L Kanz

Hospital Universitario Miguel Servet, Caesaraugusta, Aragon, Spain

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Publications (538)2775.94 Total impact

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    ABSTRACT: Background Transfusion of ABO major–incompatible red blood cells (RBCs) can activate the complement system and can cause severe and even lethal acute hemolytic reactions. The activation of the complement system with formation of C3a and C5a (anaphylatoxins) and the release of hemoglobin from the lysed RBCs are thought to mediate clinical signs like fever, hypotension, pain, and acute renal failure. Therapeutic inhibition of the complement cascade in case of ABO-incompatible RBC transfusion would be desirable to ameliorate the signs and symptoms and to improve the outcome of the reaction.Study Design and MethodsA patient with blood group B was erroneously transfused with a unit of group A2 RBCs. Within 1 hour after transfusion she received eculizumab, a monoclonal antibody that binds to the complement component C5 and blocks its cleavage. Clinical and immunohematologic observations are reported here.ResultsHemoglobinemia and hemoglobinuria were present for several hours after transfusion, but she developed no hypotension, no renal failure, and no disseminated intravascular coagulation. As shown by flow cytometry, group A cells survived in the peripheral blood for more than 75 days. No immunoglobulin G was detectable by column agglutination technique on these cells.ConclusionA low isoagglutinin titer and blood group A2 of the erroneously transfused cells most likely were the reason for the absence of clinical signs during and immediately after the ABO-incompatible transfusion. In the further course, eculizumab successfully protected the incompatible RBCs from hemolysis for several weeks.
    Transfusion 10/2014; · 3.53 Impact Factor
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    ABSTRACT: The impact of intraocular involvement (IOL) in primary CNS lymphoma (PCNSL) has not been sufficiently evaluated. Here, we present the analysis of IOL in the only completed randomized phase III trial in PCNSL. The G-PCNSL-SG1 study evaluated the role of whole-brain radiotherapy in primary therapy of PCNSL. Data of the 526 eligible study patients were checked, and clinical characteristics, therapy, and outcome of patients with IOL diagnosed at study inclusion were analyzed. Ophthalmologic examination at study inclusion was performed in 297 patients (56.5 %) of whom IOL was diagnosed in 19 (6.4 %). Clinical characteristics did not significantly differ between patients with IOL (IOL+) and those without (IOL-). The median progression-free survival (PFS) in the IOL+ group was 3.5 months (95 % CI 0.0-7.07) as compared to 8.3 months (95 % CI 4.78-11.78) in the IOL- group (P = 0.004), the median overall survival (OS) was 13.2 months (95 % CI 0.86-25.62) and 20.5 months (95 % CI 15.56-25.5), respectively (P = 0.155). In multivariate analysis, a significantly inferior PFS and OS for IOL+ patients were found. IOL at diagnosis of PCNSL was an independent negative prognostic indicator for PFS and OS in this analysis.
    Annals of Hematology 09/2014; · 2.87 Impact Factor
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    ABSTRACT: Diagnosis of chronic myelomonocytic leukemia (CMML) is based on a combination of clinical, laboratory and morphological parameters, including persistent peripheral blood (PB) monocytosis. Recently, mutations of serine/arginine-rich splicing factor 2 (SRSF2) have been identified in 40-50% of CMML and occasionally in other myeloid disorders. In this study, we established a robust assay for the detection of SRSF2 mutations in decalcified, paraffin-embedded bone marrow (BM) biopsies and investigated its diagnostic utility. BM biopsies of 78 patients with myeloid neoplasms, including 36 CMML, 22 myelodysplastic syndromes (MDS) and 20 Ph- myeloproliferative neoplasms (MPN) were analyzed. The region around hotspot P95 in exon 1 of SRSF2 was amplified and bidirectionally sequenced. In addition, a restriction fragment length polymorphism (RFLP) analysis was established. The JAK2 V617F mutation was investigated by allele-specific PCR. SRSF2 mutations were identified in 16/36 (44%) CMML, including 1/3 cases with associated systemic mastocytosis, 4/20 (20%) Ph- MPN, and 1/22 (4.5%) MDS. RFLP analysis detected all mutations with exception of a single P95A. Of note, two cases of JAK2 V617F + primary myelofibrosis (PMF) with SRSF2 mutation initially were diagnosed as CMML based on significant PB monocytosis. In CMML, no correlation with histopathology and/or clinical parameters was observed, but SRSF2 mutations were associated with normal karyotype (p < 0.001). In summary, SRSF2 mutations are frequent in CMML and a useful diagnostic feature demonstrable in BM biopsies, allowing a definitive diagnosis for cases with minimal dysplasia and normal karyotype. The role of SRSF2 mutations in cases with hybrid features between PMF and CMML needs further investigation.
