Evidence map›Paper›PMID 28195242›Full record

ArticleScientific reports2017

The alternative complement pathway is dysregulated in patients with chronic heart failure.

Negar Shahini, Annika E Michelsen, Per H Nilsson, Karin Ekholt, Lars Gullestad, Kaspar Broch, Christen P Dahl, Pål Aukrust, Thor Ueland, Tom Eirik Mollnes and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 76 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Negar ShahiniResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Per H NilssonK.G. Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway.
Karin EkholtK.G. Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway.
Lars GullestadCenter for Heart Failure Research, University of Oslo, Oslo, Norway.
Kaspar BrochDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Christen P DahlResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Tom Eirik MollnesK.G. Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway.
Arne YndestadResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Mieke C LouweResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system, an important arm of the innate immune system, is activated in heart failure (HF). We hypothesized that HF patients are characterized by an imbalance of alternative amplification loop components; including properdin and complement factor D and the alternative pathway inhibitor factor H. These components and the activation product, terminal complement complex (TCC), were measured in plasma from 188 HF patients and 67 age- and sex- matched healthy controls by enzyme immunoassay. Our main findings were: (i) Compared to controls, patients with HF had significantly increased levels of factor D and TCC, and decreased levels of properdin, particularly patients with advanced clinical disorder (i.e., NYHA functional class IV), (ii) Levels of factor D and properdin in HF patients were correlated with measures of systemic inflammation (i.e., C-reactive protein), neurohormonal deterioration (i.e., Nt-proBNP), cardiac function, and deteriorated diastolic function, (iii) Low levels of factor H and properdin were associated with adverse outcome in univariate analysis and for factor H, this was also seen in an adjusted model. Our results indicate that dysregulation of circulating components of the alternative pathway explain the increased degree of complement activation and is related to disease severity in HF patients.

Indexed as

Complement Pathway, AlternativeAgedBiomarkersCase-Control StudiesChronic DiseaseComorbidityComplement Factor HComplement System ProteinsFemaleHeart FailureHeart Function TestsHumansMaleMiddle AgedPrognosisProperdinBiomarkersComplement Factor HComplement System ProteinsProperdin

Identifiers

PMID28195242
PMCPMC5307342
OpenAlexW2588688617

What OpenQuestion holds

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LicenceCC BY
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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.