Autologous platelet kinetics in patients with severe thrombocytopenia: Discrimination between disorders of production and destruction

Measurements of platelet survival and turnover in severe thrombocytopenia have proven difficult to perform and interpret. To examine the mechanisms by which platelet life span is reduced and to determine the capacity of platelet kinetic studies to discriminate between increased platelet destruction and impaired platelet production in patients with moderate to severe thrombocytopenia, we developed a modified method for labeling autologous platelets with indium-111-oxine (which increases labeling efficiency, reduces the required volumes of blood, and decreases platelet manipulation in vitro) and conducted a prospective study in 26 patients with thrombocytopenia. Seventeen patients had megakaryocytic hypoplasia (platelet count 51 × 10⁹/L, range 10 × 10⁹/L to 150 × 10⁹/L; reduced megakaryocytes in marrow smears and biopsy sample), nine patients had clinical idiopathic thrombocytopenic purpura (ITP) (platelet count 79 × 10⁹/L, range 19 × 10⁹/L to 150 × 10⁹/L; normal to increased megakaryocytes with otherwise normal marrow, and seven patients displayed the presence of autoantibodies directed against platelet glycoproteins IIb-IIIa or Ib). Although platelet life span was shortened in all patients, the average platelet survival time measured in patients with megakaryocyte hypoplasia was substantially longer than that measured in patients with ITP. Only platelet survival times measured in patients with megakaryocyte hypoplasia were predicted by the degree of thrombocytopenia. Platelet turnover was reduced in all patients with megakaryocytic hypoplasia but was variable in the patients with ITP. Platelet turnover values correlated with circulating platelet counts in patients with marrow hypoplasia but not in the patients with ITP. Autologous platelet survival measurements may be reliably performed in patients with severe thrombocytopenia; this procedure may be clinically useful, particularly in patients with equivocal clinical presentations, in discriminating between thrombocytopenia caused by impaired platelet production and increased platelet destruction.