Short-term warfarin reversal for elective surgery–using low-dose intravenous vitamin K: safe, reliable and convenient*.
Br J Haematol. 2011 Sep;154(5):626-34
Authors: Burbury KL, Milner A, Snooks B, Jupe D, Westerman DA
…

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Heparin-induced thrombocytopenia: analysis of risk factors in medical inpatients.
Br J Haematol. 2011 Aug;154(3):373-7
Authors: Kato S, Takahashi K, Ayabe K, Samad R, Fukaya E, Friedmann P, Varma M, Bergmann SR
Abstrac…

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Diagnosis and management of anaemia of chronic disease: current status.
Br J Haematol. 2011 Aug;154(3):289-300
Authors: Cullis JO
Abstract
Anaemia of chronic disease is the second most common form of anaemia wo…

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The risk of spinal haematoma following neuraxial anaesthesia or lumbar puncture in thrombocytopenic individuals.

Br J Haematol. 2010 Jan;148(1):15-25

Authors: van Veen JJ, Nokes TJ, Makris M

Neuraxial anaesthesia is increasingly performed in thrombocytopenic patients at the time of delivery of pregnancy. There is a lack of data regarding the optimum platelet count at which spinal procedures can be safely performed. Reports are often confounded by the presence of other risk factors for spinal haematomata, such as anticoagulants, antiplatelet agents and other acquired or congenital coagulopathies/platelet function defects or rapidly falling platelet counts. In the absence of these additional risk factors, a platelet count of 80 x 10(9)/l is a ‘safe’ count for placing an epidural or spinal anaesthetic and 40 x 10(9)/l is a ‘safe’ count for lumbar puncture. It is likely that lower platelet counts may also be safe but there is insufficient published evidence to make recommendations for lower levels at this stage. For patients with platelet counts of 50-80 x 10(9)/l requiring epidural or spinal anaesthesia and patients with a platelet count 20-40 x 10(9)/l requiring a lumbar puncture, an individual decision based on assessment of risks and benefits should be made.

PMID: 19775301 [PubMed - indexed for MEDLINE]

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Diagnostic management of clinically suspected acute deep vein thrombosis.

Br J Haematol. 2009 Aug;146(4):347-60

Authors: Tan M, van Rooden CJ, Westerbeek RE, Huisman MV

Deep vein thrombosis (DVT) is a common disease that may lead to potentially fatal complications, such as pulmonary embolism. In the past decades several diagnostic tools and algorithms for DVT have been studied. Currently the combination of a clinical decision rule, D-dimer testing and compression ultrasonography has proved to be safe and effective for the diagnosis of DVT in the lower extremities. Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) can be useful as additional or secondary imaging modalities. This review will discuss the elements currently used in making the clinical diagnosis of DVT. These elements include clinical decision rules and D-dimer testing, different imaging investigations and the appropriate use of these within diagnostic algorithms in patients with clinically suspected DVT. Although current knowledge of the options available to diagnose DVT of the lower extremities is well established, there are still unresolved issues, including the optimal diagnosis of recurrent DVT and distal DVT. Furthermore, the diagnosis of DVT of the upper extremities will be discussed, including the different imaging modalities and the limitations of these techniques.

PMID: 19466972 [PubMed - indexed for MEDLINE]

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Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology.

Br J Haematol. 2009 Apr;145(1):24-33

Authors: Levi M, Toh CH, Thachil J, Watson HG

The diagnosis of disseminated intravascular coagulation (DIC) should encompass both clinical and laboratory information. The International Society for Thrombosis and Haemostasis (ISTH) DIC scoring system provides objective measurement of DIC. Where DIC is present the scoring system correlates with key clinical observations and outcomes. It is important to repeat the tests to monitor the dynamically changing scenario based on laboratory results and clinical observations. The cornerstone of the treatment of DIC is treatment of the underlying condition. Transfusion of platelets or plasma (components) in patients with DIC should not primarily be based on laboratory results and should in general be reserved for patients who present with bleeding. In patients with DIC and bleeding or at high risk of bleeding (e.g. postoperative patients or patients due to undergo an invasive procedure) and a platelet count of <50 x 10(9)/l transfusion of platelets should be considered. In non-bleeding patients with DIC, prophylactic platelet transfusion is not given unless it is perceived that there is a high risk of bleeding. In bleeding patients with DIC and prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), administration of fresh frozen plasma (FFP) may be useful. It should not be instituted based on laboratory tests alone but should be considered in those with active bleeding and in those requiring an invasive procedure. There is no evidence that infusion of plasma stimulates the ongoing activation of coagulation. If transfusion of FFP is not possible in patients with bleeding because of fluid overload, consider using factor concentrates such as prothrombin complex concentrate, recognising that these will only partially correct the defect because they contain only selected factors, whereas in DIC there is a global deficiency of coagulation factors. Severe hypofibrinogenaemia (<1 g/l) that persists despite FFP replacement may be treated with fibrinogen concentrate or cryoprecipitate. In cases of DIC where thrombosis predominates, such as arterial or venous thromboembolism, severe purpura fulminans associated with acral ischemia or vascular skin infarction, therapeutic doses of heparin should be considered. In these patients where there is perceived to be a co-existing high risk of bleeding there may be benefits in using continuous infusion unfractionated heparin (UFH) due to its short half-life and reversibility. Weight adjusted doses (e.g. 10 mu/kg/h) may be used without the intention of prolonging the APTT ratio to 1.5-2.5 times the control. Monitoring the APTT in these cases may be complicated and clinical observation for signs of bleeding is important. In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended. Consider treating patients with severe sepsis and DIC with recombinant human activated protein C (continuous infusion, 24 microg/kg/h for 4 d). Patients at high risk of bleeding should not be given recombinant human activated protein C. Current manufacturers guidance advises against using this product in patients with platelet counts of <30 x 10(9)/l. In the event of invasive procedures, administration of recombinant human activated protein C should be discontinued shortly before the intervention (elimination half-life approximately 20 min) and may be resumed a few hours later, dependent on the clinical situation. In the absence of further prospective evidence from randomised controlled trials confirming a beneficial effect of antithrombin concentrate on clinically relevant endpoints in patients with DIC and not receiving heparin, administration of antithrombin cannot be recommended. In general, patients with DIC should not be treated with antifibrinolytic agents. Patients with DIC that is characterised by a primary hyperfibrinolytic state and who present with severe bleeding could be treated with lysine analogues, such as tranexamic acid (e.g. 1 g every 8 h).

