Eva Birgitte Leinoe
Copenhagen University Hospital
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Eva Birgitte Leinoe.
British Journal of Haematology | 2005
Eva Birgitte Leinoe; Marianne Hutchings Hoffmann; Erik Kjærsgaard; Joern Dalsgaard Nielsen; Olav Jonas Bergmann; Tobias Wirenfeldt Klausen; Hans Erik Johnsen
Haemorrhage is often responsible for the lethal course of acute myeloid leukaemia (AML). Previously, multiple platelet function defects were identified by flow cytometric analysis of platelet activation markers in AML. The role of flow cytometric analysis of platelet function in characterization of prognostic markers of haemorrhage in AML patients has not been well elucidated. The objective of this prospective study was to analyse platelet function in 50 AML patients at diagnosis and to compare results with clinical bleeding score, graded by common toxicity criteria. Platelet activation markers CD62P, CD42b, CD63 and PAC‐1 were analysed following in vitro activation by thrombin receptor activating peptide. The following plasma haemostasis parameters were measured: soluble P‐selectin, activated partial thromboplastin time, thrombin time, prothrombin time, d‐dimer, fibrinogen, and von Willebrand factor antigen. In a multivariate analysis, P‐selectin (CD62P) <36 molecules of equivalent soluble fluorochrome × 103 (P < 0·0015) and platelet count <40 × 109/l (P = 0·01) were significant predictors of haemorrhage at diagnosis. Haemorrhage at diagnosis predicted grade 3–4 haemorrhage in the first 28 d following diagnosis (P = 0·018). The presented results indicate that low P‐selectin is a prognostic marker of haemorrhage in AML.
British Journal of Haematology | 2004
Eva Birgitte Leinoe; Marianne Hutchings Hoffmann; Erik Kjærsgaard; Hans Erik Johnsen
Previous findings of megakaryocytic hypogranulation and dysmegakaryocytopoietic features in acute myeloid leukaemia (AML) strongly indicate defects in platelet production. The bleeding tendency of these patients may result from dysregulated platelet production, resulting in thrombocytopenia as well as qualitative platelet defects. The present study examined platelet function at diagnosis in 50 AML patients by whole blood flow cytometry. Following in vitro platelet agonist stimulation, platelet activation markers were analysed and compared with 20 healthy individuals. To detect recent in vivo platelet activation, plasma soluble P‐selectin (sP‐selectin) was measured. Flow cytometric analysis of platelet activation markers demonstrated reduced CD62P [35·6 vs. 118·5 × 103 molecules of equivalent soluble fluorochrome (MESF); P < 0·0001], CD63 (11·3 vs. 50·7 × 103 MESF; P < 0·0001), and PAC‐1 (41·5 vs. 90·5%; P = 0·0001) while reductions in CD42b were abnormal (45·6 vs. 70%; P < 0·0001). sP‐selectin levels were similar in patients and healthy controls (0·04 vs. 0·27 fg/platelet; P = 0·84). The presented data indicate that AML pathogenesis may result in multiple platelet defects, involving adhesion, aggregation, and secretion and demonstrate that flow cytometry is a feasible method for platelet function analysis in patients with thrombocytopenia.
Cytometry Part B-clinical Cytometry | 2012
Marianne Hutchings Hoffmann; Tobias Wirenfeldt Klausen; Martin Boegsted; Steffen Falgreen Larsen; Alexander Schmitz; Eva Birgitte Leinoe; Kjeld Schmiegelow; Henrik Hasle; Olav Jonas Bergmann; Suzette Sørensen; Mette Nyegaard; Karen Dybkær; Hans Erik Johnsen
Individual cellular heterogeneity within the acute myeloid leukemia (AML) bone marrow samples can be observed by multi parametric flow cytometry analysis (MFC) indicating that immunophenotypic screening for leukemic blast subsets may have prognostic impact.
Leukemia Research | 2013
Anne Mette Larsen; Eva Birgitte Leinoe; Pär I. Johansson; Henrik Birgens; Sisse R. Ostrowski
The risk of hemorrhage is influenced by multiple factors in acute myeloid leukemia (AML). We investigated whether hemorrhage in AML patients was associated with endothelial perturbation, potentially caused by thrombocytopenia, platelet dysfunction and leukocytosis. Biomarkers of endothelial perturbation, coagulation and platelet activation were analyzed in 49 AML patients, along with previously collected data on bleeding status and platelet activation markers. High levels of syndecan-1, a marker of endothelial glycocalyx degradation, were associated with bleeding, impaired platelet function, higher age, endothelial cell activation and damage, and leukocytosis. We suggest that platelet dysfunction and leukocytosis in AML causes endothelial perturbation.
Vox Sanguinis | 2015
Anne Mette Larsen; Eva Birgitte Leinoe; Pär I. Johansson; Henrik Birgens; Sisse R. Ostrowski
Transfusion of red blood cells (RBC) is beneficial for the patient but can also be harmful, as randomized trials have demonstrated increased infection rates, bleeding and mortality. The study aim was to investigate the response of the vascular system (the haemostatic function and the endothelium) to RBC transfusion.