    Human pathology 09/2014; · 3.03 Impact Factor
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    ABSTRACT: Identification of physiologically relevant peptide vaccine targets calls for the direct analysis of the entirety of naturally presented HLA ligands, termed the HLA ligandome. In this study we implemented this direct approach using immunoprecipitation and mass spectrometry to define acute myeloid leukemia (AML) -associated peptide vaccine targets. Mapping the HLA class I ligandomes of 15 AML patients and 35 healthy controls, more than 25 000 different naturally presented HLA ligands were identified. Target prioritization based on AML exclusivity and high presentation frequency in the AML cohort identified a panel of 132 ligandome-derived tumor-associated antigens (LiTAAs) and 341 corresponding HLA ligands (LiTAPs) represented subset independently in >20% of AML patients. Functional characterization of LiTAPs by IFN-γ ELISPOT and intracellular cytokine staining confirmed AML-specific CD8(+) T-cell recognition. Of note, our platform identified HLA ligands representing several established AML-associated antigens (e.g. NPM1, MAGED1, PRTN3, MPO, WT1), but found 80% of them to be also represented in healthy control samples. Mapping of HLA class II ligandomes provided additional CD4(+) T cell epitopes and potentially synergistic embedded HLA ligands allowing for complementation of a multi-peptide vaccine for the immunotherapy of AML.Leukemia accepted article preview online, 5 August 2014; doi:10.1038/leu.2014.233.
    Leukemia. 08/2014;
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    ABSTRACT: Lenalidomide in combination with dexamethasone is an effective and well-established treatment of relapsed or refractory multiple myeloma (rrMM) disease. Due to the scarcity of reports assessing benefit and risk of long-term lenalidomide treatment in non-selected rrMM patients, we retrospectively analysed the long-term outcome in patients with rrMM treated with lenalidomide and dexamethasone. Sixty-seven patients (pts) who were treated with lenalidomide/dexamethasone for rrMM in the approved indication from 2007 to 2011 were included in this retrospective, single-centre analysis. Kaplan-Meier survival estimates were compared between total population, patients on lenalidomide for more than 12 months (mo) and patients discontinuing therapy earlier than 12 months. Median overall survival (OS) of the total patient population was 33.2 mo. OS of pts treated beyond 12 mo was 42.9 mo compared to 20.2 mo (p = 0.027) for pts stopping lenalidomide earlier than 12 mo for other reasons than progression disease (PD). OS of pts >12 mo on lenalidomide treatment did not significantly differ between pts who had received previous autologous transplantation, allogeneic transplantation or conventional therapy. Main non-hematologic toxicities were infections of grade 3/4 in 25 % and thrombembolic events of all grades in 18 % of patients. To the best of our knowledge, this is the first report on feasibility and efficacy of long-term lenalidomide treatment in a non-selected patient cohort. OS of pts >12 mo on lenalidomide is superior when compared to pts discontinued earlier for reasons other than PD. Our data confirm the current use of lenalidomide as a continuous long-term treatment strategy.
