Entries Tagged as 'Curr Opin Hematol'
Bridging therapy and oral anticoagulation: current and future prospects.
Curr Opin Hematol. 2010 Sep;17(5):444-9
Authors: Spyropoulos AC
Patients undergoing oral anticoagulation treatment with vitamin K antagonist (VKA) therapy are at a high risk of bleeding when undergoing an invasive surgery or procedure. Bridging therapy with parenteral heparin, usually at therapeutic doses, aims to protect these patients against thromboembolism during temporary periprocedural interruption of VKA therapy. Whether or not to interrupt VKA therapy and initiate bridging therapy is a difficult decision that is based upon both the patient’s and the procedure’s thromboembolic and bleeding risks.
PMID: 20613508 [PubMed - indexed for MEDLINE]
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Advances in diagnosis and treatment of eosinophilia.
Curr Opin Hematol. 2009 Jan;16(1):3-8
Authors: Sheikh J, Weller PF
PURPOSE OF REVIEW: Hypereosinophilic syndromes (HESs) are disorders characterized by sustained blood or tissue hypereosinophilia or both with subsequent damage to various organs due to eosinophilic infiltration and release of mediators. HES are now recognized to include varied eosinophilic disorders for some of which there are recent insights into their pathogenesis and targeted treatment. RECENT FINDINGS: Studies have helped delineate two subtypes of HES: the myeloproliferative variants of HES and the lymphocytic variants of HES. Many, but not all, myeloproliferative-HES patients have interstitial deletions on chromosome 4q12 that lead to fusion of the FIP1-like 1 and platelet-derived growth factor receptor alpha genes, with the fusion product encoding a protein that has constitutive tyrosine kinase activity. Lymphocytic-HES is a primary lymphoid disorder characterized by nonmalignant expansion of a T-cell population able to produce eosinophilopoietic cytokines, with the T-cell population being identified by flow cytometry or reverse transcriptase-PCR for T-cell receptor usage or both. Other HES subtypes are of uncertain causes and are included in recent diagnostic algorithms for the spectrum of HES. SUMMARY: The contemporary definition of the hypereosinophilic syndromes encompasses a range of eosinophilic disorders characterized by chronic blood hypereosinophilia often with eosinophil-mediated damage to various organs.
PMID: 19057198 [PubMed - indexed for MEDLINE]
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Long-term prognosis after deep venous thrombosis.
Curr Opin Hematol. 2008 Sep;15(5):494-8
Authors: Shbaklo H, Kahn SR
PURPOSE OF REVIEW: Deep vein thrombosis (DVT) is associated with significant long-term complications such as the postthrombotic syndrome (PTS). The present review focuses on the risk determinants of PTS after DVT, means to treat and prevent PTS, and the impact of PTS on patients and society. Knowledge acquired during the last decade is presented, with emphasis on reports published in the past 2 years. RECENT FINDINGS: PTS occurs in 20-50% of patients within 1-2 years after DVT. The principal risk factor for PTS identified to date is recurrent ipsilateral DVT; obesity and poor quality of anticoagulation for the treatment of DVT also appear to play a role. Although treatment options for established PTS are limited, a new battery-operated lower limb venous return assist device was recently shown in a randomized trial to reduce symptoms and signs in patients with severe PTS. Daily use of compression stockings after DVT appears to reduce the risk of PTS, and early use may be better than the later use. SUMMARY: Further studies of clinical determinants and biological markers of increased risk of PTS as well as testing of preventive and therapeutic modalities for PTS are needed to ultimately improve long-term prognosis after DVT.
PMID: 18695373 [PubMed - indexed for MEDLINE]
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Current management of thrombotic thrombocytopenic purpura.
Curr Opin Hematol. 2008 Sep;15(5):445-50
Authors: Kremer Hovinga JA, Meyer SC
PURPOSE OF REVIEW: New treatment modalities have become increasingly popular for the treatment of acute thrombotic thrombocytopenic purpura. Widespread availability of ADAMTS13 assays resulted in the increased recognition of patients with hereditary thrombotic thrombocytopenic purpura and specific issues related to acquired ADAMTS13 deficiency. These new aspects with implications on management of thrombotic thrombocytopenic purpura patients are reviewed here. RECENT FINDINGS: Today, plasma exchange with the replacement of fresh frozen plasma is still the treatment of choice in acute thrombotic thrombocytopenic purpura. The finding of circulating anti-ADAMTS13 autoantibodies in the majority of patients constitutes the rationale for the concomitant administration of immunosuppressive drugs. Rituximab seems to have a favorable benefit-risk ratio in plasma-refractory and relapsing thrombotic thrombocytopenic purpura; however, long-term follow-up data are not yet available. Constitutively lacking ADAMTS13 in hereditary thrombotic thrombocytopenic purpura can be supplemented by simple plasma infusions. Severe acquired ADAMTS13 deficiency either at presentation or in remission identifies patients at a particularly high risk of relapse. SUMMARY: Despite progress in understanding the pathophysiology of thrombotic thrombocytopenic purpura, acute bouts as well as relapses still represent serious health threats to patients and rapid initiation of plasma exchange is mandatory. Large randomized clinical trials, however, need to determine whether new treatment modalities are superior to standard plasma exchange.
PMID: 18695366 [PubMed - indexed for MEDLINE]
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Heparin-induced thrombocytopenia: some working hypotheses on pathogenesis, diagnostic strategies and treatment.
