Improvement of platelet dysfunction in chronic myelogenous leukemia following treatment with imatinib: a case report

Shimabukuro‐Vornhagen, Alexander; Rothe, Achim; Nogová, Lucia; Kochanek, Matthias; Scheid, Christoph; Bergwelt‐Baildon, Michael von

doi:10.1186/1752-1947-5-215

Cited by 11 publications

(5 citation statements)

References 12 publications

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“…1. Worldwide studies proved that: the most common adverse events associated with nilotinib therapy were thrombocytopenia (20−33%) and neutropenia (13−31%) [4], [5]. This also agreed with Tasigna prescribing information by (Novartis,2014) [23].…”

Section: Discussionsupporting

confidence: 70%

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Effects of nilotinib on platelet function in patients with chronic myeloid leukemia in chronic phase

Alqasim

Obaid

Yaseen

et al. 2019

Leukemia Research Reports

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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.

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Section: Discussionsupporting

confidence: 70%

“…Tyrosine kinase inhibitors (TKIs) are orally administered agents that compete with adenosine triphosphate (ATP) for its binding site on ABL, leading to abolishing tyrosine phosphorylation of the proteins involved in BCR-ABL signal transduction and finally resulting in apoptosis of the cancer cell [4].…”

Section: Introductionmentioning

confidence: 99%

Effects of nilotinib on platelet function in patients with chronic myeloid leukemia in chronic phase

Alqasim

Obaid

Yaseen

et al. 2019

Leukemia Research Reports

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“…This is corroborated by the observation that employing tyrosine kinase inhibitors for use in patients with CML could improve platelet dysfunction [5]. There exist very few case reports of soft tissue hematoma, such as spontaneous mediastinal hematoma, hematoma in iliac psoas muscle, spinal epidural hematoma, and acute subdural hematoma, as the initial presenting features of CML [10–12].…”

Section: Discussionmentioning

confidence: 90%

An Unusual Cause of Bleeding in a Patient with Chronic Myeloid Leukemia Chronic Phase

Kartthik

Mandal

Abdullah

2019

Case Reports in Hematology

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Chronic myelogenous leukemia (CML) is a clonal myeloproliferative neoplasm (MPN) characterized by dysregulated and uncontrolled proliferation of mature and maturing granulocytes with normal differentiation. A genetic hallmark of CML is the presence of the fusion gene product BCR-ABL. Bleeding diathesis in CML patients is rare (<10%) and primarily caused by acquired platelet dysfunction. We report a rare case of an adult CML chronic phase patient who presented with spontaneous muscle hematoma due to acquired Glanzmann’s thrombasthenia (GT). On laboratory workup, a GT was confirmed along with the diagnosis of CML in chronic phase. The muscle hematoma was completely resolved following imatinib therapy. The present case demonstrates that bleeding is a complication of MPNs and highlights the importance of both acquired GT diagnosis to determine the cause of bleeding in CML and of prompt treatment with imatinib to reverse this condition.

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“…A hypothesis also suggests that imatinib induces bleeding disorders because of BCR-ABL rearrangements in megakaryocytic cell lines, leading to clonal expansion of dysfunctional megakaryocytes. 40…”

Section: Impact On Platelet Functionsmentioning

confidence: 99%

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Haguet

Douxfils

Chatelain

et al. 2018

TH Open

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Imatinib, the first-in-class BCR-ABL tyrosine kinase inhibitor (TKI), had been a revolution for the treatment of chronic myeloid leukemia (CML) and had greatly enhanced patient survival. Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective. However, these treatments have been associated with arterial occlusive events. This review gathers clinical data and experiments about the pathophysiology of these arterial occlusive events with BCR-ABL TKIs. Imatinib is associated with very low rates of thrombosis, suggesting a potentially protecting cardiovascular effect of this treatment in patients with BCR-ABL CML. This protective effect might be mediated by decreased platelet secretion and activation, decreased leukocyte recruitment, and anti-inflammatory or antifibrotic effects. Clinical data have guided mechanistic studies toward alteration of platelet functions and atherosclerosis development, which might be secondary to metabolism impairment. Dasatinib, nilotinib, and ponatinib affect endothelial cells and might induce atherogenesis through increased vascular permeability. Nilotinib also impairs platelet functions and induces hyperglycemia and dyslipidemia that might contribute to atherosclerosis development. Description of the pathophysiology of arterial thrombotic events is necessary to implement risk minimization strategies.

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Improvement of platelet dysfunction in chronic myelogenous leukemia following treatment with imatinib: a case report

Cited by 11 publications

References 12 publications

Effects of nilotinib on platelet function in patients with chronic myeloid leukemia in chronic phase

Effects of nilotinib on platelet function in patients with chronic myeloid leukemia in chronic phase

An Unusual Cause of Bleeding in a Patient with Chronic Myeloid Leukemia Chronic Phase

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

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