mbH (Stuttgart) 74 (5) 1379-87 (1995) investigators suggested that coagulometer effects on INR may be corrected by using lyophilized plasma calibrants (7). Most authors agree that calibration of APTT methods should be per formed with ex vivo heparin samples, i.e. plasma samples from patients treated with heparin (2, 3, 4). It is not known whether lyophilized samples from heparin-treated patients can replace fresh samples for reliable calibration of APTT methods. The spread of individual patients' samples about the average line of relationship between different assay systems is considerable (8). The spread may be reduced or eliminated if pooled patients' samples are used to establish the average line of relationship between different APTT systems and/or more specific heparin assays. We suggest that future multicentric studies should include common deep-frozen pooled ex vivo samples in addition to fresh and lyophilized samples. Although deep-frozen samples require special conditions of transportation, they are more similar to fresh samples than lyophilized samples. Shipment of deep-frozen plasma samples to 131 laboratories was performed successfully in the Scandinavian external quality assessment scheme on coagulation (personal communication by Dr.

PL2-49 is a murine monoclonal IgG1 antibody obtained after immunization of Balb/c mice with EDTA washed platelets. Binding could be detected on Zwa(+) as well as Zwa(-) platelets, but not on type I Glanzmann's thrombasthenia platelets using an ELISA screening test. Immunoprecipitation studies showed that PL2-49 bound to glycoprotein IIb when the glycoprotein IIb/IIIa complex dissociation was performed after the monoclonal antibody binding. Experiments with a human alloantibody against Zwa antigen were run in parallel to control the complex dissociation. Ascitic fluid, as well as the purified antibody, induced activation and aggregation of washed platelets and ATP release. PL2-49-induced aggregation did not require exogenous fibrinogen and was inhibited, partially, in the presence of aspirin, apyrase, isosorbide dinitrate. Raising intra-platelet cyclic AMP with a stable PGI2 analogue, iloprost, and/or a phosphodiesterase inhibitor, RA 233, suppressed the responses to PL2-49. F(ab')2 fragments did not induce aggregation of normal platelets but inhibited the response to the whole immunoglobulin. Finally PL2-49 was shown to induce aequorin-detected elevations in intraplatelet Ca++ levels. Thus PL2-49 seems to differ from monoclonal antibodies so far described, since it binds to glycoprotein IIb in a complex-dependent manner at least under our experimental conditions for immunoprecipitation studies, and it induces platelet Ca++ mobilization and platelet aggregation after a lag-time. These reactions depend both on Fab and Fc domains of the antibody and require neither complement nor exogenous fibrinogen.

High-dose intravenous immunoglobulins (ivIG) were used in a 57-year-old patient with acquired von Willebrand disease in order to correct a hemostatic defect before pneumonectomy for lung carcinoma. IvIG induced a rapid and complete correction of factor VIII (F VIII) and von Willebrand factor (vWF) and allowed surgery without additional factor coverage. F VIII and vWF returned to baseline values within 10 days after ivIG.

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