Curr Opin Hematol. 2008 Sep;15(5):456-64
Authors: Alberio L
PURPOSE OF REVIEW: The present contribution will illustrate some evolving concepts on the pathogenesis and clinical management of heparin-induced thrombocytopenia (HIT) and describe how we approach patients with suspected HIT at our institution. RECENT FINDINGS: HIT is caused by an autoimmune reaction leading to the formation of antibodies directed against platelet factor 4. Conditions favoring the development of anti-platelet factor 4/heparin antibodies differ from those required for the formation of macromolecular ternary complexes (HIT antibody/platelet factor 4/heparin), which are able to activate platelets and induce clinical HIT. HIT can be diagnosed by combining its pretest probability with the quantitative result of rapid HIT-antibody assays. Treatment of acute HIT requires inhibition of in-vivo thrombin generation by means of alternative nonheparin anticoagulant drugs, whose effective dosage appears to be significantly lower than the official recommendations. As HIT antibodies are transient, HIT patients can be re-exposed to heparin, provided that previous heparin treatment is remote and that anti-platelet factor 4/heparin antibodies are undetectable. SUMMARY: In recent years, there has been a continuing elucidation of pathogenic and clinically relevant issues, which are intellectually rewarding to follow and should enable us to offer a steadily improving treatment to the HIT patients we are in charge of.
PMID: 18695368 [PubMed - indexed for MEDLINE]
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Thrombocytopenia in liver disease.
Curr Opin Hematol. 2008 Sep;15(5):473-80
Authors: Giannini EG, Savarino V
PURPOSE OF REVIEW: To evaluate recent findings in the multifaceted pathophysiological mechanisms underlying thrombocytopenia in patients with chronic liver disease and to assess its therapeutic management. RECENT FINDINGS: Antiplatelet antibodies, despite being observed rather frequently in patients with chronic viral liver disease, have minimal relevance in the determinism of thrombocytopenia, and antiviral treatment of the underlying liver disease does not seem to significantly affect their prevalence. Translational application of the results of studies evaluating coagulation disorders associated with liver disease seems to suggest that these may be improved by treating thrombocytopenia. Both splenectomy and partial splenic embolization are still part of the therapeutic approach to thrombocytopenia. As far as this latter technique is concerned, patient selection is fundamental, and its success likely depends upon thrombopoietin-mediated mechanisms. Eltrombopag is a promising thrombopoietic drug that proved to be able to safely increase platelet counts in patients with viral liver disease and allows the initiation of antiviral treatment. SUMMARY: New insights into the pathophysiological mechanisms of thrombocytopenia in patients with liver disease have provided interesting clinical reflex. In these patients, novel therapies for treating thrombocytopenia seem promising, although it remains to be established whether treating thrombocytopenia may help improve liver disease-associated coagulopathy.
PMID: 18695370 [PubMed - indexed for MEDLINE]
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Long-term outcome of pulmonary embolism.
Curr Opin Hematol. 2008 Sep;15(5):499-503
Authors: Meyer G, Planquette B, Sanchez O
PURPOSE OF REVIEW: Until recently, little was known about the long-term outcome of pulmonary embolism. Long-term mortality and recurrence rates, the case fatality rate of recurrent events, and the frequency of persistent vascular defects remained largely unknown. Improvements in our knowledge of these aspects may help to define the optimal long-term treatment of pulmonary embolism. This review will address these issues. RECENT FINDINGS: The death rate after pulmonary embolism is less than 5% during 3-6 months of anticoagulant treatment, provided that the patient is hemodynamically stable and free of major underlying disease. The rate of recurrent thromboembolism is less than 5% on anticoagulant therapy, reaching 30% after 10 years. Recurrences are more likely to take the form of a new pulmonary embolism than deep venous thrombosis. Chronic thromboembolic pulmonary hypertension occurs in less than 5% of the patients. Most patients have persistent perfusion defects after the initial episode and further studies are required to determine the long-term significance of this finding. SUMMARY: Pulmonary embolism has a higher mortality rate than deep venous thrombosis. Patients with pulmonary embolism have no higher risk of recurrence, but any recurrence is more likely to be a new pulmonary embolism than a deep venous thrombosis. A significant number of patients develop persistent perfusion defects after pulmonary embolism.
PMID: 18695374 [PubMed - indexed for MEDLINE]
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Activated protein C in sepsis: a critical review.
Curr Opin Hematol. 2008 Sep;15(5):481-6
Authors: Levi M
PURPOSE OF REVIEW: An impaired function of the protein C pathway plays a central role in the pathogenesis of sepsis. Administration of human recombinant activated protein C (Xigris) may restore the dysfunctional anticoagulant mechanism and may simultaneously modulate the pro-inflammatory response. Initial clinical studies with activated protein C in patients with sepsis showed a reduction of 28-day mortality. However, subsequent studies did cast some doubt on the efficacy and also the safety of this treatment. RECENT FINDINGS: A number of randomized controlled clinical studies confirm beneficial effects of activated protein C in patients with severe sepsis. Aggregate analyses, however, have cast some doubt on the usefulness of treatment with activated protein C. In some clinical situations, such as patients with a relatively low disease severity and pediatric patients, activated protein C was shown not to be effective. Activated protein C seems to increase the risk of (severe) bleeding, although the absolute risk is low in patients that were included in clinical trials. SUMMARY: Clinical studies support the use of activated protein C in patients with severe sepsis; however, in view of the substantial skepticism surrounding the efficacy and safety of this treatment, additional placebo-controlled data are required.
PMID: 18695371 [PubMed - indexed for MEDLINE]
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