| Autor(en) |
Titel |
Quelle |
Links |
| Yiallouros M, Misbach E, Schrappe M, Janka-Schaub G, Henze G |
Akute lymphoblastische Leukämie (ALL). |
kinderkrebsinfo.de 14.04.2006 |
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| Leukämien sind bösartige Erkrankungen des Blut bildenden Systems. Mit etwa 33 % aller bösartigen Neubildungen sind sie die häufigsten Krebserkrankungen im Kindes- und Jugendalter. Die akute lymphoblastische Leukämie (ALL) ist mit einem Anteil von etwa 80 % die häufigste Form der Leukämie bei Kindern und Jugendlichen. Bedeutend seltener ist, mit knapp 20 %, die akute myeloische Leukämie (AML). Der folgende Informationstext zur akuten lymphoblastischen Leukämie (ALL) richtet sich an Patienten und deren Angehörige. Er soll dazu beitragen, diese Erkrankung und die Möglichkeiten ihrer Behandlung zu erklären. |
| Yiallouros M, Creutzig U |
Akute myeloische Leukämie (AML). |
kinderkrebsinfo.de 14.04.2006 |
|
| Leukämien sind bösartige Erkrankungen des Blut bildenden Systems. Mit etwa 33 % aller bösartigen Neubildungen sind sie die häufigsten Krebserkrankungen im Kindes- und Jugendalter. Die akute myeloische Leukämie (AML) ist nach der akuten lymphoblastischen Leukämie (ALL) die zweithäufigste Leukämie bei Kindern und Jugendlichen: Ihr Anteil an der Gesamtheit aller bösartigen Erkrankungen beträgt 4,9 %. Der folgende Informationstext zur akuten myeloischen Leukämie (AML) richtet sich an Patienten und deren Angehörige. Er soll dazu beitragen, diese Erkrankung und die Möglichkeiten ihrer Behandlung zu erklären. |
| Yoshimi A, Bader P, Matthes-Martin S, Stary J, Sedlacek P, Duffner U, Klingebiel T, Dilloo D, Holter W, Zintl F, Kremens B, Sykora KW, Urban C, Hasle H, Korthof E, Revesz T, Fischer A, Nollke P, Locatelli F, Niemeyer CM, European Working Group of MDS in Childhood (EWOG-MDS) |
Donor leukocyte infusion after hematopoietic stem cell transplantation in patients with juvenile myelomonocytic leukemia. |
Leukemia 2005, 19: 971 |
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| Juvenile myelomonocytic leukemia (JMML) is a clonal myeloproliferative disorder of early childhood. In all, 21 patients with JMML who received donor leukocyte infusion (DLI) after allogeneic hematopoietic stem cell transplantation (HSCT) for either mixed chimerism (MC, n=7) or relapse (n=14) were studied. Six patients had been transplanted from an HLA-matched sibling and 15 from other donors. Six of the 21 patients (MC: 3/7 patients; relapse: 3/14 patients) responded to DLI. Response rate was significantly higher in patients receiving a higher total T-cell dose (> or =1 x 10(7)/kg) and in patients with an abnormal karyotype. None of the six patients receiving DLI from a matched sibling responded. Response was observed in five of six patients who did and in one of 15 children who did not develop acute graft-versus-host disease following DLI (P=0.01). The overall outcome was poor even for the responders. Only one of the responders is alive in remission, two relapsed, and three died of complications. In conclusion, this study shows that some cases of JMML may be sensitive to DLI, this providing evidence for a graft-versus-leukemia effect in JMML. Infusion of a high number of T cells, strategies to reduce toxicity, and cytoreduction prior to DLI may improve the results. |
| Yoshimi A, Niemeyer CM, Bohmer V, Duffner U, Strahm B, Kreyenberg H, Dilloo D, Zintl F, Claviez A, Wossmann W, Kremens B, Holter W, Niethammer D, Beck JF, Kontny U, Nollke P, Klingebiel T, Bader P |
Chimaerism analyses and subsequent immunological intervention after stem cell transplantation in patients with juvenile myelomonocytic leukaemia. |
British journal of haematology 2005, 129: 542 |
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| Chimaerism analysis was performed by polymerase chain reaction amplification of short-tandem repeat markers in 30 children following haematopoietic stem cell transplantation for juvenile myelomonocytic leukaemia (JMML). Fourteen patients always had complete chimaerism (CC); one of them relapsed after the discontinuation of the study and 13 continued in complete remission (CR). Mixed chimaerism (MC) was noted in 16 patients. Of those 12 patients demonstrated increasing MC (i-MC); 10 relapsed and two achieved CC following discontinuation of immunosuppressive therapy (IST). Four other patients demonstrating only transient MC are alive in CR. MC with up to 20% of autologous cells could be successfully eradicated without induction of severe graft-versus-host disease when IST was reduced or discontinued directly after the first demonstration of MC. At the same time, MC with up to 10% of autologous cells could disappear without intervention. The interval between MC and relapse ranged from 0-320 d (median 38 d). Donor leucocyte infusion was given to six patients with i-MC, but only one patient responded. Peripheral blood seems as valuable as bone marrow for chimaerism studies. In conclusion, serial quantitative chimaerism studies can identify patients with i-MC who are at high risk for relapse of JMML. Immediate withdrawal of IST is advised in these patients. |
| Yoshimi A, Niemeyer CM, Führer MM, Strahm B |
Comparison of the efficacy of rabbit and horse antithymocyte globulin for the treatment of severe aplastic anemia in children. |
Blood 2013, 121: 860 |
