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  • 1
    Abstract: BACKGROUND: For desensitization of ABO-incompatible kidney transplant recipients we recently proposed nonantigen-specific immunoadsorption (IA) and rituximab. METHODS: We now compared clinical outcomes of 34 ABO-incompatible living-donor kidney recipients who were transplanted using this protocol with that of 68 matched ABO-compatible patients. In addition, we analyzed efficacy and cost of nonantigen-specific as compared to blood group antigen-specific IA. RESULTS: Before desensitization, the median isoagglutinin titer of 34 ABO-incompatible patients was 1:64 (Coombs technique). Patients received a median of 7 preoperative IA treatments. Twenty-four patients had a median of 2 additional plasmapheresis treatments to reach the preoperative target isoagglutinin titer of 1:8 or less. After a median postoperative follow-up of 22 months, overall graft survival in the ABO-incompatible group was not significantly different from that in ABO-compatible patients (log-rank P = 0.20), whereas patient survival tended to be lower (log-rank P = 0.05). The incidence of rejection episodes was 15% in both groups. The ABO-incompatible kidney recipients had a higher incidence of BK virus replication (P = 0.04) and nephropathy (P = 0.01) and showed more often colonization with multidrug resistant bacteria (P = 0.02). In comparison to blood group antigen-specific IA, nonantigen-specific IA showed equal efficacy but was associated with reduction in cost. CONCLUSIONS: Clinical outcomes of ABO-incompatible patients desensitized with a nonantigen-specific IA device and rituximab do not differ from that of matched ABO-compatible patients although a trend toward reduced patient survival was noted. Special attention must be paid to the higher incidence of BK virus infection in recipients of ABO-incompatible grafts.
    Type of Publication: Journal article published
    PubMed ID: 25989497
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  • 2
    Keywords: DIAGNOSIS ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; PCR ; MUTATIONS ; UNITED-STATES ; CHRONIC MYELOID-LEUKEMIA ; CHRONIC LYMPHOCYTIC-LEUKEMIA
    Abstract: Bone marrow biopsy of the iliac crest is the first and most important step in the diagnostics of hematopoietic disorders. The biopsies of the years 2006 and 2007 from the Institute of Pathology of the Jena University Hospital were retrospectively analyzed for clinicopathological parameters. In addition, the Mitelman database was retrieved for chromosomal aberrations. The analysis of 2820 reports from 1185 patients revealed that lymphomas, plasma cell myeloma and acute leukemia were most frequent. Males predominated in myeloproliferative neoplasms and lymphoma subtypes, particularly CLL, except for plasma cell myeloma and acute leukemia. A peak incidence was seen between 61 and 70 years of age with a varying pattern for single entities. The database search revealed that ALL, AML, CLL and CML were mainly diploid while Hodgkin lymphoma, mature B-cell lymphoma and multiple myeloma mostly carried hyperdiploid chromosome numbers. Numerical aberrations like chromosome 8 gains in hyperdiploid CML were prominent in specific subgroups. Molecular testing is exemplified in CML, plasma cell myeloma and hairy cell leukemia. The study highlights typical clinicopathological characteristics and new genetic findings in hematopoietic and lymphoid neoplasms with relevance for the new WHO classification and beyond. We hope that it may help in the differential diagnosis of bone marrow biopsies.
    Type of Publication: Journal article published
    PubMed ID: 22795690
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  • 3
    Abstract: BACKGROUND: In simultaneous pancreas-kidney transplantation (SPKT), monitoring of the pancreas allograft is more complex than the kidney allograft due to difficulties in obtaining pancreas histology and weak clinical evidence supporting the role of donor-specific antibodies (DSA). METHODS: We performed a single-center retrospective analysis of all 17 SPKT recipients who underwent a total of 22 pancreas allograft indication biopsies from October 2009 to September 2012. Fifteen patients had at least 2 DSA measurements: pretransplantation and at the time of biopsy. RESULTS: All 7 patients (100%) with post-transplantation DSA-positivity (de novo: n = 6; persistent: n = 1) at biopsy had at least 1 rejection episode either of the pancreas (n = 4) or the kidney (n = 3), with 3 antibody-mediated rejections (AMR). In contrast, only 4 of 8 patients (50%) without post-transplantation DSA had evidence of rejection, with 1 AMR. Findings during pancreas allograft biopsy procedures led to a change of immunosuppressive therapy in 11 of 15 (73%) patients. Patient survival, graft survival, and function were not adversely affected by the presence of post-transplantation DSA. One major and 2 minor procedure-related complications occurred during the pancreas biopsies. CONCLUSIONS: In this small retrospective analysis, pancreas allograft histology provided the most therapeutically relevant information, rather than the kidney histology or DSA monitoring.
    Type of Publication: Journal article published
    PubMed ID: 26518960
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  • 4
    Keywords: NECROSIS-FACTOR-ALPHA ; EPITHELIAL-CELLS ; LUNG-DISEASE ; HEPCIDIN EXPRESSION ; HEREDITARY HEMOCHROMATOSIS ; HUMAN MONOCYTES ; IFN-BETA ; IRON HOMEOSTASIS ; DIFFERENTIAL REGULATION ; LEUKOCYTE MIGRATION
    Abstract: Regulation of iron homeostasis and the inflammatory response are tightly linked to protect the host from infection. Here we investigate how imbalanced systemic iron homeostasis in a murine disease model of hereditary hemochromatosis (Hfe(-/-) mice) affects the inflammatory responses of the lung. We induced acute pulmonary inflammation in Hfe(-/-) and wild-type mice by intratracheal instillation of 20 microg of lipopolysaccharide (LPS) and analyzed local and systemic inflammatory responses and iron-related parameters. We show that in Hfe(-/-) mice neutrophil recruitment to the bronchoalveolar space is attenuated compared to wild-type mice although circulating neutrophil numbers in the bloodstream were elevated to similar levels in Hfe(-/-) and wild-type mice. The underlying molecular mechanisms are likely multifactorial and include elevated systemic iron levels, alveolar macrophage iron deficiency and/or hitherto unexplored functions of Hfe in resident pulmonary cell types. As a consequence, pulmonary cytokine expression is out of balance and neutrophils fail to be recruited efficiently to the bronchoalveolar compartment, a process required to protect the host from infections. In conclusion, our findings suggest a novel role for Hfe and/or imbalanced iron homeostasis in the regulation of the inflammatory response in the lung and hereditary hemochromatosis.
    Type of Publication: Journal article published
    PubMed ID: 22745741
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