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Published on: December 7, 2012
Indirect platelet radioactive antiglobulin test in patients with lymphoproliferative disease
An indirect platelet radioactive antiglobulin test (PRAT) was used to evaluate serum antiplatelet antibody and complement activation in 114 patients with lymphoproliferative disease. Overall, 60% of serum samples gave a positive indirect PRAT. Positive PRAT was observed in 85% of patients with chronic lymphocytic leukemia (CLL) and megakaryocytic thrombocytopenia, as well as in about half the patients with CLL and a normal platelet count or amegakaryocytic thrombocytopenia. In contrast to findings in patients with idiopathic autoimmune thrombocytopenic purpura or in those with leukemia who were alloimmunized, positive PRAT in patients with lymphoproliferative disease was predominantly caused by C3-only sensitization of platelets. Results were analyzed in relation to other clinical and laboratory findings. There was no significant difference in antiglobulin sensitization pattern between CLL and other lymphomas, different cell type, stage of disease, presence or absence of splenomegaly, recent or distant chemotherapy, sex, or history of pregnancy. Previous transfusion did affect antiglobulin sensitization patterns, as did presence of autoimmune hemolytic anemia. A high frequency of low serum complements (CH50, C3, C4, and factor B) and increased circulating immune complexes was observed; these did not correlate with frequency or sensitization pattern of positive PRAT. Amounts of bound anti-C3 and anti-IgG were significantly higher in patients with lymphoproliferative disease and positive antiglobulin test than in normal individuals; there was, however, no correlation between amount of antiglobulin serum bound and platelet counts. There was an 87% correlation in direct and indirect PRAT in 24 patients tested.(ABSTRACT TRUNCATED AT 250 WORDS)
An indirect platelet radioactive antiglobulin test (PRAT) was used to evaluate serum antiplatelet antibody and complement activation in 114 patients with lymphoproliferative disease. Overall, 60% of serum samples gave a positive indirect PRAT. Positive PRAT was observed in 85% of patients with chronic lymphocytic leukemia (CLL) and megakaryocytic thrombocytopenia, as well as in about half the patients with CLL and a normal platelet count or amegakaryocytic thrombocytopenia. In contrast to findings in patients with idiopathic autoimmune thrombocytopenic purpura or in those with leukemia who were alloimmunized, positive PRAT in patients with lymphoproliferative disease was predominantly caused by C3-only sensitization of platelets. Results were analyzed in relation to other clinical and laboratory findings. There was no significant difference in antiglobulin sensitization pattern between CLL and other lymphomas, different cell type, stage of disease, presence or absence of splenomegaly, recent or distant chemotherapy, sex, or history of pregnancy. Previous transfusion did affect antiglobulin sensitization patterns, as did presence of autoimmune hemolytic anemia. A high frequency of low serum complements (CH50, C3, C4, and factor B) and increased circulating immune complexes was observed; these did not correlate with frequency or sensitization pattern of positive PRAT. Amounts of bound anti-C3 and anti-IgG were significantly higher in patients with lymphoproliferative disease and positive antiglobulin test than in normal individuals; there was, however, no correlation between amount of antiglobulin serum bound and platelet counts. There was an 87% correlation in direct and indirect PRAT in 24 patients tested.(ABSTRACT TRUNCATED AT 250 WORDS)

