Evidence map›Paper›PMID 27477022›Full record

ReviewBritish journal of haematology2016

Bleeding related to disturbed fibrinolysis.

Krasimir Kolev, Colin Longstaff

Abstract readReview
In one paragraph

Review in British journal of haematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

55 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Krasimir KolevDepartment of Medical Biochemistry, Semmelweis University, Budapest, Hungary.
Colin LongstaffBiotherapeutics Group, National Institute for Biological Standards and Control, South Mimms, UK. colin.longstaff@nibsc.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The components and reactions of the fibrinolysis system are well understood. The pathway has fewer reactants and interactions than coagulation, but the generation of a complete quantitative model is complicated by the need to work at the solid-liquid interface of fibrin. Diagnostic tools to detect disease states due to malfunctions in the fibrinolysis pathway are also not so well developed as is the case with coagulation. However, there are clearly a number of inherited or acquired pathologies where hyperfibrinolysis is a serious, potentially life-threatening problem and a number of antifibrinolytc drugs are available to treat hyperfibrinolysis. These topics will be covered in the following review.

Indexed as

FibrinolysisAnimalsAntifibrinolytic AgentsBlood CoagulationBlood Coagulation Disorders, InheritedBlood Coagulation TestsHemorrhageHumansLeukemia, Promyelocytic, AcuteLysinePhenotypeSerpinsThrombolytic TherapyAntifibrinolytic AgentsLysineSerpinsacute promyelocytic leukaemiaantiplasminbleeding disordersfibrinolysisplasminogen activator inhibitor type 1

Identifiers

PMID27477022
PMCPMC5096260

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.