Reversion of Thrombocytopenia Using Bovine Serum Albumin (BSA) (original) (raw)
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Journal of Cellular Physiology, 1989
Thrombopoiesis was studied in mice after the induction of acute immune thrombocytopenia with platelet antiserum (PAS). Utilizing electron microscopy, we examined platelets and megakaryocytes (MK) obtained 4, 8, 12, 24, 48, 72, and 120 hr after administration of PAS. Four to 24 hr after injection of PAS, the majority of bone marrow MK were normal in size and organelle distribution. The demarcation membrane system (DMS) extended normally throughout the mature cell cytoplasm at these times. However, approximately 50% of MK observed 48 hr and 72 hr after injection of PAS were significantly larger than normal, and often had demarcation membranes confined to an area between a peripheral organelledeficient zone and a central nuclear zone. The median values for sectional areas of platelets obtained 8-72 hr after administration of PAS were significantly greater than the median value for sectional areas of platelets in a pooled control sample. The proportion of cytoplasm to surface-connected canalicular system appeared greater than normal in most large platelets from the PAS samples; and increased numbers of profiles of Golgi complex and endoplasmic reticulum were observed. By 48 hr post-injection of PAS (at which time the modal ploidy class of MK has shifted from 1 6 N to 32N; Corash et al., Blood 70: 177, 1987), most platelets were normal in size and cytoplasmic appearance. At 120 hr post-injection of PAS, virtually all platelets exhibited a normal size and complement of organelles, and MK also had returned to normal. Our data indicate that in response to acute thrombocytopenia, MK prematurely release platelets which differ from normal platelets in size and cytoplasmic appearance. There was a marked dissociation between alterations in platelets and MK, since a statistically significant increase in platelet sectional area occurred 40 hr before the shift in modal ploidy class of MK, and platelet size subsequently decreased toward normal during the period that has been shown to be associated with the maximum shift in MK ploidy. These results strongly suggest that the characteristics of platelet release do not depend on the ploidy or cytoplasmic characteristics of MK.
Blood, 1987
We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thromboc...
Evaluation of platelet function in thrombocytopenia
Platelets, 2017
Whole blood aggregometry is a functional assay for determination of platelet function. Until now, whole blood aggregometry has not been considered feasible at low platelet counts. Hence, the objectives of the present study were to explore platelet function in thrombocytopenia using a novel index of impedance aggregometry adjusted for platelet count and evaluate the association to platelet function assessed by flow cytometry. Hirudin anticoagulated blood was collected from 20 healthy volunteers, 20 patients with primary immune thrombocytopenia (ITP), and 17 hematological cancer patients. Platelet function was analyzed by impedance aggregometry and by flow cytometry. Collagen, adenosine diphosphate, thrombin receptor agonist peptide-6, and ristocetin were used as agonists for both analyses. Thrombocytopenia in healthy whole blood was induced in vitro employing a recently published method. Platelet aggregation of thrombocytopenic patients was evaluated relative to the aggregation of he...
Physiology of the Regulation of Platelet Production
British Journal of Haematology, 1967
RED CELL production is known to be regulated by a humoral factor, Erythropoietin, and it has been suggested that platelet production may be controlled by the same, or a similar mechanism. Thus, Van Dyke, Lawrence, Polycove and Lowy (1963) reported that preparations of human urinary Erythropoietin stimulate platelet production in rats. Hirsh and Dacie (1966), from studies on anaemic patients following splenectoniy, have suggested that in the presence of active haemopoiesis, anaemia stimulates thrombopoiesis as well as erythropoiesis.
Detection of thrombopoietic activity in plasma by stimulation of suppressed thrombopoiesis
Journal of Clinical Investigation, 1970
Rabbits in which thrombocytosis had been produced by five daily transfusions of platelet concentrates had suppressed endogenous thrombopoiesis, as reflected by decreased incorporation of selenomethionine-75 Se (75 SeM) into the circulating platelet mass. Rabbits in which endogenous thrombopoiesis had been suppressed by transfusion-induced thrombocytosis were used to detect thrombopoietic activity in rabbit plasma. Thrombopoietic activity was demonstrated in the plasma of both normal and thrombocytopenic donor rabbits. A dose response relationship was observed between the incorporation of 75 SeM into platelets and the dose of plasma administered. Infusion of 20-150 ml of plasma from thrombocytopenic donors increased the incorporation of 75 SeM into platelets from 52 to 107% above control values. A dose response effect also was seen after infusion of normal plasma, but normal plasma produced less effect than comparable doses of plasma from thrombocytopenic donors. Rabbits with transfusion-induced thrombocytosis appear to be more sensitive assay animals for the detection of thrombopoietic activity than animals with normal platelet counts. Changes in the rate of appearance and levels of 75 SeM may primarily indicate changes in platelet protein or platelet size and are apparently more sensitive indicators of the state of thrombopoiesis than are alterations in the numbers of circulating platelets. The results strongly support the concept of a humoral agent, i.e. thrombopoietin, that acts on megakaryocytes to regulate platelet production.
