Evidence map›Paper›PMID 35723762›Full record

Observational studyAngiogenesis2022

Microvascular and proteomic signatures overlap in COVID-19 and bacterial sepsis: the MICROCODE study.

Alexandros Rovas, Konrad Buscher, Irina Osiaevi, Carolin Christina Drost, Jan Sackarnd, Phil-Robin Tepasse, Manfred Fobker, Joachim Kühn, Stephan Braune, Ulrich Göbel and 7 more

Open access · hybridAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Angiogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 21 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

17 authors at 4 institutions in 2 countries.

Alexandros Rovas *Department of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Konrad Buscher *Department of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Irina OsiaeviDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Carolin Christina DrostDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Jan SackarndDepartment of Cardiology and Angiology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Phil-Robin TepasseDepartment of Medicine B for Gastroenterology, Hepatology, Endocrinology, Clinical Infectiology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Manfred FobkerCenter for Laboratory Medicine, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Joachim KühnInstitute of Virology, University Hospital Münster, Von-Stauffenberg-Straße 36, 48151, Münster, Germany.
Stephan BrauneDepartmenf of Intensive Care and Emergency Medicine, St. Franziskus-Hospital GmbH, Hohenzollernring 70, 48145, Münster, Germany.
Ulrich GöbelDepartment of Anaesthesiology and Critical Care, St. Franziskus-Hospital GmbH, Hohenzollernring 70, 48145, Münster, Germany.
Gerold ThölkingDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Andreas GröschelDepartment of Pulmonology, Clemens Hospital, Düesbergweg 124, 48153, Münster, Germany.
Jan RossaintDepartment of Anaesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Hans VinkDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 ER, Maastricht, the Netherlands.
Alexander LukaszDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Hermann PavenstädtDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany.
Philipp KümpersDepartment of Medicine D, Division of General Internal and Emergency Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer Campus 1, 48149, Münster, Germany. philipp.kuempers@ukmuenster.de.ORCID 0000-0001-9929-0703
University Hospital Münster · DESt. Franziskus Hospital · DEClemenshospital Münster · DEMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAlthough coronavirus disease 2019 (COVID-19) and bacterial sepsis are distinct conditions, both are known to trigger endothelial dysfunction with corresponding microcirculatory impairment. The purpose of this study was to compare microvascular injury patterns and proteomic signatures in COVID-19 and bacterial sepsis patients. METHODS AND

resultsThis multi-center, observational study included 22 hospitalized adult COVID-19 patients, 43 hospitalized bacterial sepsis patients, and 10 healthy controls from 4 hospitals. Microcirculation and glycocalyx dimensions were quantified via intravital sublingual microscopy. Plasma proteins were measured using targeted proteomics (Olink). Coregulation and cluster analysis of plasma proteins was performed using a training-set and confirmed in a test-set. An independent external cohort of 219 COVID-19 patients was used for validation and outcome analysis. Microcirculation and plasma proteome analysis found substantial overlap between COVID-19 and bacterial sepsis. Severity, but not disease entity explained most data variation. Unsupervised correlation analysis identified two main coregulated plasma protein signatures in both diseases that strictly counteract each other. They were associated with microvascular dysfunction and several established markers of clinical severity. The signatures were used to derive new composite biomarkers of microvascular injury that allow to predict 28-day mortality or/and intubation (area under the curve 0.90, p < 0.0001) in COVID-19.

conclusionOur data imply a common biological host response of microvascular injury in both bacterial sepsis and COVID-19. A distinct plasma signature correlates with endothelial health and improved outcomes, while a counteracting response is associated with glycocalyx breakdown and high mortality. Microvascular health biomarkers are powerful predictors of clinical outcomes.

Indexed as

COVID-19SepsisAdultBiomarkersHumansMicrocirculationProteomeProteomicsBiomarkersProteomeBiomarkerCOVID-19MicrocirculationMicrovascular dysfunctionProteomic signatureSepsis

Identifiers

PMID35723762
PMCPMC9208353
OpenAlexW4283167487

What OpenQuestion holds

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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.