Circulating antiplatelet antibodies in pregnant women with immune thrombocytopenic purpura as predictors of thrombocytopenia in the newborns.

Newborns from mothers with immune thrombocytopenic purpura (ITP) have a risk of thrombocytopenia due to passage of maternal antiplatelet antibodies into fetal/neonatal circulation. We looked for predictors of neonatal thrombocytopenia (nTP) in pregnant women with ITP. One hundred pregnant women with platelet count <100 × 109/l, no non-immune causes of thrombocytopenia and increased platelet associated IgG (PA-IgG) were included in the study. Thirty seven and 63 of them gave birth to babies with and without nTP, respectively (nTP+ and nTP- groups). Platelet count, mean platelet volume, PA-IgG, antiplatelet circulating antibodies (cAB), time of ITP onset (before or during pregnancy), and frequency of corticosteroid treatment were compared in these groups. There were no differences in all test parameters between nTP+ and nTP- groups except cAB. These antibodies were detected in 33 out of 37 in nTP+ group and in 2 out of 63 mothers in nTP- group (p < 0.001). The sensitivity of this test was 89% and its specificity was 97%. A strong reverse correlation (r = -0.749, p < 0.001) was established between maternal cAB titer and neonatal platelet count. Antibodies against glycoproteins IIb-IIIa and/or Ib were identified in antigen specific MAIPA (Monoclonal Antibody Immobilization of Platelet Antigen) assay only in 10 out of 19 (53%) test sera with cAB. Antiplatelet cAB in pregnant women with ITP could serve as reliable predictors of nTP in their babies.

Differential procoagulant activity of microparticles derived from monocytes, granulocytes, platelets and endothelial cells: impact of active tissue factor.

: Microparticles released by activated/apoptotic cells exhibit coagulation activity as they express phosphatidylserine and some of them - tissue factor. We compared procoagulant properties of microparticles from monocytes, granulocytes, platelets and endothelial cells and assessed the impact of tissue factor in observed differences. Microparticles were sedimented (20 000g, 30 min) from the supernatants of activated monocytes, monocytic THP-1 cells, granulocytes, platelets and endothelial cells. Coagulation activity of microparticles was examined using plasma recalcification assay. The size of microparticles was evaluated by dynamic light scattering. Tissue factor activity was measured by its ability to activate factor X. All microparticles significantly accelerated plasma coagulation with the shortest lag times for microparticles derived from monocytes, intermediate - for microparticles from THP-1 cells and endothelial cells, and the longest - for microparticles from granulocytes and platelets. Average diameters of microparticles ranged within 400-600 nm. The largest microparticles were produced by endothelial cells and granulocytes, smaller - by monocytes, and the smallest - by THP-1 cells and platelets. The highest tissue factor activity was detected in microparticles from monocytes, lower activity - in microparticles from endothelial cells and THP-1 cells, and no activity - in microparticles from platelets and granulocytes. Anti-tissue factor antibodies extended coagulation lag times for microparticles from monocytes, endothelial cells and THP-1 cells and equalized them with those for microparticles from platelets and granulocytes. Higher coagulation activity of microparticles from monocytes, THP-1 cells and endothelial cells in comparison with microparticles from platelets and granulocytes is determined mainly by the presence of active tissue factor.

Relationships of mean platelet volume and plasma thrombopoietin with glycocalicin levels in thrombocytopenic patients.

BACKGROUNDS/AIMS: Relationships of mean platelet volume (MPV) and thrombopoietin (TPO) with platelet turnover assessed by glycocalicin measurement were evaluated in thrombocytopenic patients. METHODS: MPV, glycocalicin and platelet-associated IgG (PA-IgG) were measured in 107 patients with idiopathic thrombocytopenic purpura (ITP) and 19 patients with hypoproductive thrombocytopenia (HPT; aplastic anemia or leukemia), and TPO was measured in 53 ITP and 12 HPT patients. All the included ITP patients had PA-IgG ≥300% and glycocalicin ≥50% of control values, and HPT patients had PA-IgG <300% and glycocalicin <50% of control values. RESULTS AND CONCLUSIONS: MPV was higher in ITP than in HPT patients: 9.56 ± 1.69 and 7.59 ± 0.90 fl (p < 0.001). In the ITP group a direct correlation was detected between MPV and glycocalicin (r = 0.344, p < 0.001). This interaction was essentially expressed in patients with normal/increased glycocalicin (≥100% of control; r = 0.470, p < 0.001, n = 64). TPO was greatly enhanced in HPT in comparison with ITP patients (958 ± 659 and 11 ± 27 pg/ml, p < 0.001). In the ITP group a reverse correlation was detected between TPO and glycocalicin (r = -0.373, p = 0.006).