We report on a new method based on speckle size analysis and devoted to particle aggregation measurements. The experimental measurements give the speckle size variation during a salt aggregation process of polystyrene microspheres. The measurements are taken at a fixed monomer concentration, varying the salt concentration. Moreover, we applied this technique to follow blood platelet aggregation, usually monitored with a visible light transmittance photometer (aggregometer). Aggregation process was induced by ADP (adenosine diphosphate) addition, then we measured the speckle size variation versus time at two different ADP concentrations.

Inhibitors against factor XI (FXI) have been frequently described in patients who acquired inhibitors (due to auto-immune disorders, malignancies or infections), but less often in those with a congenital deficiency of this factor, who had received plasma infusions. The present report concerns one such inhibitor found in the plasma of a patient with chronic myelomonocytic leukaemia and infected by B19 parvovirus, who was neither a heterozygote nor a homozygote for FXI deficiency, and who had no bleeding tendency despite a very low FXI level. Taking this case into account, we discuss and present the clinical and biological features of acquired FXI deficiency caused by an inhibitor.

No abstract

Inhibitors against factor XI (FXI) have been frequently described in patients who acquired inhibitors (due to auto‐inmune disorders, malignancies or infections), but less often in those with a congenital deficiency of this factor, who had received plasma infusions. The present report concerns one such inhibitor found in the plasma of a patient with chronic myelomonocytic leukaemia and infected by B19 parvovirus, who was neither a heterozygote nor a homozygote for FXI deficiency, and who had no bleeding tendency despite a very low FXI level. Taking this case into account, we discuss and present the clinical and biological features of acquired FXI deficiency caused by an inhibitor.

Seventeen patients with primary thrombocythemia (PT) were evaluated for in vitro bone marrow megakaryocyte progenitors (CFU-MK) using a plasma clot system. The aim of this study was to find out whether spontaneous growth of CFU-MK could be used in the diagnosis of PT. The number of CFU-MK was normal in 7 patients and reduced in 10 patients. In the absence of stimulating factor, CFU-MK grew spontaneously in 12 patients, while in 5 patients no spontaneous CFU-MK were observed. The mean plasma level of platelet factor 4 (PF4) was significantly higher (p < 0.05) in patients without spontaneous CFU-MK (59.8 ± 59.6 IU/ml; mean ± SD) compared to patients with (18.1 ± 20.7 IU/ml). The mean plasma level of β-thromboglobulin did not differ between patients with or without spontaneous CFU-MK. The β-thromboglobu-lin/PF4 ratio was significantly higher (p < 0.01) in patients with spontaneous CFU-MK (9.9 ± 7.1) compared to patients without (3.1 ± 1.4). These results suggest that PF4 could inhibit in vitro spontaneous growth of CFU-MK.