135 research outputs found
High iron content of Ankaferd hemostat as a clue for its hemostatic action of red blood cell origin
No full textHaznedaroglu, Ibrahim C./0000-0001-8028-9462
Echocardiographic Dilemma: Misleading Thrombus Appearance Due to Cavitation With Intravascular Hemolysis on a Mechanical Prosthetic Valve
No full textEchocardiographic Dilemma: Misleading Thrombus Appearance Due to Cavitation With Intravascular Hemolysis on a Mechanical Prosthetic Valve Ibrahim Akpinar, MD, Muhammet Rasit Sayin, MD, Turgut Karabag, MD, Mehmet Emin Kalkan, MD, Sait Mesut Dogan, MD, Mustafa Aydin, MD, and Ibrahim C. Haznedaroglu, MD a Zonguldak Karaelmas University, Faculty of Medicine, Department of Cardiology, Zonguldak, Turkey b Ataturk State Hospital, Department of Cardiology, Zonguldak, Turkey c Hacettepe University, Faculty of Medicine, Department of Hematology, Ankara, Turke
Autoimmune hemolytic anemia in Philadelphia positive chronic myeloid leukemia with t(7;14) anomaly after 5 years of interferon alpha treatment
No full textKarakus, sema/0000-0001-7615-4581; Haznedaroglu, Ibrahim C./0000-0001-8028-9462; Haznedaroglu, Ibrahim C./0000-0001-8028-9462A 41-year-old woman, Philadelphia positive chronic myeloid leukemia patient, had progressive decline in hemoglobin levels. She had been receiving interferon alpha treatment for five years. Autoimmune hemolytic anemia was diagnosed. Subsequent bone marrow examination revealed translocation t(7;14). She was placed on prednisone treatment. The patient responded to prednisone as treatment for the hemolytic process. The result of a direct Coombs' test remained positive. The patient died shortly after the diagnosis of autoimmune hemolytic anemia. Autoimmune hemolytic anemia should be considered in the evaluation of chronic myeloid leukemia patients with a sudden decrease in hemoglobin levels
Key Decision Just After 3 Months Following TKI Initiation in CML: Better and not Difficult
No full textMONITORING THE RESPONSE TO TYROSINE KINASE INHIBITOR (TKI) TREATMENT IN CHRONIC MYELOID LEUKEMIA (CML)
No full textThe aim of oral tyrosine kinase inhibitor (TKI) treatment in chronic myeloid leukemia (CML) is to get ideal hematological, cytogenetic, molecular responses at the critical time-points. The depth of the response obtained with TKI and time to achieve this response are important for the prediction of prognosis in the patient with CML. The high efficacy of the TKI treatment of CML has prompted the need for accurate methods to monitor response at levels below the landmark of CCyR. Quantification of BCR-ABL transcripts has proven to be the most sensitive method available and has shown prognostic impact with regard to progression-free survival. European LeukemiaNet (ELN) molecular program harmonized the reporting of results according to the IS (Internatıonal harmonization of Scale) in Europe. The aim of this review is to outline monitoring the response to optimal TKI treatment based on the ELN CML 2013 recommendations from the clinical point of view as a physician. Careful cytogenetic and molecular monitoring could help selecting the most convenient TKI drug and to optimize TKI treatment. Excessive monitoring may have an economical cost but failure to optimize TKI treatment may result in CML disease acceleration and death
Monitoring the response to tyrosine kinase inhibitor (TKI) treatment in chronic myeloid leukemia (CML)
No full textAbstract
The aim of oral tyrosine kinase inhibitor (TKI) treatment in chronic myeloid leukemia (CML) is to get ideal hematological, cytogenetic, molecular responses at the critical time-points. The depth of the response obtained with TKI and time to achieve this response are important for the prediction of prognosis in the patient with CML. The high efficacy of the TKI treatment of CML has prompted the need for accurate methods to monitor response at levels below the landmark of CCyR. Quantification of BCR-ABL transcripts has proven to be the most sensitive method available and has shown prognostic impact with regard to progression-free survival. European LeukemiaNet (ELN) molecular program harmonized the reporting of results according to the IS (Internat?onal harmonization of Scale) in Europe. The aim of this review is to outline monitoring the response to optimal TKI treatment based on the ELN CML 2013 recommendations from the clinical point of view as a physician. Careful cytogenetic and molecular monitoring could help selecting the most convenient TKI drug and to optimize TKI treatment. Excessive monitoring may have an economical cost but failure to optimize TKI treatment may result in CML disease acceleration and death
Current concerns of undertreatment and overtreatment in chronic myeloid leukemia based on European LeukemiaNet 2013 recommendations
No full textIntroduction: The aim of this paper is to indicate optimal tyrosine kinase inhibitor (TKI) administration practices based on European LeukemiaNet (ELN) 2013 recommendations for chronic myeloid leukemia (CML). Likewise, current concerns of undertreatment and overtreatment with TKIs during the long-term clinical course of CML will be outlined
The therapeutic goals of essential thrombocythemia under the clouds of over-treatment and under-treatment
No full textIntroduction: Therapeutic stratification after the accurate essential thrombocythemia (ET) diagnosis is made based on the medical history (age, previous thrombosis), clinical assessments (cardiovascular [CV] risk factors, comorbidities, systemic diseases), laboratory examinations (leukocytosis, extreme thrombocytosis, anemia) and if available further sophistical analyses (CD34 count, JAK2V617F homozygosity, and mutant allele burden)
DRUG THERAPY IN THE PROGRESSED CML PATIENT WITH MULTI-TKI FAILURE
No full textThe aim of this paper is to outline pharmacotherapy of the ‘third-line management of CML’ (progressive disease course after sequential TKI drugs. Current management of CML with multi-TKI failure is reviewed. TKI (bosutinib, ponatinib, dasatinib, nilotinib) and non-TKI (omacetaxine mepussecinate, IFN or PEG-IFN) drugs are available. The literature search was made in PubMed with particular focus on the clinical trials, recommendations, guidelines and expert opinions, as well as international recommendations. Progressing CML disease with multi-TKI failure should be treated with alloSCT based on the availability of the donor and EBMT transplant risk scores. The TKI and non-TKI drugs shall be used to get best promising (hematological, cytogenetic, molecular) response. During the CP-CML phase of multi-TKI failure, 2nd generation TKIs (nilotinib or dasatinib) are used if they remained. Bosutinib and ponatinib (3rd generation TKIs) can be administered in triple-TKI failed (imatinib and nilotinib and dasatinib) patients. The presence of T315I mutation at any phase requires ponatinib or omacetaxine mepussecinate therapy before allografting. During the AP/BC-CML phase of multi-TKI failure, the most powerful TKI available (ponatinib or dasatinib if remained) together with chemotherapy should be given before alloSCT. Monitoring of CML disease and drug off-target risks (particularly vascular thrombotic events) are vital
- …
