Blood coagulation and platelet profiles in persistent post-splenectomy thrombocytosis. The relationship to thromboembolism

Biomed Pharmacother. 1985;39(6):264-71.


To clarify the possible role of persistent thrombocytosis after splenectomy being a predisposing factor causing development of thromboembolism, blood coagulation profiles and platelet functions were studied in 34 cases being 1-18 years post-splenectomy from non-malignant diseases. Persistent thrombocytosis was observed in 16 with significant negative correlation between hemoglobin level and platelet count indicated the role of anemia on persistent post-splenectomy thrombocytosis. Blood coagulation profiles showed accelerated thrombin formation or hypercoagulability as measured by thrombin generation test especially in cases with thrombocytosis, together with decreased fibrinolytic activity and high fibrinogen, but in presence of high antithrombin III activity. Concerning the platelet, the aggregation to ristocetin was defective, the improved aggregation to ADP and adrenaline was achieved only in whom with intact spleen giving defective platelet aggregation. The finding indicated the role of spleen contributing to abnormal platelet aggregation. Another interesting observation was the decreased platelet 5-hydroxytryptamine content in splenectomized cases. The overall changes on blood coagulation and platelets post-splenectomy including those with persistent thrombocytosis did not thoroughly shift to hypercoagulable state, since a high antithrombin III activity and some platelet defect remained. These present findings, therefore, unlikely predisposed to the occurrence of thromboembolism even in those with persistent thrombocytosis.

MeSH terms

  • Adolescent
  • Adult
  • Blood Coagulation Tests
  • Blood Coagulation*
  • Blood Platelets / physiology*
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Middle Aged
  • Platelet Aggregation
  • Platelet Count
  • Splenectomy / adverse effects*
  • Thrombocytosis / blood*
  • Thromboembolism / blood
  • Thromboembolism / etiology*