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Updated: Oct 11, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
Published on: January 29, 2014
Immunoglobulin classes and subclasses of platelet antibodies in a case of post-transfusion purpura
L Porretti1, F Marangoni, E Cofrancesco
1Centro Trasfusionale e di Immunologia dei Trapianti, Ospedale Maggiore, Milano, Italia.
A multiparous white woman developed severe thrombocytopenia following transfusion of red blood cells. Six ineffective platelet transfusions (a total of 42 random donor concentrates) were given from day 0 to day +6, high-dose steroids from day +1, progressively tapered until day +30, and a total of 150 g of intravenous immunoglobulins from day +2 to day +6. As platelet count had not increased significantly by day +8, four plasma exchange procedures, each consisting of 2,000 ml of plasma exchanged with 5% albumin solution, were performed on days +8, +10, +14 and +18. Platelet count was 5, 50, 100 and 234 x 10(9)/l on days +8, +14, +26 and +32 (discharge), respectively. The patient's acute phase serum contained increased levels of platelet alloantibodies with anti-HPA-1a (PlA1, Zwa) specificity and a titer of 3,200. IgG1, IgG2 and IgG3 subclasses of platelet-reactive antibodies in the patient's serum were elevated, whereas IgG4, IgM and IgA were within the reference values. Levels of IgG1, IgG2 and IgG3 of antiplatelet antibodies showed a marked and parallel reduction during treatment, but were still above the reference values at the end of treatment and 1 year later, when the patient platelet count was normal. Although a failure of intravenous immunoglobulins cannot be proven in this case, plasma exchange seems to have contributed more than intravenous immunoglobulins to clinical remission.
A multiparous white woman developed severe thrombocytopenia following transfusion of red blood cells. Six ineffective platelet transfusions (a total of 42 random donor concentrates) were given from day 0 to day +6, high-dose steroids from day +1, progressively tapered until day +30, and a total of 150 g of intravenous immunoglobulins from day +2 to day +6. As platelet count had not increased significantly by day +8, four plasma exchange procedures, each consisting of 2,000 ml of plasma exchanged with 5% albumin solution, were performed on days +8, +10, +14 and +18. Platelet count was 5, 50, 100 and 234 x 10(9)/l on days +8, +14, +26 and +32 (discharge), respectively. The patient's acute phase serum contained increased levels of platelet alloantibodies with anti-HPA-1a (PlA1, Zwa) specificity and a titer of 3,200. IgG1, IgG2 and IgG3 subclasses of platelet-reactive antibodies in the patient's serum were elevated, whereas IgG4, IgM and IgA were within the reference values. Levels of IgG1, IgG2 and IgG3 of antiplatelet antibodies showed a marked and parallel reduction during treatment, but were still above the reference values at the end of treatment and 1 year later, when the patient platelet count was normal. Although a failure of intravenous immunoglobulins cannot be proven in this case, plasma exchange seems to have contributed more than intravenous immunoglobulins to clinical remission.
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