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[51Cr]Platelet Kinetics in Thrombocytopenia: Correlation Between Splenic Sequestration of Platelets and Response to Splenectomy

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Presented in abstract form at the annual meeting of the American Society of Hematology, Chicago, Illinois, December 1973.

▸Requests for reprints should be addressed to Curt A. Ries, M.D., University of California Hospital, Room 125-U, San Francisco, CA 94143.

San Francisco, California

Ann Intern Med. 1974;80(6):702-707. doi:10.7326/0003-4819-80-6-702
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Twenty-five patients with thrombocytopenia caused by excessive destruction or pooling of platelets had [51,Cr]platelet kinetic studies before splenectomy. Seventeen patients had kinetic patterns typical of idiopathic thrombocytopenic purpura, with normal or near-normal platelet recoveries and shortened platelet survivals; 8 patients had kinetic evidence of enlarged splenic platelet pools, with low platelet recoveries and normal or slightly shortened platelet survivals. All patients showed splenic sequestration by external counting. The 17 patients with idiopathic thrombocytopenic purpura patterns had progressive splenic sequestration; 2 also had hepatic sequestration. Significant splenic sequestration was detected in seven of these patients only by posterior counting. The eight patients with enlarged splenic platelet pools had immediate splenic sequestration. Twenty-three patients (92%) had complete or good partial remissions after splenectomy. The spleen is the major site of platelet destruction and pooling in most patients with thrombocytopenia associated with shortened platelet survival or abnormal pooling; splenectomy produces a prolonged remission in most of them.





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