    Annals of Hematology 07/2014; · 2.87 Impact Factor
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    ABSTRACT: While paraneoplastic leukocytosis is a common phenomenon in solid tumors, extreme elevations of white blood counts (WBC) in the range of more than 100,000/mul are uncommon in patients with non-hematologic malignancies. Leukocytosis with mature neutrophils due to a granulocyte colony-stimulating factor (G-CSF) producing tumor is only seen on rare occasions.
    BMC Research Notes 05/2014; 7(1):313.
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    ABSTRACT: The vast majority of chronic myeloid leukemia patients express a BCR-ABL1 fusion gene mRNA encoding a 210 kDa tyrosine kinase which promotes leukemic transformation. A possible differential impact of the corresponding BCR-ABL1 transcript variants e13a2 (b2a2) and e14a2 (b3a2) on disease phenotype and outcome is still conflicting. A total of 1,105 newly diagnosed imatinib-treated patients were analyzed according to transcript type at diagnosis (e13a2, n=451; e14a2, n=496; e13a2+e14a2, n=158). No differences regarding age, sex, and Euro risk score were observed. A significant difference was found comparing white blood cells (88 vs. 65 x 109/L, p<0.001) and platelets (296 vs. 430 x 109/L, p<0.001) at diagnosis indicating a distinct disease phenotype (e13a2 vs. e14a2, respectively). No significant difference was observed regarding other hematologic features including spleen size and hematologic adverse events during imatinib-based therapies. Cumulative molecular response was inferior in e13a2 patients (p=0.002 for major molecular response, p<0.001 for MR4). No difference was observed with regard to cytogenetic response and overall survival. In conclusion, e13a2 and e14a2 chronic myeloid leukemia seem to represent distinct biological entities. However, clinical outcome under imatinib treatment was comparable and no prediction can be made by e13a2 vs. e14a2 BCR-ABL1 transcript type at diagnosis. ClinicalTrials.gov identifier: NCT00055874 (http://clinicaltrials.gov).
    Haematologica 05/2014; · 5.94 Impact Factor
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    ABSTRACT: Early assessment of response at 3 months of tyrosine kinase inhibitor (TKI) treatment has become an important tool to predict favorable outcome. We sought to investigate the impact of relative changes of BCR-ABL transcript levels within the initial 3 months of therapy. In order to achieve accurate data for high BCR-ABL levels at diagnosis, Beta-Glucuronidase (GUS) was used as reference gene. Within the German CML-Study IV, samples of 408 imatinib-treated patients were available in a single laboratory for both times, diagnosis and 3 months on treatment. 301 of these were treatment-naïve at sample collection. Results: i) With regard to absolute transcript levels at diagnosis no predictive cut-off could be identified. ii) At 3 months an individual reduction of BCR-ABL transcripts to the 0.35 fold of baseline level (0.46-log reduction, i.e. roughly half-log) separated best (high-risk: 16% of patients, 5-year overall survival 83 vs 98%, HR 6.3, P=0.001). iii) At 3 months, a 6% BCR-ABL(IS) cut-off derived from BCR-ABL/GUS yielded a good and sensitive discrimination (high-risk: 22% of pts, 5-year overall survival 85% vs. 98%, HR 6.1, P=0.002). Patients at risk of disease progression can be identified precisely by the lack of a half-log reduction of BCR-ABL transcripts at 3 months.Leukemia accepted article preview online, 06 May 2014; doi:10.1038/leu.2014.153.
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 05/2014; · 10.16 Impact Factor
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    ABSTRACT: Natural killer (NK)-cell alloreactivity after allogeneic hematopoietic cell transplantation (HCT) is influenced by the interaction of killer-cell immunoglobulin-like receptors (KIRs) on donor NK cells and human leukocyte antigen (HLA) class I ligands on recipient cells. We investigated the influence of donor KIR haplotype and KIR-ligand mismatch (MM) on relapse in 57 patients with hematologic malignancies receiving haploidentical HCT after reduced intensity conditioning and graft CD3/CD19 depletion. Of the 57 donors, 17 had KIR haplotype A (29.8 %) and 40 had KIR haplotype B (70.2 %). A KIR-ligand MM was found in 34 of 57 patients (59.6 %). There was no difference between donor KIR haplotypes in non-relapse mortality (NRM, p = 0.200) but had a significantly reduced incidence of relapse for patients with a haplotype B donor (p = 0.001). In particular, patients in partial remission (PR) benefited more from a haplotype B graft (p = 0.008) than patients in complete remission (CR, p = 0.297). Evaluating KIR-ligand MM cumulative incidences of relapse (p = 0.680) or NRM (p = 0.579), we found no significant difference. In conclusion, in the setting of reduced intensity conditioning (RIC) and CD3/CD19-depleted haploidentical HCT, we could not confirm the positive data with KIR-ligand MM but observed a significant lower risk of relapse with a KIR haplotype B donor.
