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Objective: Chronic myeloid leukemia (CML), is a clonal myeloproliferative disease due to neoplastic transformation of immature hematopoietic stem cells. The introduction of imatinib mesylate, specific BCR-ABL tyrosine kinase inhibitor (TKİ), opened a new era in treatment of CML. Currently, imatinib is considered as the first line treatment regime for CML however nonresponse or intolerance to imatinib therapy may develop. The aim of our study is to evaluate the prognosis and the efficacy of treatment in CML patients treated with TKİ. Methods: In the study; 16 years old and older 54 patients with CML who had been followed-up at Adult Hematology Department in the university hospital between November 1995 and December 2009, were analyzed retrospectively. The disease phases of patients when the TKİ was started were defined according to criteria proposed by World Health Organization (WHO). Risk profiles of patients at the time of diagnosis were determined by Sokal risk scoring system. Response rates (hematologic and cytogenetic), relapse rate (hematologic, cytogenetic or molecular relapse), relapse free survival and overall survival were evaluated. The survival curves were evaluated by Kaplan Meier method. Results: In our study, complete hematologic response(CHR) and complete cytogenetic response (CCR) rates were 94.4% and 75.9%, respectively. Relapse rate was 31.5%. Imatinib therapy was discontinued 40% of patients. Causes for imatinib discontinuation were primary imatinib resistance (40%), secondary imatinib resistance (46.6%) and side effects (13.4%). Estimated rate of relapse free survival was86.7% at 18 months and 56.2% at 5 years. Estimated three-year and five-year overall survival rates were 93.7%. Conclusion: It was concluded that imatinib mesylate is an effective and tolerable treatment choice but further studies that compares TKİ' s or combinations in terms of efficacy and tolerabilitiy are required to decide the most appropriate treatment choice in CML treatment. [ABSTRACT FROM AUTHOR]

Objective: Acute kidney injury (AKI) is an important clinical entity that is known to increase mortality in patients with sepsis. Erythrocyte maturation and proliferation are inhibited by pro-inflammatory cytokines; these cytokines exert effects on red cell distribution width (RDW) well. Based on this knowledge; our aim in this study was to evaluate the impact of RDW on acute kidney injury in patients with sepsis. Methods: 120 patients diagnosed with sepsis and admitted to intesive care unit (ICU) and treated between 2009-2013 were retrospectively evaluated. Patients were divided into two groups as follows: group 1 (RDW≥16.8) and group 2 (RDW<16.8). Multiple logistic regression analysis was used to determine the association between RDW and AKI and mortality. Results: There was a statistically significant relationship between AKI and RDW (p<0.001, OR=11.52) but there were no statistically significant relationship between AKI and sex, age, serum lactate levels as well as SOFA score. Also, there were statistically significant relationship between mortality and RDW (p=0.044, OR=5), serum lactate levels (p=0.030) and SOFA score (p<0.001). RDW was found associated with both AKI and mortality. Conclusions: Results suggest that RDW is an important parameter for predicting development of AKI and mortality in ICU patients with sepsis. [ABSTRACT FROM AUTHOR]

Objectives: The early diagnosis of volume overload in chronic kidney disease (CKD) is very important. N-terminal probrain natriuretic peptide (NT-proBNP) is a valuable biomarker for this purpose. Our study aimed to detect the relationship between NT-proBNP and left ventricular hypertrophy (LVH), hypertension (HT), GFR, and proteinuria among diabetic patients with stage 3-4 CKD. Methods: 160 diabetic patients with stage 3-4 CKD [80 patients in stage 3 CKD (group 1) and 80 patients in stage 4 CKD (group 2)] were enrolled. NT-proBNP levels were evaluated in serum, and proteinuria was determined from 24-hour collected urine. Left ventricular hypertrophy was evaluated by M-mode echocardiography. NT-proBNP levels were compared according to their left ventricular hypertrophy, hypertension, and proteinuria levels. Results: NT-proBNP levels was significantly higher, and GFR was lower in group 2 compared to group1 (p < 0.05). NTproBNP was higher in patients with LVH (+) HT (+) and proteinuria = 1gr/d than patients with LVH (-), HT (-), and proteinuria < 1g/d (p < 0.05). We found a significant correlation between NT-proBNP levels and left ventricular posterior wall thickness, diastole (LVPWTd), proteinuria, SBP, and DBP. Proteinuria was the major contributor to increased NTproBNP levels among the independent variables. Conclusion: We detected that NT-proBNP levels are increased during the progression of CKD, and proteinuria is the major cause of increased NT-proBNP levels among the independent variables. [ABSTRACT FROM AUTHOR]

Objectives: The early diagnosis of volume overload in chronic kidney disease (CKD) is very important. N-terminal probrain natriuretic peptide (NT-proBNP) is a valuable biomarker for this purpose. Our study aimed to detect the relationship between NT-proBNP and left ventricular hypertrophy (LVH), hypertension (HT), GFR, and proteinuria among diabetic patients with stage 3-4 CKD. Methods: 160 diabetic patients with stage 3-4 CKD [80 patients in stage 3 CKD (group 1) and 80 patients in stage 4 CKD (group 2)] were enrolled. NT-proBNP levels were evaluated in serum, and proteinuria was determined from 24-hour collected urine. Left ventricular hypertrophy was evaluated by M-mode echocardiography. NT-proBNP levels were compared according to their left ventricular hypertrophy, hypertension, and proteinuria levels. Results: NT-proBNP levels was significantly higher, and GFR was lower in group 2 compared to group1 (p < 0.05). NTproBNP was higher in patients with LVH (+) HT (+) and proteinuria = 1gr/d than patients with LVH (-), HT (-), and proteinuria < 1g/d (p < 0.05). We found a significant correlation between NT-proBNP levels and left ventricular posterior wall thickness, diastole (LVPWTd), proteinuria, SBP, and DBP. Proteinuria was the major contributor to increased NTproBNP levels among the independent variables. Conclusion: We detected that NT-proBNP levels are increased during the progression of CKD, and proteinuria is the major cause of increased NT-proBNP levels among the independent variables. [ABSTRACT FROM AUTHOR]