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Background After cardiopulmonary bypass (CPB) thrombocytopenia is a relatively common pattern which may trigger postoperative bleeding. The purpose of this study is to verify if the endogenous fibrinogen levels are independent determinants of chest drain blood loss and need for allogeneic blood products transfusions in a clinical model of post-CPB thrombocytopenia. Methods Retrospective analysis on 445 consecutive patients having a platelet count < 100 × 1000 cells/μL after CPB. Based on the fibrinogen levels the patients were divided into three groups with similar platelet count and low (LF, median 170 mg/dL), intermediate (IF, median 215 mg/dL), and high (HF, median 280 mg/dL), fibrinogen levels. Chest drain blood loss (mL/12 h), transfusion rate of red blood cells (RBC), fresh frozen plasma (FFP) and platelet concentrates were assessed and compared between groups. Results There was a significant (P = 0.001) difference in chest drain blood loss with higher values in the LF group (487 mL/12 h, IQR 300–600 mL/12 h) than in the IF group (350 mL/12 h, IQR 200–500 mL/12 h) and the HF group (300 mL/12 h, IQR 200–475 mL/12 h). Transfusion rates of FFP significantly (P = 0.014) differed between groups (LF: 18.4%, IF: 7.9%, HF: 9.2%) and platelet concentrate transfusions significantly (P = 0.020) differed between groups (LF: 23.5%, IF: 16.5%, HF: 10.7%). In multivariable models, these differences were confirmed. Thromboelastography parameters showed an effective compensation of clot firmness in group HF vs. IF and LF. Conclusions Levels of fibrinogen > 240 mg/dL compensate the decrease in clot firmness observed in thrombocytopenic patients following CPB, and reduce bleeding and transfusion needs. [ABSTRACT FROM AUTHOR]

Anaemia is the commonest cytopenia seen in patients with myelodysplastic syndrome ( MDS), and the majority of patients will require transfusion support at some point. Blood transfusions are rich in iron, which leads to the accumulation of body iron over time. It is accepted that this ultimately causes end organ damage and may impact on both morbidity and mortality. In addition, recent data has increased our interest in the subject with regard to the potential impact on stem cell transplant outcome and an anti-leukaemic effect of iron chelation therapy. There is still debate over which patients should receive iron chelation therapy, but the emergence of new diagnostic and prognostic markers in MDS may help decision making in the clinic setting. [ABSTRACT FROM AUTHOR]

Patients with upper gastrointestinal (GI) bleeding frequently require hospitalization and have a mortality rate that ranges from 6% to 14%. These patients need rapid clinical assessment to determine the urgency of endoscopy and the need for endoscopic treatment. Risk-scoring tools, such as the Rockall score and the Glasgow-Blatchford score, are commonly used in this assessment. These tools clearly help identify high-risk patients but do not necessarily have good predictive value in identifying important outcomes. Their diagnostic accuracy in identifying rebleeding and mortality ranges from poor to fair. The shock index (heart rate divided by systolic blood pressure) provides an integrated assessment of the cardiovascular status. It can be easily calculated during the initial evaluation of patients and monitoring after treatment. The shock index has been used in a few studies in patients with acute GI bleeding, including studies to determine which patients need emergency endoscopy, to predict complications after corrosive ingestions, to identify delayed hemorrhage following pancreatic surgery, and to evaluate the utility of angiograms to identify sites of GI bleeding. Not all studies have found the shock index to be useful in patients with GI bleeding, however. This may reflect the unpredictable natural history of various etiologies of GI bleeding, comorbidity that may influence blood pressure and/or heart rate, and inadequate data acquisition. The shock index needs more formal study in patients with GI bleeding admitted to medical intensive care units. Important considerations include the initial response to resuscitation, persistent bleeding following initial treatment, and rebleeding following a period of stabilization. In addition, it needs correlation with other risk-scoring tools. [ABSTRACT FROM AUTHOR]

Red blood cell (RBC) alloimmunization can be a life-threatening complication for patients with sickle cell disease (SCD) receiving therapeutic transfusions. Despite provision of extended antigen-matched donor RBCs, patients continue to develop antibodies due to high degree of polymorphisms in the immunogenic antigens in individuals of African ancestry. Identification of biomarkers of alloimmunization in this patient population is therefore of great interest and will help to identify in advance patients most likely to make antibodies in response to transfusion. We have recently identified altered T cell responses and innate immune abnormalities in alloimmunized SCD patients. In this paper, we summarize this work and propose our working model of how innate immune abnormalities can contribute to pathogenic T cell responses in alloimmunized SCD patients. We believe that unravelling the basis of such altered interactions at the cellular and molecular level will help future identification of biomarkers of alloimmunization with the goal that this information will ultimately help guide therapy in these patients. [ABSTRACT FROM AUTHOR]

Abstract: Most patients with myelodysplastic syndromes (MDS) require transfusions due to chronic anemia. Apart from the acute risks associated with transfusions, chronic anemia and red blood cell (RBC) transfusion dependence impact negatively on survival and quality of life (QoL), and are associated with iron overload, potentially leading to organ damage. QoL studies demonstrate that regular transfusions do not correct the impact of chronic anemia. Furthermore, chronic transfusion support requires substantial resources. Therefore, major goals are to prevent or effectively treat anemia. Indeed, innovative drugs have been shown to be effective in achieving transfusion independence by altering the natural course of MDS. [Copyright &y& Elsevier]

To better understand the detection and management of iron overload in transfusion-dependent patients with myelodysplastic syndromes (MDS), a 15-min web- or paper-based survey was conducted among 338 European physicians from 27 countries. Respondents had a mean of 18 years of clinical experience. Forty-six percent and 27% of physicians noted that detecting and treating iron overload were either "very important" or "important," respectively. The main reason for not actively exploring iron overload was related to poor patient prognosis, while the main reasons for not initiating iron chelation therapy were poor patient prognosis and older patient age. Thirty-seven percent and 31% of physicians believed that treating iron overload in these patients was "very important" or "important," respectively. Ninety percent of physicians prescribed iron chelation therapy, and 38% of transfusion-dependent patients received iron chelation therapy. The key reasons for not initiating iron chelation therapy were related to poor patient prognosis (72%), patient age ≥85 years (50%), and comorbidities (34%). The views of these experienced MDS physicians reflect available international MDS treatment guidelines. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension is common in adults with thalassaemia and other haemolytic anaemias. It was hypothesised that regular transfusions in thalassaemia major should both decrease the chronic haemolytic rate and be protective from pulmonary hypertension (PHT). To reduce the contribution of existing cardiac disease to PHT, the subjects were limited to patients with normal left ventricular shortening fractions. Associations with multiple laboratory markers of haemolysis, serum ferritin levels, chest X-rays findings and splenectomy status were also considered. We found no biochemical, transfusional, or clinical (except gender) differences in transfused thalassaemia patients with or without pulmonary hyper tension. [ABSTRACT FROM AUTHOR]