Seminars in thrombosis and hemostasis
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Physical injuries, especially road traffic injuries, are a leading cause of death and morbidity worldwide, ranking fifth among the leading causes of death in the United States. Immediate and early trauma deaths are mainly determined by primary brain injuries and/or hemorrhages, whereas late mortality is caused by secondary brain injuries, host defense failure, and superimposed complications including also disseminated intravascular coagulation (DIC). Trauma patients are particularly susceptible to the early development of coagulopathy, and the most severely injured patients are coagulopathic on hospital admission. ⋯ As such, the multifaceted derangement of hemostasis occurring after massive traumatic injuries, especially those involving the brain, is mainly sustained by release of procoagulants (fats, phospholipids) and constitutive tissue factor from the injured tissue into the circulation, associated with a systemic inflammatory response that also promotes tissue factor hyperexpression on monocytes and the other cells. The excessive, non-wound-related thrombin generation is insufficiently antagonized by physiological anticoagulant pathways and amplified by impaired endogenous fibrinolysis. The resulting burst of systemic thrombin generation, coupled with platelet hyperaggregability, shock, hypothermia, and tissue hypoperfusion, further contribute to the development of DIC and microvascular bleeding.
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Semin. Thromb. Hemost. · Jun 2010
ReviewDisseminated intravascular coagulation in infectious disease.
Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. Systemic inflammation as a result of severe infection leads to activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. ⋯ Apart from the general coagulation response to inflammation associated with severe infection, specific infections may cause distinct features, such as hemorrhagic fever or thrombotic microangiopathy. The relevance of the cross-talk between inflammation and coagulation is underlined by the results of the treatment of severe systemic infection with modulators of coagulation and inflammation.
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Semin. Thromb. Hemost. · Feb 2010
ReviewInfluenza and cardiovascular disease: does swine-origin, 2009 H1N1 flu virus represent a risk factor, an acute trigger, or both?
Influenza infection has become an important focus of both public and medical attention because of high-level perceived clinical and public health effects, enormously amplified by the current and ongoing 2009 H1N1 flu pandemic, sustained by the swine-origin influenza A (H1N1) virus (S-OIV). The current transmission of this virus among humans appears much higher than that traditionally observed with seasonal influenza, raising several outbreaks of febrile respiratory infection ranging in severity from self-limited to severe, even life-threatening disease. Reliable biological and clinical evidence support a significant association between influenza infection and cardiovascular disorders, so that S-IOV might also be regarded as a potential multifaceted bioweapon able to affect the function of the cardiovascular system through a kaleidoscope of humoral, biological, and biochemical mechanisms. ⋯ Comprehensive information regarding the 2009 H1N1 infection remains limited, so that it seems unreasonable to draw definitive conclusions. Nevertheless, current recorded mortality data would lead us to conclude that this new virus might represent a sinister threat to humankind, with cardiovascular mortality risk highlighting an additional crucial role for increasing further the alert against this threat. It also seems reasonable to support calls for vaccination against these viruses, both the seasonal and the new S-OIV, because this might represent a feasible strategy for short- and long-term prevention of virus-associated cardiovascular disease.
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Semin. Thromb. Hemost. · Nov 2009
ReviewRecent improvements in the clinical treatment of coagulation factor inhibitors.
The mainstay of therapy in patients with congenital hemophilia is factor replacement. However, the development of inhibitors in these patients is a major complication that represents an important challenge in hemophilia care. ⋯ The management of severe bleeding episodes and the definitive eradication of the autoantibody are also the two main options of the clinical management of patients with acquired hemophilia, a rare but life-threatening hemorrhagic condition. The most recent options available for treating patients with acquired hemophilia and congenital hemophilia with inhibitors are addressed in this review.
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Semin. Thromb. Hemost. · Nov 2009
ReviewTwelve years of experience of acquired hemophilia A: trials and tribulations in South Australia.
Acquired hemophilia A (AH) is a rare and serious acquired bleeding disorder where prompt and correct diagnosis is crucial, and immune suppression is often required for factor VIII (FVIII) autoantibody eradication. The acquired FVIII deficiency usually manifests as bruises and bleeding, and treatment such as FVIII has limited efficacy because of the neutralizing FVIII inhibitor. Expensive bypassing agents such as recombinant activated factor VII (rFVIIa) may be required to treat clinically significant bleeding. ⋯ Overall mortality was 25% ( N = 6), five of whom were not treated. Advanced age and lack of treatment were predictive of poor survival outcomes. The very elderly (>75 years of age) may warrant a different treatment modality such as rituximab, which is potentially more tolerable and efficacious.