Background
Tyrosine kinases are highly expressed in platelets and play an important role in their activation process. Some studies have reported the blocking effects of tyrosine kinase inhibitors on different platelet functions.
Objectives
Evaluate the effects of nilotinib on platelets aggregation in 42 patients with chronic phase of CML and correlate the results with clinical and hematological parameters: age, complete blood count and presentation.
Patients and methods
This study was conducted on 42 patients diagnosed as Chronic Phase of Chronic Myeloid Leukemia based on clinical, morphological and cytogenetic study. All patients were on Nilotinib treatment and were attending the National Center of Hematology in Baghdad. About 9 mL of venous blood sample were collected from each patient and control subjects, samples divided into 3 parts for complete blood count, platelet aggregation test and PT and aPTT.
Results
The mean age was 41.3 ± 1.7 (mean ± SEM) years old. M:F ratio of 1.2:1. Mean duration of nilotinib therapy(1.4 years). All patients had normal PT and aPTT.
Only 16 (38%) patients had abnormal aggregation response to epinephrine, but there was no statistically significant differences with control group.
Conclusion
Nilotinib had no adverse effect on platelet function nor patients clotting tests.
This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
A 15 year child is presented with transfusion dependent chronic anemia.
The clinical and laboratory features suggested a chronic nonspherocytic
hemolytic anemia (CNSHA) with bone marrow suggestive of congenital
dyserythropoietic anemia (CDA). DNA studies revealed the underlying
novel mutation in the PKLR gene responsible for pyruvate kinase
deficiency.
Hematopoietic stem-cell transplantation (HSCT) refers to a procedure in which hematopoietic stem cells are infused to restore bone marrow function in cancer patients who receive bone-marrow-toxic doses of cytotoxic drugs, with or without whole-body radiation therapy. Stem cells may be obtained from the transplant recipient (autologous HSCT) or can be harvested from a donor (allogeneic HSCT). Stem cells may be harvested from bone marrow, peripheral blood, or umbilical cord blood shortly after delivery of neonates. The perception of the mechanisms through which malignant cells are eradicated following allogeneic hematopoietic cell transplantation (HCT) has evolved substantially over the past four decades. No longer merely thought of as a means to rescue hematopoietic function following myeloablative conditioning, allogeneic transplantation is now known to be a powerful type of immunotherapy capable of curing patients with other-wise fatal malignant diseases. This conceptual evolution has translated into a diversification of the indications for allotransplants and led to the development of reduced intensity transplant approaches whose beneficial antineoplastic effects occur as a consequence of the transplanted donor immune system. Recently, investigators have begun to test whether non-hematologic malignancies might likewise be susceptible to allogeneic immune attack.
This is an open access article under the terms of the Creative Commons Attribution NonCommercial NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non commercial and no modifications or adaptations are made.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.