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Journal of Intensive Care

, 2:61

Recent advances in disseminated intravascular coagulation


In the blurring boundaries between clinical practice and scientific observations, it is increasingly attractive to propose shared disease mechanisms that could explain clinical experience. With the advent of available therapeutic options for complement inhibition, there is a push for more widespread application in patients, despite a lack of clinically relevant research. Patients with disseminated intravascular coagulation DIC and thrombotic microangiopathies TMA frequently exhibit complement activation and share the clinical consequences of thrombocytopenia, microangiopathic hemolytic anemia, and microvascular thrombosis. However, they arise from very different molecular etiologies giving rise to cautious questions about inclusive treatment approaches because most clinical observations are associative and not cause-and-effect. Complement inhibition is successful in many cases of atypical hemolytic uremic syndrome, greatly reducing morbidity and mortality of patients by minimizing thrombocytopenia, microangiopathic hemolytic anemia, and microvascular thrombosis. But is this success due to targeting disease etiology or because complement is a sufficiently systemic target or both? These questions are important because complement activation and similar clinical features also are observed in many DIC patients, and there are mounting calls for systemic inhibition of complement mediators despite the enormous differences in the primary diseases complicated by DIC. We are in great need of thoughtful and standardized assessment with respect to both beneficial and potentially harmful consequences of complement activation in these patient populations. In this review, we discuss about what needs to be done in terms of establishing the strategy for complement inhibition in TMA and DIC, based on the current knowledge.

KeywordsComplement Blood coagulation Thrombotic microangiopathy Disseminated intravascular coagulation Hemolytic uremic syndrome Thrombocytopenia Microangiopathic hemolytic anemia Acute kidney injury AbbreviationsDICdisseminated intravascular coagulation

TMAthrombotic microangiopathy

SIRSsystemic inflammatory response syndrome

TCCterminal complement complex

C1qcomplement component 1 q subcomponent

C3complement component 3

C5complement component 5

FSAPfactor seven activating protease

StxShiga toxin

EHECenterohemorrhagic Escherichia coli

HUShemolytic uremic syndrome

p-HUSHUS associated with invasive pneumococcal disease

TTPthrombotic thrombocytopenic purpura

TFtissue factor

Gb3globotriaosylceramide CD77

BUNblood urea nitrogen

DAMPsdamage-associated molecular patterns

CR2-CD21complement receptor type 2

Electronic supplementary materialThe online version of this article doi:10.1186-s40560-014-0061-4 contains supplementary material, which is available to authorized users.

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Autor: Shinichiro Kurosawa - Deborah J Stearns-Kurosawa


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