    Annals of Hematology 04/2014; · 2.87 Impact Factor
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    ABSTRACT: Objective. The aim of this study was to find a new and less cardiotoxic conditioning regimen for high-dose chemotherapy and autologous stem cell transplantation (aSCT) in patients with severe SSc and pre-existing cardiac involvement.Methods. Six patients with cardiac involvement were treated for SSc with a conditioning regimen including reduced-dose CYC plus the non-cardiotoxic alkylant thiotepa. All patients received an implantable cardioverter defibrillator (ICD) before aSCT. The response at months 6 and 12 was measured according to reduction of the modified Rodnan skin score (mRSS). CT histography was used to monitor pulmonary manifestations, as were echocardiography, N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin for the cardiac involvement. Cardiac events were defined as death or hospitalisation due to heart failure or appropriate discharge of the ICD.Results. Between December 2008 and May 2012, four male and two female patients with a median age of 41 years received aSCT. The median mRSS significantly decreased from 26.5 to 18 and 17.5 at month 6 and 12, respectively. The total lung volume also significantly improved. Within the median follow-up of 1.6 years (range 1-3.8) two patients experienced a relapse of SSc, which results in a progression-free survival rate of 66.6%. Three patients experienced ICD discharge.Conclusion. For patients with SSc and cardiac involvement, the use of thiotepa and reduced-dose CYC is feasible and effective. The rate of ICD discharge underlines the need for protection in these endangered patients. This preliminary experience allowed us to use this regimen for our currently recruiting prospective trial (NCT01895244).
    Rheumatology (Oxford, England) 01/2014; · 4.24 Impact Factor
  • Katja Weisel, Lothar Kanz
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    ABSTRACT: Lenalidomide is an immunomodulatory drug (IMiD), which is well established and approved in the treatment of multiple myeloma (MM) and 5q-myelodysplastic syndrome (MDS). The mode of action includes immune modulation, anti-angiogenetic, anti-inflammatory, and anti-proliferative effects. Development of lenalidomide initiated a profound shift in therapeutic approaches especially toward MM. This chapter will discuss the mode of action of lenalidomide as well as its clinical applications. Important clinical phase II and III data of lenalidomide are presented. Currently, lenalidomide is not only investigated in MM and MDS, but also in malignant lymphomas and other entities.
    Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer 01/2014; 201:347-57.
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    ABSTRACT: Deep molecular response (MR(4.5)) defines a subgroup of patients with chronic myeloid leukemia (CML) who may stay in unmaintained remission after treatment discontinuation. It is unclear how many patients achieve MR(4.5) under different treatment modalities and whether MR(4.5) predicts survival. Patients from the randomized CML-Study IV were analyzed for confirmed MR(4.5) which was defined as ≥ 4.5 log reduction of BCR-ABL on the international scale (IS) and determined by reverse transcriptase polymerase chain reaction in two consecutive analyses. Landmark analyses were performed to assess the impact of MR(4.5) on survival. Of 1,551 randomly assigned patients, 1,524 were assessable. After a median observation time of 67.5 months, 5-year overall survival (OS) was 90%, 5-year progression-free-survival was 87.5%, and 8-year OS was 86%. The cumulative incidence of MR(4.5) after 9 years was 70% (median, 4.9 years); confirmed MR(4.5) was 54%. MR(4.5) was reached more quickly with optimized high-dose imatinib than with imatinib 400 mg/day (P = .016). Independent of treatment approach, confirmed MR(4.5) at 4 years predicted significantly higher survival probabilities than 0.1% to 1% IS, which corresponds to complete cytogenetic remission (8-year OS, 92% v 83%; P = .047). High-dose imatinib and early major molecular remission predicted MR(4.5). No patient with confirmed MR(4.5) has experienced progression. MR(4.5) is a new molecular predictor of long-term outcome, is reached by a majority of patients treated with imatinib, and is achieved more quickly with optimized high-dose imatinib, which may provide an improved therapeutic basis for treatment discontinuation in CML.
