Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Improvement of platelet dysfunction in chronic myelogenous leukemia following treatment with imatinib: a case report. | Shimabukuro-Vornhagen et al. Journal of Medical Case Reports 2011 5 215 http content 5 1 215 JOURNALOF medical Ur Case REPORTS CASE REPORT Open Access Improvement of platelet dysfunction in chronic myelogenous leukemia following treatment with imatinib a case report Alexander Shimabukuro-Vornhagen Achim Rothe Lucia Nogova Matthias Kochanek Christoph Scheid and Michael von Bergwelt-Baildon Abstract Introduction In patients with chronic myeloid leukemia tyrosine kinase inhibitors suppress the BCR-ABL clone and often induce complete molecular remissions. Megakaryocytes in such patients have been shown to be derived from the BCR-ABL clone and abnormal platelet function is frequent in chronic myeloid leukemia. However little is known about the influence of modern targeted therapy on chronic myeloid leukemia-associated platelet disorders. Case presentation We report the case of a massive hemorrhage in a 32-year-old Caucasian man caused by chronic myeloid leukemia-associated platelet dysfunction which improved after treatment with imatinib. Conclusion This report demonstrates that platelet dysfunction and bleeding disorder in BCR-ABL chronic myeloid leukemia can successfully be treated with imatinib. We suggest the monitoring of platelet function in future studies using imatinib to treat patients with chronic myeloid leukemia. Introduction Chronic myeloid leukemia CML is a clonal myeloproliferative disorder that results from the malignant transformation of a hematopoietic stem cell. It is characterized by the Philadelphia chromosome Ph which is formed by translocation and fusion of the long arms of chromosomes 9 and 22 in a pluripotent hematopoietic progenitor cell. At the molecular level the fusion generates a BCR-ABL protein with constitutive tyrosine kinase activity. Tyrosine kinase inhibitors such as imati-nib are able to suppress the BCR-ABL clone and induce molecular remission. Megakaryocytes are thought to belong to the BCR-ABL clone and
