Evidence map›Paper›PMID 25705421›Full record

ReviewJournal of intensive care2014

Complement, thrombotic microangiopathy and disseminated intravascular coagulation.

Shinichiro Kurosawa, Deborah J Stearns-Kurosawa

Open access · goldAbstract readReview
In one paragraph

Review in Journal of intensive care, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 58 citations in OpenAlex.

  1. Lessons from a case report of thrombocytopenia-associated multiple organ failure secondary to Streptococcus suis infection: Diagnosis and treatment strategies.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
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  14. Mechanistic inferences from clinical reports of SARS-CoV-2.Infectious diseases (London, England) · 2020
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Shinichiro KurosawaBoston University School of Medicine, 670 Albany Street, Boston, MA 02118 USA.
Deborah J Stearns-KurosawaBoston University School of Medicine, 670 Albany Street, Boston, MA 02118 USA.
Boston University · USUniversity School · US

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI COGGESHALL, KENNETH MARK · 2004 to 2023
$56.2M
Role of Inter-alpha Inhibitors in Anthrax IntoxicationR42AI062095 · NIAID · PROTHERA BIOLOGICS, LLC · PI OPAL, STEVEN M. · 2010 to 2012
$2.7M
Development and Treatment of Pre-Clinical EHEC Models with HUSR01AI102931 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KUROSAWA, SHINICHIRO · 2013 to 2016
$1.6M
NIAID NIH HHS R01 AI102931NIAID NIH HHS R42 AI062095NIAID NIH HHS U19 AI062629
6 · The paper itself

Abstract

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.

Indexed as

Acute kidney injuryBlood coagulationComplementDisseminated intravascular coagulationHemolytic uremic syndromeMicroangiopathic hemolytic anemiaThrombocytopeniaThrombotic microangiopathy

Identifiers

PMID25705421
PMCPMC4336180
OpenAlexW1976249816

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.