Radiometric Quantitation of PAIgG Stratified Treatment Response in ITP Patients.

Because treatment response in ITP is variable, it would be useful to be able to assess which patients are likely to respond to conventional treatment. Toward this goal we correlated the number of platelet surface IgG molecules measured with a quantitative radiometric platelet antibody assay (PAIgG) with treatment related changes in platelet count. We tested the hypothesis that patients’ response to conventional treatment could be stratified based on quantitation of the patients’ PAIgG. Data was obtained via a retrospective chart review. Patients with a diagnosis of idiopathic thrombocytopenic purpura (ITP), age 18 or older with an initial platelet count of <150,000, and quantitation of antiplatelet IgG performed at the time of diagnosis were included in the study. Patients were treated using conventional approaches that included steroids, IVIgG, anti-D antibody, splenectomy, and or cytotoxic medications. Patient response to therapy was evaluated as the change in platelet count, computed as the difference in platelet count obtained at diagnosis and the latest stable platelet count available. There were 64 patients with at least 90 days between initial and follow-up platelet counts. Of the 31 patients whose PAIgG were ≤1,000 molecules/platelet (m/plt), only 1 had an initial platelet count of <50,000. Of the 33 patients who’s PAIgG were >1,000 m/plt 16 had platelet counts of <50,000 (p≤0.001. Patients with PAIgG levels >1000 m/plt exhibited a significantly greater increase in platelet count μ=73,000 ±92,000 as compared to those with PAIgG levels ≤1000 m/plt, μ=18,000 ±43,000 (p=0.03). Although a PAIgG level of 500 m/plt is 3 standard deviations above the mean of normals, a greater response to treatment was noted in patients if their PAIgG level was >1000 m/plt. Patients with PAIgG levels between 500 and 1000 m/plt respond in a similar fashion to those with PAIgG levels <499. In addition, more patients with PAIgG levels >1000 m/plt received conventional treatment (19/33 vs. 10/31; p<0.05). In particular, there were more patients who received cytotoxic treatment in this cohort, (11/33 vs. 3/31; p≤0.025). Similar results were observed in 74 patients with at least 30 days between initial and follow-up platelet counts. This study suggests that measuring the amount of antiplatelet IgG stratifies ITP patients into 2 groups: patients with PAIgG ≤1,000 m/plt with platelet counts over 50,000 and patients with PAIgG >1,000 m/plt platelet counts that are less than 50,000. Those patients whose PAIgG is >1,000 m/plt are more likely to receive treatment and have an increase in platelet count with conventional therapy. We conclude that radiometric quantitation of PAIgG is helpful for predicting a patient’s response to therapy.