Summary. Platelet‐associated IgG (PAIgG) was studied by a quantitative platelet radioactive anti‐IgG test (PRAT) in 298 patients. At the time of investigation, 171 patients were thrombocytopenic (platelet count <100 × 109/1), 127 had normal platelet counts. Patients fell into the following disease categories: Idiopathic thrombocytopenic purpura (ITP) (N=81), possible ITP (19), acute ITP (9), systemic lupus erythematosus (22), autoimmune haemolytic anaemia of warm‐type (18), systemic blood disease (65), liver diseases (35), others (49). A significant elevation of PAIgG was found in all disease categories. There was a significant correlation between PAIgG and the reciprocal values of platelet counts for most disease groups. No relationship was discernible between PAIgG and hypergammaglobulinaemic states (serum IgG >1.8 g/l), Platelet survival studies (N=30) revealed that normal and increased values of PAIgG were associated with normal or shortened platelet mean life span. It is concluded that an elevated PAIgG is only one of several factors involved in the development of immunologically mediated thrombocytopenia.

Platelet-associated IgG (PAIgG), platelet mean life span (MLS), and platelet sequestration sites were studied in 69 patients with immune (ITP) and presumed nonimmune thrombocytopenias (NTP). A shortened MLS was associated with elevated PAIgG (N = 46), and with normal PAIgG (N = 15). Four patients had a normal MLS, but elevated PAIgG, four patients were normal for both parameters. The highest PAIgG values occurred in ITP patients with a very short MLS. Nine NTP patients had also elevated PAIgG, but a normal or slightly shortened MLS. There was a significant double log correlation between PAIgG and MLS for ITP, but not for NTP patients. Judged from the coefficient of determination, only 10% of PAIgG were directly related to a shortened MLS. 70% of patients (N = 63) had exclusively splenic and 30% hepatosplenic sequestration. PAIgG was elevated in 29/44 patients with splenic (66%) and in 16/19 patients with hepatosplenic sequestration (84%). In ITP, PAIgG-positive cases were observed in 69% of splenic v 82% of hepatosplenic sequestration, while in NTP the corresponding figures were 6/11 and 2/2. No significant correlation between PAIgG and either sequestration type was demonstrable. We conclude that in immunologically mediated thrombocytopenia only a small portion of PAIgG accounts for a decreased MLS, and that the concentration of PAIgG per se does not determine the platelet sequestration type.

A radioassay for the detection of complement activating autoantibodies (autohaemolysins) in patients with autoimmune haemolytic anaemia (AIHA) is described. The method is based on immunoradiometric quantitation of the cytolytic C5b-9 complement complex following its antibody-dependent deposition on red blood cells (RBC). The use of affinity-purified, radiolabelled antibodies directed against the neoantigens of the C5b-9 complex ensured specificity of the test which proved more sensitive than conventional haemolytic assays and was not subject to disturbances by haemolytic sera. The results obtained in 70 patients with various forms of AIHA (warm type N = 45); cold type (N = 22); Donath-Landsteiner type (N = 3] support the prevailing assumption that autohaemolysins can trigger the complement cascade to completion. Since intact RBC from patients with detectable autohaemolysins carried C3/C4 components but never C5b-9, it is inferred that regulatory mechanisms operate in vivo at the level of C4b/C3b inactivation to arrest the cascade and rescue the autologous cells.

The direct demonstration of HLA–C antigens Cw2, Cw3, and Cw4 on human platelets is described. The antigens were detected by means of a platelet radioimmune anti‐IgG test using acid eluates from platelets and lymphocytotoxic antisera. It is concluded that HLA–C determinants are only weakly expressed on platelets. Individual differences observed reflect antigenic variations.

A technique is described which permits the detection of platelet-specific, noncomplement-fixing ('blocking') PIA' antibodies in serologically negative sera of mothers from children suffering from neonatal alloimmune thrombocytopenia. The technique consists of (1) antibody enrichment in eluates prepared from maternal serum and PIAl-positive platelets, and (2) quantitation of antibodies in eluates by the platelet radioactive anti-IgG test. With this assay, PIA1 antibodies were demonstrated in 6 out of 7 maternal sera, and anti-A antibodies in one. It proved valuable also for longitudinal studies for periods up to 30 months after delivery.