Endothelial Damage, Platelet Activation, Thrombin Generation and Fibrinolytic Activity in Patients With Hypertensive Crisis: 2C.05

Born, B.J.H. van den; Hoeven, Nina van der; Owenberg, EL; Laat, Bas de; Meijers, Jcm; Levi, Marcel; Montfrans, Gert van

doi:10.1097/01.hjh.0000378282.51813.79

Cited by 1 publication

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“…9 Hypertension can be interpreted as a prothrombotic condition characterized by endothelial cell dysfunction, platelet activation, and increased thrombin generation. 239,240 A healthy endothelium maintains vascular tone and structure by keeping vasodilatation and constriction in balance. The main modulator is nitric oxide (NO), a molecule produced by the endothelium.…”

Section: Thrombotic Microangiopathy Associated With Malignant Hypertementioning

confidence: 99%

Spectrum of Complement-Mediated Thrombotic Microangiopathies: Pathogenetic Insights Identifying Novel Treatment Approaches

Riedl

Fakhouri

Quintrec

et al. 2014

Semin Thromb Hemost

125

116

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Thrombotic microangiopathy (TMA) is a rare but severe disorder characterized by endothelial cell activation and thrombus formation. It manifests with the triad of hemolytic anemia, thrombocytopenia, and organ failure. Prompt diagnosis and treatment initiation are crucial for long-term outcome. TMA often manifests subsequent to infectious events, of which (enterohemorrhagic) Escherichia coli is the most frequently reported. TMA also occurs on the background of genetic/autoimmune defects in the complement system (atypical hemolytic uremic syndrome [aHUS]) and underlying conditions, such as pregnancy, transplantation, drugs, other glomerulopathies, vasculitides, or metabolic defects. Complement activation or defects in its regulation have now been described in an increasing number of acquired diseases with TMA. Coinciding with this expanding spectrum of complement-mediated diseases, the question arises which patients might benefit from a complement-targeted therapy. Success of therapy depends on the individual contribution of complement activation in disease pathogenesis. The advent of eculizumab, a monoclonal antibody that blocks terminal complement activation, has markedly improved outcome and quality of life in patients with aHUS. This review discusses the contribution of complement and highlights its complex interaction with inflammation, coagulation, and the endothelium. Treatment experiences focusing on eculizumab therapy are discussed in detail across the emerging spectrum of complement-mediated thrombotic microangiopathies.

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Section: Thrombotic Microangiopathy Associated With Malignant Hypertementioning

confidence: 99%

Spectrum of Complement-Mediated Thrombotic Microangiopathies: Pathogenetic Insights Identifying Novel Treatment Approaches

Riedl

Fakhouri

Quintrec

et al. 2014

Semin Thromb Hemost

125

116

View full text Add to dashboard Cite

show abstract

Endothelial Damage, Platelet Activation, Thrombin Generation and Fibrinolytic Activity in Patients With Hypertensive Crisis: 2C.05

Cited by 1 publication

References 0 publications

Spectrum of Complement-Mediated Thrombotic Microangiopathies: Pathogenetic Insights Identifying Novel Treatment Approaches

Spectrum of Complement-Mediated Thrombotic Microangiopathies: Pathogenetic Insights Identifying Novel Treatment Approaches

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