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Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Allogeneic stem cell transplantation is curative but it carries a significant risk of morbidity and mortality. Prognosis in older patients depends on what treatment can safely be given. Thrombopoietin agonists have been shown to improve all cytopenias and immunosuppression can be effective.
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Platelets are derived from megakaryocytes (giant cells restricted to the bone marrow) developed from pluripotent stem cells in the bone marrow (Figure 51.12). The megakaryoblasts undergo non-mitotic nuclear replication with increasing cytoplasmic volume. As the cell enlarges, the cell membrane invaginates and platelets bud off from the surface. The time taken for the stem cell to produce platelets is approximately 10 days. The production of platelets is under the control of thrombopoietin.
Pharmacologic alternatives to blood
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Thrombopoietin is the hematopoietic growth factor responsible for megakaryocytic growth, development, and platelet production. While its existence had been postulated for almost half a century, it was not until the early 1990s that real progress was made in identifying this elusive factor. Vigon et al67 cloned the human homologue of the v-mpl oncogene transduced in the myeloproliferative leukemia retrovirus and described its striking similarities to members of the hematopoietic growth receptor superfamily. c-mpl knockout mice have approximately a 90% reduction in platelet count as a result of a reduction in megakaryocyte progenitors and a decrease in megakaryocyte ploidy.67,68 In 1994, cloning of the gene for the c-Mpl ligand led to the identification of thrombopoietin.69,70 Thrombopoietin promotes the full spectrum of megakaryocyte growth and development.71 Two forms of recombinant thrombopoietin were developed for human studies: pegylated recombinant human megakaryocyte growth and development factor (PEG–rHuMGDF) and recombinant human thrombopoietin (rhTPO).
Introduction of direct-acting antiviral agents alters frequencies of anti-GPIIb/IIIa antibody-producing B cells in chronic hepatitis C patients with thrombocytopenia
Published in Platelets, 2023
Takashi Satoh, Haruki Uojima, Naohisa Wada, Hayato Takiguchi, Mei Kaneko, Marina Nakamura, Natsuki Gonda, Michika Homma, Hisashi Hidaka, Chika Kusano, Ryouichi Horie
The changes in laboratory findings and thrombopoietin levels at the baseline and EOT are summarized in Table 2. A significant improvement in platelet count from the baseline to EOT was observed in CHC patients with thrombocytopenia [median (range), 8.45 (4.3–8.8) × 104/μL vs. 9.35 (5.8–12.2) × 104/μL; p = .016). In addition, the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly improved from the baseline to EOT in patients with CHC with or without thrombocytopenia. However, no correlation between AST or ALT and platelet count was observed at baseline (r = 0.249, p = .249 or r = 0.231, p = .519) and EOT (r = −0.488, p = .155 or r = −0.384, p = .272) in CHC patients with thrombocytopenia. In contrast, AST and platelet count were negatively correlated at the baseline (r = −0.778, p < .001) and EOT (r = −0.674, p = .002) in patients with CHC without thrombocytopenia; ALT was negatively correlated with platelet count only at the baseline in CHC patients without thrombocytopenia (r = −0.643, p = .004). Other laboratory data, including plasma TPO levels, showed no significant improvement.
Tirofiban-induced thrombocytopenia
Published in Annals of Medicine, 2023
The treatment strategies for tirofiban-induced thrombocytopenia included modification of the drug regimen, other interventions to minimize the risk of bleeding, and supportive care. The risk of bleeding increases when the patient’s platelet count is below 100 × 109/L, and the therapies which affect hemostasis may need to be discontinued [57]. After discontinuation of treatment, the platelet count might normalize within 1–6 days (mean of 2.1 days) [11]. However, platelet count recovery might be slower in individuals with decreased metabolism due to renal or hepatic insufficiency [33]. Platelet transfusions were recommended in the presence of active bleeding associated with profound thrombocytopenia (platelet count < 20 × 109/L) by the European Society of Cardiology [58], but maybe little effect while reversibly binding GP IIb/IIIa inhibitor tirofiban remains in circulation (half-life 2 h) [59]. In patients with persistent major bleeding, fibrinogen supplementation with cryoprecipitate or fresh frozen plasma may be considered [46]. Supportive treatments for profound thrombocytopenia might include corticosteroid and immunoglobulin therapy [58]. Intravenous immunoglobulin (IVIG) was frequently used to successfully treat thrombocytopenia caused by tirofiban [10,15,17], resulting in an immediate increase in the platelet count and rapid return to normal levels. However, due to thrombocytopenia evolving, inadequate antiplatelet therapy and the use of thrombopoietin may increase the risk of thrombosis, occasionally leading to the occurrence of thrombotic events [38].
Clinical, Laboratory Features and Clinical Courses of Patients with Wiskott Aldrich Syndrome and X–linked Thrombocytopenia–A single center study
Published in Immunological Investigations, 2022
Hacer Neslihan Bildik, Deniz Cagdas, Aysenur Ozturk Kura, Sevil Oskay Halacli, Ozden Sanal, Ilhan Tezcan
The clinical score of five patients in the study was 5, according to a published scoring system for WAS (Ochs et al. 2009); none of them scored 5 due to severe refractory thrombocytopenia (Mahlaoui et al. 2013). We did not have any patients with early-onset severe refractory thrombocytopenia in this study, so none of our patients were treated with thrombopoietin analogs. We treated the patients with autoimmune hemolytic anemia with transfusion, high-dose methylprednisolone, and intravenous immunoglobulin (IVIG) in line with the literature (Fan et al. 2016). HSCT was performed on one patient, one patient underwent splenectomy and one died due to GIS bleeding. Because of the severe course of immunological findings and bleeding complications, HSCT and splenectomy were carried out without applying to second-line treatment for hemolytic anemia.