Objectives Use of potent antiplatelet drugs requires evaluation of platelet function. While platelet function in elective cases is usually assessed in a central laboratory environment, there is also an urgent need for rapid perioperative point-of-care assessment. Recently, multiple electrode platelet aggregometry has been developed and assumed to measure platelet function independent from platelet count. We tested the hypothesis that results of multiple electrode platelet aggregometry are affected by platelet count, in particular if platelet count is below normal range. Methods Whole blood samples from 20 healthy volunteers were prepared containing platelet concentrations of 50,000, 100,000, 150,000, 200,000, and 250,000 μl -1 while maintaining hematocrit. Platelet aggregation was induced by collagen, thrombin receptor activating peptide 6 (TRAP-6), adenosine-diphoshate (ADP), and arachidonic acid, respectively, and aggregation was measured by multiple electrode platelet aggregometry (Multiplate™). Results Results of multiple electrode platelet aggregometry significantly decreased in blood samples with platelet count below normal range. Compared to results measured in blood samples with platelet count within normal range, aggregometry results decreased by 18.4% (p < 0.001) and 37.2% (p < 0.001) in blood samples with a platelet count of 100.000 and 50.000 μl -1 , respectively. On the other hand, large interindividual variation has been observed and some blood samples showed normal results even with platelet counts of 50.000 μl -1 . Conclusion The results obtained with Multiplate™ Analyzer are influenced by platelet function as well as platelet count thus displaying the overall platelet aggregability within the blood sample rather than platelet function alone.

Allogeneic hematopoietic stem cell transplantation (HSCT) is the only definitive treatment for severe bone marrow dysfunction and clonal disorders in patients diagnosed with Shwachman-Diamond syndrome (SDS).In an attempt to minimize regimen-related toxicity (RRT), we have initiated a fludarabine/treosulfan/ melphalan-based pilot protocol avoiding the combination of busulfan and cyclophosphamide. Median age at transplantation was 9.6 years (range 1.5-17 years). All three patients received conditioning with fludarabine (30 mg/m 2 / day  6), treosulfan (12 g/m 2 /day  3) and melphalan (140 mg/m 2 /day  1). CAMPATH-1H (0.1 mg/kg  2) was added in two cases, while rabbit ATG (Genzyme; 3  2.5 mg/kg) was given to the cord blood recipient. One patient was transplanted with a non-manipulated marrow graft from an HLA-identical sibling, one with a marrow graft from a 10/10 matched unrelated donor, and one with a 9/10 matched unrelated umbilical cord blood (UCB) unit. Mean cell doses given were 3.6  10 8 nucleated cells/ kg BW for the bone marrow recipients and 4.2  10 7 nucleated cells/kg BW for UCB recipient. Overall, two of three patients are alive and display 100% donor chimerism. Acute graft-versus-host disease grade II was seen in one patient, while no GVHD exceeding grade I occurred in the remaining two.

The main cause of death in the patient group less than 45 years is trauma. Beside severe traumatic brain injury, bleeding remains a leading cause of death in this group. For a causal therapy, it is necessary to understand the pathophysiology of trauma-induced coagulopathy (TIC). Beside the well-known lethal triad of trauma (hypothermia, acidosis, and coagulopathy), dilution and hypoperfusion with activation of the protein C pathway play a crucial role. TIC is a complex independent syndrome which may be present without initial hypercoagulopathy. A rapid and differentiated diagnosis and goal-directed therapy is crucial for causal therapy.