Vicente-Ayuso Carmen, Papadopoulos Petros, Villa-Fajardo María, Prieto Blanca, Álvarez-Carmona Ana María, Mateo-Morales Marta, Pérez-López Cristina, Peña-Cortijo Ascensión, Polo-Zarzuela Marta, Sáez Isabel, Martín María Paz, Benavente-Cuesta Celina, González-Fernández Ataúlfo, Martínez-Martínez Rafael, Zwaginga Jaap Jan, Seghatchian Jerard, Gutiérrez Laura
Department of Hematology, Instituto de Investigación Sanitaria San Carlos (IdISSC), Hospital Clínico San Carlos, Madrid, Spain.
Servicio de Hematología y Hemoterapia, Hospital Clínico San Carlos, Madrid, Spain.
Transfus Apher Sci. 2017 Oct;56(5):756-768. doi: 10.1016/j.transci.2017.08.020. Epub 2017 Aug 31.
Hemato-oncologic patients with chemotherapy-induced thrombocytopenia are one of the populations receiving platelet transfusions. The general practice with these patients is to give prophylactic platelet transfusions when platelet counts fall below 10×10PLT/L. However, in more than 40% of these patients, platelet transfusion does not prevent bleeding. The reason of the low efficacy of platelet transfusion in the context of chemotherapy patients is not entirely understood. We therefore aimed at immunophenotyping the expression of platelet surface and activation markers and thrombopoietin levels from hemato-oncologic patients before and after transfusion. A more detailed follow-up was performed in three patients that underwent autologous bone marrow transplantation. As previously reported, basal platelet activation was observed in hemato-oncologic patients. Based on flow cytometry parameters, i.e. the percentage of positivity and mean fluorescence intensity (MFI) distribution, our data provide an additional interpretation of platelet acquired qualitative changes in the hemato-oncologic patient. From our results we propose: first, the underlying activation of platelets in the hemato-oncologic patient is accompanied by loss of expression of the platelet receptors that are susceptible to protease-mediated shedding; second, soon after transfusion, the newly circulating donor platelets show additional activation, which may result in subsequent platelet receptor recycling and potential accelerated clearance of these activated platelets. In conclusion, the immunophenotype of circulating platelets changes after prophylactic platelet transfusion. Next to platelet count increment, exploration of this immunophenotype might help to explain transfusion refractory bleeding in hemato-oncologic patients. Eventually this may lead to personalization and improvement of the present platelet transfusion support regime.
化疗诱导的血小板减少症的血液肿瘤患者是接受血小板输注的人群之一。对于这些患者的一般做法是,当血小板计数降至10×10⁹/L以下时给予预防性血小板输注。然而,在超过40%的此类患者中,血小板输注并不能预防出血。化疗患者中血小板输注疗效低下的原因尚未完全明确。因此,我们旨在对血液肿瘤患者输血前后血小板表面和活化标志物的表达以及血小板生成素水平进行免疫表型分析。对3例接受自体骨髓移植的患者进行了更详细的随访。如先前报道,血液肿瘤患者中观察到基础血小板活化。基于流式细胞术参数,即阳性百分比和平均荧光强度(MFI)分布,我们的数据为血液肿瘤患者血小板获得性质量变化提供了额外的解释。根据我们的结果,我们提出:第一,血液肿瘤患者血小板的潜在活化伴随着易受蛋白酶介导脱落影响的血小板受体表达丧失;第二,输血后不久,新循环的供体血小板显示出额外的活化,这可能导致随后的血小板受体再循环以及这些活化血小板的潜在加速清除。总之,预防性血小板输注后循环血小板的免疫表型发生变化。除了血小板计数增加外,探索这种免疫表型可能有助于解释血液肿瘤患者的输血难治性出血。最终,这可能会导致目前血小板输注支持方案的个性化和改进。