    Journal of Clinical Oncology 12/2013; · 18.04 Impact Factor
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    ABSTRACT: Since the advent of tyrosine kinase inhibitors, the impact of age on outcome of chronic myeloid leukemia (CML) patients has changed. We therefore analyzed patients from the randomized CML study IV to investigate disease manifestations and outcome in different age groups. One thousand five hundred twenty-four patients with BCR-ABL-positive chronic phase CML were divided into four age groups: (1) 16–29 years, n = 120; (2) 30–44 years, n = 383; (3) 45–59 years, n = 495; and (4) ≥60 years, n = 526. Group 1 (adolescents and young adults (AYAs)) presented with more aggressive disease features (larger spleen size, more frequent symptoms of organomegaly, higher white blood count, higher percentage of peripheral blasts and lower hemoglobin levels) than the other age groups. In addition, a higher rate of patients with BCR-ABL transcript levels >10 % on the international scale (IS) at 3 months was observed. After a median observation time of 67.5 months, no inferior survival and no differences in cytogenetic and molecular remissions or progression rates were observed. We conclude that AYAs show more aggressive features and poor prognostic indicators possibly indicating differences in disease biology. This, however, does not affect outcome.
    Annals of Hematology 10/2013; · 2.87 Impact Factor
  • Clinical lymphoma, myeloma & leukemia 10/2013;
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    ABSTRACT: The exact prevalence of psoriatic arthritis (PsA) among patients with psoriasis is still not conclusive. Data in the literature vary between 5.8 and 30 %. Objective of this study was to gain more information on the prevalence of PsA among patients with psoriasis in Germany. Between 09/2010 and 05/2011, consecutive patients from dermatological private practices and a university hospital with psoriasis were asked to fill out the validated German Psoriatic Arthritis Diagnostic (GEPARD) Questionnaire. Patients who answered ≥4 questions with "yes" were invited to come for a rheumatological check up. Those patients who refused a rheumatological examination were counted as "absence of PsA". Laboratory tests for inflammatory markers as well as the severity of skin manifestations were assessed. The diagnosis of PsA was made according to the CASPAR criteria, and imaging was performed in addition. A total of 404 questionnaires were evaluated; 50.5 % answered ≥4 questions positively; 19.3 % had a history of PsA confirmed by a rheumatologist; and in 10.9 %, PsA or spondyloarthritis was newly diagnosed during the present study. This leads to an overall prevalence of PsA in patients with psoriasis of 30.2 %. The frequency of psoriatic arthritis in the present study is higher than expected from previous studies in Germany. The prevalence is consistent with findings of a large observational survey from Scandinavia. Using the CASPAR criteria and imaging in all patients, certainty of the diagnosis is very high. The GEPARD Questionnaire is a helpful tool to identify people at risk for psoriatic arthritis.
