A prospective comparison of four techniques for measuring platelet‐associated IgG

Abstract

We describe a prospective study comparing four different assays for PAIgG. Platelets from patients with a variety of thrombocytopenic disorders were collected into ACD, washed, and the PAIgG then measured using three assays for surface PAIgG. These included: (a) a direct binding assay using 125I-monoclonal anti-IgG (MoAb); (b) a direct binding assay using 125I-staphylococcal protein A (SPA); and (c) a two-stage assay. PAIgG also was measured using an assay for 'total' PAIgG following platelet lysis. The mean +/- SD number of molecules of IgG per platelet on washed platelets from 29 healthy, non-thrombocytopenic controls was: 86 +/- 80 (125I-MoAb); 94 +/- 96 (125I-SPA); 3520 +/- 1890 (two-stage surface assay); and 10,850 +/- 3720 (total PAIgG). A total of 62 different patients with idiopathic thrombocytopenic purpura or thrombocytopenia complicating systematic lupus erythematosus, and 73 different patients with 'non-immune' thrombocytopenia, were tested using each of the four assays. These 'non-immune' thrombocytopenic patients included patients with carcinoma, septicaemia, pre-eclampsia, chronic leukaemia, thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, acute leukaemia and myelodysplasia. All four assays gave similar results for both the immune and non-immune thrombocytopenic patients. The sensitivity of the assays for the most severely thrombocytopenic patients with immune thrombocytopenia was: MoAb 60%; SPA 88%; two-stage 82%; and 'total' PAIgG 88%. The specificity of the four assays in the non-immune thrombocytopenic patients was 57% 'total' PAIgG; 63% two-stage surface; 25% SPA; 38% MoAb.(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet size deviation width, platelet large cell ratio, and mean platelet volume have sufficient sensitivity and specificity in the diagnosis of immune thrombocytopenia

“…For this purpose, PAIgG and bone marrow aspiration are sometimes used. However, elevated levels of PAIgG are often found in various diseases, such as infection, autoimmune disease, and liver cirrhosis (MuellerEckhardt et al, 1980;Von dem Borne et al, 1986;Kelton et al, 1989), and PAIgG was not recommended as a diagnostic measure in recent guidelines (British Committee for Standards in Haematology General Haematology Task Force, 2003). Bone marrow sampling is invasive and not necessary as the first-line diagnostic procedure; it was recommended that it should be reserved for older patients, or patients with atypical features (George et al, 1996;Mak et al, 2000;Marsh et al, 2003).…”

A prospective study of protein‐specific assays used to investigate idiopathic thrombocytopenic purpura

“…Often assays that are thought to be useful in ITP have proved not to be diagnostically useful after prospective evaluation. For example, assays that measure IgG associated with platelets (PAIgG) (also known as phase II assays) have shown that patients with ITP have increased levels of PAIgG, but this finding is non-specific as patients with non-immune thrombocytopenia also have elevated levels of PAIgG (Kelton et al, 1982(Kelton et al, , 1989Kiefel, 1992;Mueller-Eckhardt et al, 1980;Sinha & Kelton, 1990). Protein-specific assays (phase III), which measure antibody directed against specific platelet glycoproteins, have been proposed to be diagnostically useful (Macchi et al, 1996;McMillan, 1995).…”

“…The diagnosis of ITP is based on the finding of thrombocytopenia with normal bone marrow megakaryocytes, and the exclusion of other causes for the thrombocytopenia (George et al, 1996). Assays that measure IgG associated with platelets, termed platelet-associated IgG (PAIgG), have not proved to be useful diagnostic tests because patients with immune as well as non-immune thrombocytopenia have elevated levels of PAIgG (Kelton et al, 1989;MuellerEckhardt et al, 1980). Nonetheless, these assays for PAIgG continue to be widely used.…”

Impact of immune thrombocytopenia on the clinical course of chronic lymphocytic leukemia

“…Assuming a low platelet count in CLL patients is usually due to involvement of the bone marrow by the primary disease, no recognized criteria have been postulated so far for IT diagnosis. The lack of sufficient sensitivity and specificity in available platelet auto-antibody tests, 5,6 which would parallel the direct Coomb test for red blood cells, certainly limits the interpretation of some acute thrombocytopenias. However, the occurrence of a rapid and deep "unexplained" fall in the platelet count, together with some adjuvant conditions, such as platelet rise after therapy with prednisone or high-dose intravenous immunoglobulins (IVIg), an augmented number of megakaryocytes in the bone marrow, or the absence of hypersplenism, have been used for IT diagnosis in past reports.…”