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| Yoshimi A, Niemeyer C, Baumann I, Schwarz-Furlan S, Schindler D, Ebell W, Strahm B |
High incidence of Fanconi anaemia in patients with a morphological picture consistent with refractory cytopenia of childhood. |
British journal of haematology 2013, 160: 109 |
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| Yoshimi A, Strahm B, Baumann I, Furlan I, Schwarz S, Teigler-Schlegel A, Walther JU, Schlegelberger B, Göhring G, Nöllke P, Führer M, Niemeyer CM |
Hematopoietic stem cell transplantation in children and young adults with secondary myelodysplastic syndrome and acute myelogenous leukemia after aplastic anemia. |
Biology of blood and marrow transplantation 2014, 20: 425 |
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| Secondary myelodysplastic syndrome and acute myelogenous leukemia (sMDS/sAML) are the most serious secondary events occurring after immunosuppressive therapy in patients with aplastic anemia. Here we evaluate the outcome of hematopoietic stem cell transplantation (HSCT) in 17 children and young adults with sMDS/sAML after childhood aplastic anemia. The median interval between the diagnosis of aplastic anemia and the development of sMDS/sAML was 2.9 years (range, 1.2 to 13.0 years). At a median age of 13.1 years (range, 4.4 to 26.7 years), patients underwent HSCT with bone marrow (n = 6) or peripheral blood stem cell (n = 11) grafts from HLA-matched sibling donors (n = 2), mismatched family donors (n = 2), or unrelated donors (n = 13). Monosomy 7 was detected in 13 patients. The preparative regimen consisted of busulfan, cyclophosphamide, and melphalan in 11 patients and other agents in 6 patients. All patients achieved neutrophil engraftment. The cumulative incidence of grade II-IV acute graft-versus-host disease (GVHD) was 47%, and that of chronic GVHD was 70%. Relapse occurred in 1 patient. The major cause of death was transplant-related complication (n = 9). Overall survival and event-free survival at 5 years after HSCT were both 41%. In summary, this study indicates that HSCT is a curative therapy for some patients with sMDS/sAML after aplastic anemia. Future efforts should focus on reducing transplantation-related mortality. |
| Youngster I, Arcavi L, Schechmaster R, Akayzen Y, Popliski H, Shimonov J, Beig S, Berkovitch M |
Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review. |
Drug safety 2010, 33: 713 |
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| Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect and one of the most common genetic disorders worldwide, with an estimated 400 million people worldwide carrying a mutation in the G6PD gene that causes deficiency of the enzyme. Although drug-induced haemolysis is considered the most common adverse clinical consequence of G6PD deficiency, significant confusion exists regarding which drugs can cause haemolytic anaemia in patients with G6PD deficiency. In the absence of consensus among physicians, patients are subject to conflicting advice, causing uncertainty and distress. In the current review we aimed, by thorough search of the medical literature, to collect evidence on which to base decisions either to prohibit or allow the use of various medications in patients with G6PD deficiency. A literature search was conducted during May 2009 for studies and case reports on medication use and G6PD deficiency using the following sources: MEDLINE (1966-May 2009), PubMed (1950-May 2009), the Cochrane database of systematic reviews (2009), and major pharmacology, internal medicine, haematology and paediatric textbooks. After assessing the literature, we divided medications into one of three groups: medications that should be avoided in individuals with G6PD deficiency, medications that were considered unsafe by at least one source, but according to our review can probably be given safely in normal therapeutic dosages to individuals with G6PD deficiency as evidence does not contravene their use, and medications where no evidence at all was found to contravene their use in G6PD-deficient patients. It is reasonable to conclude that, over time, many compounds have been wrongly cited as causing haemolysis because they were administered to patients experiencing an infection-related haemolytic episode. We found solid evidence to prohibit only seven currently used medications: dapsone, methylthioninium chloride (methylene blue), nitrofurantoin, phenazopyridine, primaquine, rasburicase and tolonium chloride (toluidine blue). Regarding all other medications, our review found no evidence to contravene their use in normal therapeutic doses to G6PD-deficient patients. There is a need for evidence-based global consensus regarding medication use in G6PD-deficient patients |
| Yu A, Uttenreuther-Fischer M, Huang C, Tsui C, Gillies S, Reisfeld R, Kung F |
Phase I trial of a human-mouse chimeric anti-disialoganglioside monoclonal antibody ch14. 18 in patients with refractory neuroblastoma and osteosarcoma. |
J Clin Oncol 1998, 16: 2169 |
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| Yu Y, Fuhr J, Boye E, Gyorffy S, Soker S, Atala A, Mulliken JB, Bischoff J |
Mesenchymal stem cells and adipogenesis in hemangioma involution. |
Stem cells (Dayton, Ohio) 2006, 24: 1605 |
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