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Quantitative Determination of Antibody in Idiopathic Thrombocytopenic Purpura
449
Citations
19
References
1975
Year
ImmunohematologyImmunodeficienciesSurface IggImmunologyQuantitative DeterminationPathologyImmune SystemImmunotherapyThrombosisHematologyPlatelet ConcentratesImmunohaematologyImmunochemistryAutoantibodiesNormal PlateletsClinical ChemistryPlatelet AntagonistLaboratory MedicineHealth SciencesAutoimmune DiseaseAllergyAutoimmunityAntibody ScreeningBlood PlateletPlatelet SurfaceMedicine
Normal platelets contain less than 0.4 pg of surface IgG. The study examined the clinical applicability of a new technique that measures antiplatelet antibody directly on platelet surfaces or in serum. The technique is a quantitative complement lysis‑inhibition assay used to assess surface IgG on platelets or in serum. Patients with idiopathic thrombocytopenic purpura had surface IgG levels above 0.4 pg, inversely related to platelet count, with levels >1.1 pg predicting prednisone non‑response, and quantitative surface IgG measurement proved useful for predicting treatment response. Published in N Engl J Med 292:230–236 (1975).
We studied the clinical applicability of a recently developed technic that determines antiplatelet antibody directly on the platelet surface or in serum. The technic is a quantitative complement lysis-inhibition assay. Normal platelets have less than 0.4 pg of surface IgG. All patients with idiopathic thrombocytopenic purpura who were studied had greater than that value. Surface IgG was increased in inverse proportion to the platelet count. Surface levels of greater than 1.1 pg correlated with failure to respond to prednisone therapy. Incubation of normal serums with normal platelets did not increase surface IgG of such platelets, but their incubation with thrombocytopenic serums increased their surface IgG 0.5 to 100 times. The degree of increase did not predict response to treatment. However, quantitation of surface IgG of thrombocytopenic platelets was useful in predicting response to treatment. (N Engl J Med 292:230–236,1975)
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