related disease: mutations in nonmuscle MYH9 Mouse models of http://bloodjournal.hematologylibrary.org/content/119/1/238.full.html Updated information and services can be found at: (381 articles) Platelets and Thrombopoiesis Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub\_requests
Blood, 2000
The effects of thrombopoietic stimulation on megakaryocytopoiesis, platelet production, and platelet viability and function were examined in normal volunteers randomized to receive single bolus subcutaneous injections of 3 g/kg pegylated recombinant megakaryocyte growth and development factor (PEG-rHuMGDF) or placebo in a 3:1 ratio. PEG-rHuMGDF transiently doubled circulating platelet counts, from 237 ؎ 41 ؋ 10 3 /L to 522 ؎ 90 ؋ 10 3 /L (P F .0001), peaking on day 12. Baseline and day-12 samples showed no differences in responsiveness of platelets to adenosine diphosphate or thrombin receptor agonist peptide (P G .4 in all cases); expression of platelet ligand-induced binding sites or annexin V binding sites (P G .6 in both cases); or density of platelet TPO-receptors (P G .5). Platelet counts normalized by day 28. The life span of autologous 111 In-labeled platelets increased from 205 ؎ 18 hours (baseline) to 226 ؎ 22 hours (P F .01) on day 8. Platelet life span decreased from 226 ؎ 22 hours (day 8) to 178 ؎ 53 hours (P F .05) on day 18. The theoretical basis for senescent changes in mean platelet life span was illustrated by biomathematical modeling. Platelet turnover increased from 43.9 ؎ 11.9 ؋ 10 3 platelets/L/d (baseline) to 101 ؎ 27.6 ؋ 10 3 platelets/ L/d (P ؍ .0009), and marrow megakaryocyte mass expanded from 37.4 ؎ 18.5 fL/kg to 62 ؎ 17 ؋ 10 10 fL/kg (P ؍ .015). Although PEG-rHuMGDF initially increased megakaryocyte volume and ploidy, subsequently ploidy showed a transient reciprocal decrease when the platelet counts exceeded placebo values. In healthy human volunteers PEG-rHuMGDF transiently increases megakaryocytopoiesis 2-fold. Additionally, peripheral platelets expand correspondingly and exhibit normal function and viability during the ensuing 10 days. The induced perturbation in steady state thrombopoiesis resolves by 4 weeks. (Blood. 2000; 95:2514-2522) 2000 by The American Society of Hematology Patients and methods Subjects and study design This placebo-controlled, blinded study, approved by the Institutional Review Board, involved 16 healthy human volunteers recruited from the Emory campus community. Informed consent was obtained from each participant on admission to the General Clinical Research Center (GCRC)
Blood, 2011
This study investigated the immature platelet fraction (IPF) in assessing treatment effects in immune thrombocytopenia (ITP). IPF was measured on the Sysmex XE2100 autoanalyzer. The mean absolute-IPF (A-IPF) was lower for ITP patients than for healthy controls (3.2 vs 7.8 × 109/L, P < .01), whereas IPF percentage was greater (29.2% vs 3.2%, P < .01). All 5 patients with a platelet response to Eltrombopag, a thrombopoietic agent, but none responding to an anti-FcγRIII antibody, had corresponding A-IPF responses. Seven of 7 patients responding to RhoD immuneglobulin (anti-D) and 6 of 8 responding to intravenous immunoglobulin (IVIG) did not have corresponding increases in A-IPF, but 2 with IVIG and 1 with IVIG anti-D did. This supports inhibition of platelet destruction as the primary mechanism of intravenous anti-D and IVIG, although IVIG may also enhance thrombopoiesis. Plasma glycocalicin, released during platelet destruction, normalized as glycocalicin index, was higher in I...