    Rheumatology International 10/2013; · 2.21 Impact Factor
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    ABSTRACT: Klippel-Trénaunay syndrome (KTS) is a rare congenital anomaly characterized by malformation of lymph and blood vessels as well as growth disturbance of soft tissue and bone. The clinical picture is variable and associated with an increased risk of thromboembolic events mediated by intravascular coagulopathy in venous malformations. Here, we report on a male patient with KTS suffering from recurrent deep vein thrombosis (DVT) and life-threatening bleeding due to consumptive coagulopathy. Furthermore, we describe the successful long-term anticoagulant management with rivaroxaban.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 09/2013; · 1.25 Impact Factor
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    ABSTRACT: The SRY-related HMG-box family of transcription factors member SOX2 regulates stemness and pluripotency in embryonic stem cells and plays important roles during early embryogenesis. More recently, SOX2 expression was documented in several tumor types including ovarian carcinoma, suggesting an involvement of SOX2 in regulation of cancer stem cells. Intriguingly, however, studies exploring the predictive value of SOX2 expression with respect to histopathological and clinical parameters report contradictory results in individual tumors, indicating that SOX2 may play tumor-specific roles. In this report, we analyze the functional relevance of SOX2 expression in human ovarian carcinoma. We report that in human serous ovarian carcinoma (SOC) cells SOX2 expression increases the expression of cancer stem cell markers, the potential to form tumor spheres and the in vivo tumor-initiating capacity, while leaving cellular proliferation unaltered. Moreover, SOX2-expressing cells display enhanced apoptosis resistance in response to conventional chemotherapies and TRAIL. Hence, our data demonstrate that SOX2 associates with stem cell state in ovarian carcinoma and induction of SOX2 imposes cancer stem cell properties on SOC cells. We propose the existence of SOX2-expressing ovarian cancer stem cells as a mechanism of tumor aggressiveness and therapy resistance in human SOC.
    Cancer Research 07/2013; · 9.28 Impact Factor
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    ABSTRACT: The transcription factor SOX2 has been extensively studied for its role in embryonic stem cell self-renewal and pluripotency. More recent data suggest oncogenic functions of SOX2 and demonstrate expression in several carcinoma types, predominantly of squamous cell origin. The gene SOX2 is located at chromosome 3q26, a region that is frequently amplified in ovarian high-grade serous carcinoma. In this study, we correlate SOX2 protein expression and gene-amplification status in ovarian carcinomas with histopathologic criteria and disease outcome. A total of 215 cases of ovarian carcinomas (154 serous, 39 endometrioid, 11 clear cell, 5 mucinous, and 6 transitional cell carcinomas) were analyzed by immunohistochemistry in a tissue microarray for nuclear expression of SOX2. A total of 60.5% of all carcinomas showed SOX2 expression with no significant difference between the major histologic types. Interestingly, SOX2 expression was predominantly a feature of high-grade tumors (G1: 36.4%, G2: 55.6%, G3: 64.0%, P=0.040). In 21.2% of these cases, fluorescence in situ hybridization analysis detected low-level SOX2 gene amplification which was not significantly associated with SOX2 protein expression. However, survival analysis of Stage II to IV high-grade serous carcinomas revealed a favorable effect of SOX2 expression (median disease-free survival 27 vs. 21 mo, P=0.041; median overall survival 39 vs. 25 mo, P=0.062). Further studies are needed to explore whether expression of SOX2 has a specific role in prognosis and therapy response.
    International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists 05/2013; · 2.07 Impact Factor
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    ABSTRACT: Patients with primary refractory or relapsed acute myeloid leukemia (AML) have a dismal prognosis. We report a retrospective single center analysis of aplasia-inducing chemotherapy using fludarabine, cytarabine, and amsacrine (FLAMSA) followed by reduced-intensity conditioning (RIC) for allogeneic hematopoietic cell transplantation (HCT) in 62 consecutive primary refractory or relapsed AML patients. Two-year event-free survival and overall survival (OS) were 26 and 39 %, respectively. Risk stratification according to cytogenetic and molecular genetic markers showed superior survival in patients in the intermediate-1 risk group (2-year OS 70 %) compared to the intermediate-2 risk (2-year OS 34 %, p = 0.03) and adverse risk (2-year OS 38 %, p = 0.06) group. The use of HLA-matched versus HLA-mismatched donors had no significant influence on survival (p = 0.98). Two-year OS in the elderly subgroup defined by age ≥60 years was 31 % compared to 46 % in the group of younger patients <60 years (p = 0.19). Cumulative incidence of non-relapse mortality at 2 years adjusted for relapse as competing risk was 20 % for patients <60 years and 26 % for older patients (p = 0.55). Chronic graft-versus-host disease was associated with a statistically significant superior survival (p < 0.01). FLAMSA-RIC followed by allogeneic HCT enables long-term disease-free survival in primary refractory or relapsed AML even in the elderly patient population.
