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Teke H.U.,Eskiehir Osmangazi University | Gunduz E.,Eskiehir Osmangazi University | Akay O.M.,Eskiehir Osmangazi University | Gulbas Z.,Bone Marrow Transplantation Center

Primer immunologic defect in patients with idiopathic thrombocytopaenic purpura (ITP) result from autoreactive B-lymphocytes secreting antiplatelet antibodies. Dysfunctional cellular immunity has also great importance in ITP pathogenesis. CD4+CD25+ regulatory T-cells have immunoregulatory features and it is able to inhibit CD4+CD25 - and CD8+ responses. ITP is also an autoimmune disease; the CD4+CD25+ T-cell levels of the patients decrease during the active state. According to our findings, immunosuppressive treatments increase the CD4+CD25+ Treg cell levels in the non-remission ITP patients. However, this level is not enough to overcome the resistance. CD4+CD25-Foxp3+ and CD4 +Foxp3+ Treg cells are responsible for the pathogenesis of the non-remission ITP patients and other factors exist, which are responsible for the resistance of ITP treatment. © 2013 Informa UK Ltd. Source

Hammadi A.A.,Bone Marrow Transplantation Center | Marino A.,Stamina Foundation | Farhan S.,Almustansyrea Medical College
International Journal of Stem Cells

Background and Objectives: Spinal cord injury is a common neurological problem secondary to car accidents, war injuries and other causes, it may lead to varying degrees of neurological disablement, and apart from physiotherapy there is no available treatment to regain neurological function loss. Our aim is to find a new method using autologous hematopoietic stem cells to gain some of the neurologic functions lost after spinal cord injury. Methods and Results: 277 patients suffering from spinal cord injury were submitted to an intrathecally treatment with peripheral stem cells. The cells were harvested from the peripheral blood after a treatment with G-CSF and then concentrated to 4~6 ml. 43% of the patients improved; ASIA score shifted from A to B in 88 and from A to C in 32. The best results were achieved in patients treated within one year from the injury. Conclusions: Since mesenchymal cells increase in the peripheral blood after G-CSF stimulation, a peripheral blood harvest seems easier and cheaper than mesenchymal cell cultivation prior to injection. It seems reasonable treatment for spinal cord injury. Source

Sahin D.G.,Eskiehir Osmangazi University | Gunduz E.,Eskiehir Osmangazi University | Kasifoglu N.,Eskiehir Osmangazi University | Akay O.M.,Eskiehir Osmangazi University | And 2 more authors.
Advances in Therapy

Introduction: Cytomegalovirus (CMV) infections continue to cause significant morbidity and mortality in hematopoietic stem cell transplant (HSCT) recipients. Successful pre-emptive therapy in transplant patients depends on the availability of reliable diagnostic tests for CMV infections. The purpose of this retrospective study was to evaluate CMV DNA viral load, incidence of CMV disease and CMV seropositivity, risk factors and correlation between CMV DNA positivity and clinical course in HSCT patients. Methods: Two hundred and twenty-five patients who underwent peripheral blood stem cell or bone marrow transplantation between June 2003 and April 2010 were included. A realtime polymerase chain reaction (RT-PCR) assay was used for CMV monitoring. Results: Recipient median age was 42.5 years. CMV seropositivity was 95.6%. CMV DNA positivity determined by RT-PCR was 24.9% among the entire patient group. CMV DNA positivity with RT-PCR was found to be significantly higher in allogeneic transplant recipients than autologous transplant recipients (46.7% vs 14.0%; P<0.0001). Gender, age, conditioning regimen, stem cell source, underlying disease and recipient and donor seropositivity (alone or paired) were not significant risk factors for CMV DNAemia. We did not observe any CMV end-organ disease. Conclusion: CMV DNAemia was significantly higher in allogeneic transplant recipients than in autologous transplant patients. End-organ disease could be prevented with appropriate pre-emptive therapy. © Springer Healthcare 2013. Source

Aktas A.,Celal Bayar University | Kurt E.,Eskiehir Osmangazi University | Gulbas Z.,Bone Marrow Transplantation Center

Aspirin exacerbated respiratory disease (AERD) is induced by acetylsalicylic acid (ASA) and/or nonsteroidal antiinflammatory drugs (NSAIDs). Effects of desensitization on many mediators have been examined previously, but few studies addressed the influence of desensitization on T lymphocytes and T lymphocyte-derived cytokines. This study was performed to examine peripheral blood lymphocyte (PBL) cytokine expression in aspirin-sensitive patients who have asthma before and after aspirin desensitization. In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-γ) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated. Twelve patients with AERD were included in the study. Two different control groups were formed, one consisted of 15 healthy people and second 12 aspirin tolerant asthmatic (ATA) patients using aspirin. A blood sample was collected prior to desensitization, and the tests were repeated by taking a second blood sample 1 month after the 4-day desensitization treatment. The proportion of lymphocytes secreting IFN-γ in the study group was 15.61 ± 4.40 % before desensitization and 15.08 ± 5.89 % after desensitization. The rate of IFN-γ secreting CD4+ T lymphocytes was 20.51 ± 4.41 % in the normal control group and 16.07 ± 5.7 % in the ATA group (p = 0.021). The ratio of CD4+ T lymphocyte secreting IFN-γ was reduced in patients with AERD before desensitization compared to normal control group (p = 0.040). The levels of IL-2, IL-4, and the subsets of lymphocyte were not different before and after desensitization compared to control groups. © 2013 Springer Science+Business Media New York. Source

Arora M.,University of Minnesota | Klein J.P.,Medical College of Wisconsin | Weisdorf D.J.,University of Minnesota | Hassebroek A.,Center for International Blood and Marrow Transplant Research | And 21 more authors.

Several risk factors are associated with increased mortality in patients with chronic graft-versus-host disease (cGVHD), but there is considerable variability in the reported factors. Therefore, we evaluated patient, transplantation, and cGVHD characteristics to develop a risk score in 5343 patients with cGVHD. Ten variables were identified as being significant in multivariate analysis of overall survival and nonrelapse mortality (NRM): age, prior acute GVHD, time from transplantation to cGVHD, donor type, disease status at transplantation, GVHD prophylaxis, gender mismatch, serum bilirubin, Karnofsky score, and platelet count. These 10 variables were used to build a cGVHD risk score, and 6 risk groups (RGs) were identified. The 5-year NRM was 5% (1%-9%) in RG1, 20% (19%-23%) in RG2, 33% (29%-37%) in RG3, 43% (40%-46%) in RG4, 63% (53%-74%) in RG5, and 72% (59%-85%) in RG6. The 5-year overall survival was highest at 91% (95% confidence interval [CI]:85%-97%) in RG1, followed by 67% (65%-69%) in RG2, 51% (46%-55%) in RG3, 40% (37%-43%) in RG4, 21% (12%-30%) in RG5, and 4% (0%-9%) in RG6 (all P < .01). This analysis demonstrates the usefulness of data from a large registry to develop risk-score categories for major transplantation outcomes. Validation of this cGVHD risk score is needed in a different population to ensure its broad applicability. © 2011 by The American Society of Hematology. Source

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