GTX is safe and effective in controlling the life-threatening infections. Further randomized controlled studies with long-term follow-up are needed to assess the exact role of GTX in the outcome of patients with neutropenia and patients with defective granulocyte functions.

Granulocyte colony-stimulating factor (G-CSF) is widely used to reduce the risk of infection resulting from neutropenias and to mobilize and collect CD34+ hematopoetic progenitor cells (HPCs) for autologous and allogenic transplantation. The safety of recombinant human G-CSF (rhG-CSF) administration in healthy donors has been investigated in several studies. However, there are limited cumulative data about the effects of rhG-CSF on hemostasis. Hemostatic parameters, including urokinase-type plasminogen activator antigen (u-PA:Ag) and nitric oxide in 17 healthy granulocyte apheresis donors who donated for neutropenic patients were evaluated. rhG-CSF (single dose, 10 microg/kg subcutaneously) and dexamethasone (8 mg, single dose oral) were given to donors 12 hours before granulocyte apheresis. Two blood samples were drawn at time 0 (T(0)) before rhG-CSF and dexamethasone administration and at time 1 (T1), immediately before the apheresis. A statistically significant rise in coagulant factor VIII (FVIII) and von Willebrand factor (vWF), and slightly rise in u-PA:Ag were observed after G-CSF plus dexamethasone administration. In addition, there were positive correlations between vWF-D-dimer and FVIII-D-dimer. A significant decrease in mean total nitric oxide (NOx), nitrite, and nitrate levels was also found after G-CSF plus dexamethasone administration. Moreover, there was a strong negative correlation between nitrite and D-dimer levels (r = -0.611; P = .009). Even if partially compensated with u-PA and protein C, increased FVIII and vWF activity, and decreased nitric oxide levels may still partially contribute to progress of thrombosis risk in rhG-CSF plus dexamethasone administered healthy granulocyte donors. Large numbers of healthy donors exposed to G-CSF plus dexamethasone will be needed to evaluate the risk of thrombosis in this population.

Objective: In humans, 38 different critical blood type classification systems are currently recognized. They differ in frequencies in distinct populations. It is aimed to visualize ABO and Rh(D) groups distribution in Istanbul as having the largest community in Turkey. Method: Volunteered blood donor's data on the automation system were screened retrospectively. Blood donation acceptance criteria were based on the guidelines prepared by the Ministry of Health. ABO and Rh(D) groups were analyzed using column agglutination/gel centrifugation methods. Results: The study covered six years' data between the dates of January 2014 and December 2019, including 136,231 donors. The majority of the donors were found to have blood group A with a frequency of 41.88%(n=57,059). The second most common blood group was group O, and had a frequency of 34.92%(n=47,576). The blood group B (n=20,790;15.26%) and group AB (n=10,806;7.93%) were found to be the rare encountered blood groups. Among the Rh(D) group, 85.02% of the donors were Rh(D) positive. Conclusion: In transfusion medicine, ABO and Rh(D) groups' compatibility is mandatory. According to the monthly and or annual blood products requirement, there are some suggested quantities of blood units to be available at blood centres. Determining the frequency of blood group distribution of populations will help to coordinate the ratio of blood groups to be storaged. The Turkish genetic makeup is a fascinating mixture of European and Asian DNA, necessitates to find out the countries' specific ABO and Rh(D) groups ratio. We compared our results with the previously reported studies performed in different cities of Turkey and the world around. Thus, our research as giving the overall distribution of ABO and Rh(D) groups from the largest city of Turkey reflecting the general ethnic background of the country, would help to the establishment of a databank of ABO and Rh(D) group's ratio.

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4770 Hematopoietic stem cells which can self-renew, are very important for regeneration of hematopoietic system. Because, in chemotherapy applications, malign cells are killed but on the other hand normal cells are also damaged. It is known that corticosteroids, which is essential drug for all chemotherapy protocols, efficiently induce apoptosis not only in malign cells also in normal hematopoietic cells. But, there are no comprehensive studies about the apoptotic effects of glucocorticoids on pure CD34+ hematopoietic cell population. In several studies, it has been showed that hematopoietic cytokines can prevent apoptosis caused by chemotherapy and decrease toxic effects of this drugs. In this study, for the first time, we investigated apoptotic effects of corticosteroids on CD34+ hematopoietic stem cell population collected from human peripheral blood buffy coats by using immunomagnetic positive selection method and protective effects of hematopoietic cytokines. Buffy coats were obtained from standard blood collection bags of voluntary blood donors. Two control groups are composed that is not including cytokines in serum free medium (SFC) and induced with cytokine coctail that including interleukin 3, thrombopoietin, stem cell factor and flt3/flk2 ligand (CC). Test groups are dexamethasone group (D), prednisolone group (P) and groups induced with cytokines before drug application (CD, CP). High concentrations of dexamethasone (10-3 M) and prednisolone (10-3 M) were used in vitro in concordance with clinical treatment doses. To determine apoptotic mechanisms, immunohistochemical staining was carried out by using monoclonal antibodies against fas, caspase 3, sitocrom c, bax and bcl2. Then cells were counting and determining degree of peroxidase reactions were quantified using H-score. For statistical analysis paired t-test and one sample t-test were used. As a result, both dexamethasone and prednisolon induce apoptosis in pure CD34+ cells. When compared with control groups, corticosteroids caused significant increase for apoptotic fas, caspase 3, sitocrom c and bax (p<0,05), and a significant decrease for antiapoptotic bcl2 (p<0,05). In control that is not including cytokines (SFC) apoptosis induced and same results were determined. When cytokines were added before, it was observed a significant decrease for all apoptotic markers (p<0,05) and a significant increase for antiapoptotic bcl2 (p<0,05) (Figure 1). So that, corticosteroids induce apoptosis in human pure CD34+ hematopoietic stem cells and cytokines decrease apoptotic effects of this drugs and prevent apoptosis in vitro. As a results, our findings demonstrated that may be useful cytokine treatment in order to minimize hematopoietic toxicity and to protect CD34+ cells from high-dose corticosteroid damage.Figure 1:Pure CD34+ cells of peroxidase levels calculated using H-score by immunohistochemical stainingFigure 1:. Pure CD34+ cells of peroxidase levels calculated using H-score by immunohistochemical staining Disclosures: Cetin: Istanbul University Research Fund: Employment, Research Funding. Kuruca:Istanbul University Research Fund: Research Funding.