    Annals of Hematology 05/2013; · 2.87 Impact Factor
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    ABSTRACT: History and admission findings: We report on a 24-year-old male patient who presented with worsening of the general condition and abdominal pain.Investigations: On physical examination, gynecomastia was noted. Laboratory tests showed manifest hyperthyroidism. The beta-hCG levels were markedly increased. By ultrasound, the thyroid gland was hyperperfused without thyroid nodules. Several large echo mixed lesions were found in the liver. The testes appeared normal. Diagnosis: In light of the typical laboratory findings, a non-seminomatous extragonadal germ cell tumor was diagnosed. Hyperthyroidism was most probably HCG induced. Treatment and course: Initially the patient was treated with thyreostatic drugs. After initiation of chemotherapy and a marked decrease in beta-hCG, thyreostatic therapy could be terminated. Conclusions: Germ cell tumors may cause an increase in beta-hCG concentration. By cross-reacting with the TSH-receptor this could induce hyperthyroidism. Germ cell tumors are therefore a rare differential diagnosis of hyperthyreoidism.
    DMW - Deutsche Medizinische Wochenschrift 04/2013; 138(17):908. · 0.65 Impact Factor

Publication Stats

13k Citations
2,775.94 Total Impact Points

Institutions

  • 2014
    • Hospital Universitario Miguel Servet
      Caesaraugusta, Aragon, Spain
  • 1997–2014
    • Universitätsklinikum Tübingen
      • • Internal Medicine II - Oncology, haematology, clinical immunology, rheumatology and pneumology
      • • Department of Medicine
      Tübingen, Baden-Württemberg, Germany
    • Hohenheim University
      Stuttgart, Baden-Württemberg, Germany
    • Goethe-Universität Frankfurt am Main
      • Institut für Medizinische Virologie
      Frankfurt, Hesse, Germany
  • 1995–2014
    • University of Tuebingen
      • • Department of Internal Medicine
      • • Centre for Geriatric Medicine
      Tübingen, Baden-Württemberg, Germany
  • 2013
    • Universitätsmedizin Mannheim
      Mannheim, Baden-Württemberg, Germany
  • 2009–2011
    • Universität Heidelberg
      • • Medical University Clinic and Polyclinic
      • • II. Medical Clinic
      Heidelberg, Baden-Wuerttemberg, Germany
  • 2010
    • Charité Universitätsmedizin Berlin
      • Department of Pediatrics, Division of Oncology and Hematology
      Berlin, Land Berlin, Germany
  • 2005–2007
    • University of Hamburg
      • Center for Oncology
      Hamburg, Hamburg, Germany
    • University Medical Center Hamburg - Eppendorf
      Hamburg, Hamburg, Germany
    • Hertie-Institute for Clinical Brain Research
      Tübingen, Baden-Württemberg, Germany
  • 1996–2003
    • Martin Luther University of Halle-Wittenberg
      Halle-on-the-Saale, Saxony-Anhalt, Germany
  • 2001
    • Haematology Oncology Practice Altona
      Hamburg, Hamburg, Germany
  • 2000
    • Universität Ulm
      Ulm, Baden-Württemberg, Germany
  • 1999
    • Ninewells Hospital
      Dundee, Scotland, United Kingdom
  • 1991–1999
    • Universitätsklinikum Freiburg
      • Department of Internal Medicine
      Freiburg, Lower Saxony, Germany
  • 1988–1998
    • University of Freiburg
      • Institute of Forensic Medicine
      Freiburg, Lower Saxony, Germany