PMID: 19222477 [PubMed - indexed for MEDLINE]

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Multivariate analysis of febrile neutropenia occurrence in patients with non-Hodgkin lymphoma: data from the INC-EU Prospective Observational European Neutropenia Study.

Br J Haematol. 2009 Mar;144(5):677-85

Authors: Pettengell R, Bosly A, Szucs TD, Jackisch C, Leonard R, Paridaens R, Constenla M, Schwenkglenks M,

Myelosuppression, particularly febrile neutropenia (FN), are serious dose-limiting toxicities that occur frequently during the first cycle of chemotherapy. Identifying patients most at risk of developing FN might help physicians to target prophylactic treatment with colony-stimulating factor (CSF), in order to decrease the incidence, or duration, of myelosuppression and facilitate delivery of chemotherapy as planned. We present a risk model for FN occurrence in the first cycle of chemotherapy, based on a subgroup of 240 patients with non-Hodgkin lymphoma (NHL) enroled in our European prospective observational study. Eligible patients had an International Prognostic Index of 0-3, and were scheduled to receive a new myelosuppressive chemotherapy regimen with at least four cycles. Clinically relevant factors significantly associated with cycle 1 FN were older age, increasing planned cyclophosphamide dose, a history of previous chemotherapy, a history of recent infection, and low baseline albumin (<35 g/l). Prophylactic CSF use and higher weight were associated with a significant protective effect. The model had high sensitivity (81%) and specificity (80%). Our model, together with treatment guidelines, may rationalise the clinical decision of whether to support patients with CSF primary prophylaxis based on their risk factor profile. Further validation is required.

PMID: 19055662 [PubMed - indexed for MEDLINE]

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Advances in understanding of pathogenesis of aHUS and HELLP.

Br J Haematol. 2008 Nov;143(3):336-48

Authors: Fang CJ, Richards A, Liszewski MK, Kavanagh D, Atkinson JP

Both atypical haemolytic uraemic syndrome (aHUS) and the HELLP syndrome (haemolytic anaemia, elevated liver enzymes, and low platelets) are thrombotic microangiopathies characterized by microvascular endothelial activation, cell injury and thrombosis. aHUS is a disease of complement dysregulation, specifically a gain of function of the alternative pathway, due to mutations in complement regulatory proteins and activating components. Recently, the same complement mutation identified in multiple patients with aHUS was found in a patient with the HELLP syndrome. The pathogeneses of both diseases are reviewed focusing on the role of the complement system and how its dysfunction could result in a thrombotic microangiopathy in the kidney in the case of aHUS and in the liver in the case of the HELLP syndrome.

PMID: 18691170 [PubMed - indexed for MEDLINE]

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Phase I study of eptifibatide in patients with sickle cell anaemia.

Br J Haematol. 2007 Nov;139(4):612-20

Authors: Lee SP, Ataga KI, Zayed M, Manganello JM, Orringer EP, Phillips DR, Parise LV

The alphaIIbbeta3 antagonist eptifibatide is an effective treatment for patients with acute coronary syndromes (ACS). Platelet reactivity and CD40 ligand (CD40L) may play a role in the pathophysiology of sickle cell anaemia (SCA) similar to that in ACS, suggesting that inhibition of platelet aggregation and CD40L release by eptifibatide may benefit patients with SCA. Following eptifibatide infusion, safety and pharmacodynamic data were obtained from four SCA patients in their non-crisis, steady states. Eptifibatide was well tolerated, with no adverse changes in the haematological, biochemical or coagulation parameters studied. Eptifibatide did not increase plasma levels of platelet factor 4 or beta-thromboglobulin, P-selectin exposure or platelet:leucocyte aggregate formation. Moreover, decreases in platelet aggregation and soluble CD40L (sCD40L) levels achieved in SCA patients were comparable to those observed in the treatment of ACS. Finally, indicators of inflammation, macrophage inflammatory protein-1alpha, tumour necrosis factor-alpha and myoglobin were reduced following eptifibatide infusion, while vasodilation correlatives, matrix metalloproteinases (MMP-2 and MMP-9) and leptin were increased. Based on these phase I results, eptifibatide may benefit SCA patients by inhibiting platelet aggregation, decreasing sCD40L levels and favourably altering plasma levels of inflammatory mediators.

PMID: 17916103 [PubMed - indexed for MEDLINE]

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