESs) (liver, bone marrow,
lymphnodes, etc.) other than the spleen are also responsible for the destruction of
platelets. We therefore consider the W/B F1 mouse to be a useful model of human ITP, and believe that it provides valuable information
for the development of new therapeutic agents in patients with ITP, especially those
who do not respond to splenectomy.