British Journal of Haematology | 2017
Eva Birgitte Leinoe; Eva Zetterberg; Savvas Kinalis; Olga Østrup; Peter Kampmann; Eva Norström; Nadine Gretenkort Andersson; Jenny Klintman; Klaus Qvortrup; Finn Cilius Nielsen; Maria Rossing
Rare inherited bleeding disorders (IBD) are a common cause of bleeding tendency. To ensure a correct diagnosis, specialized laboratory analyses are necessary. This study reports the results of an upfront diagnostic strategy using targeted whole exome sequencing. In total, 156 patients with a significant bleeding assessment tool score participated in the study, of which a third had thrombocytopenia. Eighty‐seven genes specifically associated with genetic predisposition to bleeding were analysed by whole exome sequencing. Variants were classified according to the five‐tier scheme. We identified 353 germline variants. Eight patients (5%) harboured a known pathogenic variant. Of the 345 previously unknown variants, computational analyses predicted 99 to be significant. Further filtration according to the Mendelian inheritance pattern, resulted in 59 variants being predicted to be clinically significant. Moreover, 34% (20/59) were assigned as novel class 4 or 5 variants upon targeted functional testing. A class 4 or 5 variant was identified in 30% of patients with thrombocytopenia (14/47) versus 11% of patients with a normal platelet count (12/109) (P < 0·01). An IBD diagnosis has a major clinical impact. The genetic investigations detailed here extricated our patients from a diagnostic conundrum, thus demonstrating that continuous optimization of the diagnostic work‐up of IBD is of great benefit.
Transfusion Medicine | 2015
Anne Mette Larsen; Eva Birgitte Leinoe; Pär I. Johansson; R. Larsen; P. Wantzin; Henrik Birgens; Sisse R. Ostrowski
The beneficial effect of platelet transfusion on haemostasis is well established, but there is emerging evidence that platelet transfusion induces an inflammatory response in vascular endothelial cells.
Vox Sanguinis | 2013
R. T. Hoeg; Eva Birgitte Leinoe; P. Andersen; T. W. Klausen; Henrik Birgens
Interventions to change physician transfusion behavior are often evaluated by examining the amount of red blood cell (RBC) units transfused or the proportion of patients transfused before and after the intervention. The pre‐transfusion haemoglobin concentration is a sensitive measure of transfusion practice, but has not been used to evaluate behavioral interventions. We examined the effect of a Danish National Board of Health December 2007 transfusion guideline on the behavior of clinicians treating acute myeloid leukaemia (AML). We compared the effect of the guideline on pre‐transfusion haemoglobin concentrations with other measures of transfusion behavior, including use of RBC units and proportion of patients transfused. No change in transfusion behavior could be demonstrated by examining amount of RBC units transfused and proportion of patients transfused. Conversely, the pre‐transfusion haemoglobin concentration fell significantly. Pre‐transfusion haemoglobin determination is a sensitive measure of the effect of an intervention to change physician transfusion behaviour.
Platelets | 2018
Marcus Fager Ferrari; Eva Birgitte Leinoe; Maria Rossing; Eva Norström; Karin Strandberg; Tobias Steen Sejersen; Klaus Qvortrup; Eva Zetterberg
Abstract Familial hemophagocytic lymphohistiocytosis (FHL) is caused by biallelic variants in genes regulating granule secretion in cytotoxic lymphocytes. In FHL3–5, the affected genes UNC13D, STX11 and STXBP2 have further been shown to regulate the secretion of platelet granules, giving rise to compromised platelet function. Therefore, we aimed to investigate platelet degranulation in patients heterozygous for variants in UNC13D, STX11 and STXBP2. During the work-up of patients referred to the Coagulation Unit, Skåne University Hospital, Malmö, Sweden and the Department of Hematology, Rigshospitalet, Copenhagen, Denmark due to bleeding tendencies, 12 patients harboring heterozygous variants in UNC13D, STX11 or STXBP2 were identified using targeted whole exome sequencing. Transmission electron microscopy (TEM) was used to assess the secretion of platelet dense granules following thrombin stimulation. Platelet degranulation, activation and aggregation were further assessed by flow cytometry (FC) and light transmission aggregometry (LTA) with lumi-aggregometry. In total, eight out of twelve (67%) patients showed impaired degranulation by at least one of the assays (TEM, FC and LTA). In the 12 patients, eight different heterozygous variants were identified. One variant was strongly associated with impaired degranulation, while four of the variants were associated with impaired granule secretion to a slightly lesser extent. One additional variant was found in six out of the twelve patients, and was associated with varying degrees of degranulation impairment. Accordingly, six out of the eight (75%) identified variants were associated with impaired platelet degranulation. Our results suggest that heterozygous variants in UNC13D, STX11 and STXBP2 are sufficient to cause platelet secretion defects resulting in increased bleeding.
Haematologica | 2018
Loredana Bury; Eva Zetterberg; Eva Birgitte Leinoe; Emanuela Falcinelli; Alessandro Marturano; Giorgia Manni; Alan T. Nurden; Paolo Gresele
We report a novel form of autosomal dominant variant Glanzmann thrombasthenia (GT) with, unlike all previously reported cases, the proband showing compound heterozygosity for two ITGB3 variants. Expression studies in CHO cells of the two previously undescribed ITGB3 variants, and studies in