Evidence map›Paper›PMID 29360169›Full record

ArticleJournal of leukocyte biology2018

Adrenomedullin surges are linked to acute episodes of the systemic capillary leak syndrome (Clarkson disease).

Zhihui Xie, Wei-Sheng Chen, Yuzhi Yin, Eunice C Chan, Kaoru Terai, Lauren M Long, Timothy G Myers, Arkadiusz Z Dudek, Kirk M Druey

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  16. Adrenomedullin in COVID-19 induced endotheliitis.Critical care (London, England) · 2020
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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

9 authors at 1 institution in 1 country.

Zhihui XieMolecular Signal Transduction Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
Wei-Sheng ChenMolecular Signal Transduction Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
Yuzhi YinMast Cell Biology Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
Eunice C ChanMolecular Signal Transduction Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
Kaoru TeraiHealthPartners Neuroscience Center, St. Paul, Minnesota, USA.
Lauren M LongMolecular Signal Transduction Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
Timothy G MyersResearch Technologies Branch, NIAID/NIH, Bethesda, Maryland, USA.
Arkadiusz Z DudekHealthPartners Neuroscience Center, St. Paul, Minnesota, USA.
Kirk M DrueyMolecular Signal Transduction Section, Laboratory of Allergic Diseases, St. Paul, Minnesota, USA.
HealthPartners · US

Funding

Infectious Diseases Research Technologies Core - BethesdaZICAI001051 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$226.1M
Studies in the Pathogenesis of Systemic Capillary Leak SyndromeZIAAI001083 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$11.5M
Intramural NIH HHS ZIA AI001083
6 · The paper itself

Abstract

backgroundSystemic Capillary Leak Syndrome (SCLS) is an extremely rare and life-threatening vascular disorder of unknown etiology. SCLS is characterized by abrupt and transient episodes of hypotensive shock and edema due to plasma leakage into peripheral tissues. The disorder has garnered attention recently because its initial presentation resembles more common vascular disorders including systemic anaphylaxis, sepsis, and acute infections with the Ebola/Marburg family of filoviruses. Although approximately 70-85% of patients with SCLS have a concurrent monoclonal gammopathy of unknown significance (MGUS), any contribution of the paraprotein to acute flares is unknown. PROCEDURE: To identify circulating factors that might trigger acute SCLS crises, we profiled transcriptomes of paired peripheral blood mononuclear cell fractions obtained from patients during acute attacks and convalescent intervals by microarray.

resultsThis study uncovered 61 genes that were significantly up- or downregulated more than 2.5-fold in acute samples relative to respective baselines. One of the most upregulated genes was ADM, which encodes the vasoactive peptide adrenomedullin. A stable ADM protein surrogate (pro-ADM) was markedly elevated in SCLS acute sera compared to remission samples or sera from healthy controls. Monocytes and endothelial cells (ECs) from SCLS subjects expressed significantly more ADM in response to proinflammatory stimuli compared to healthy control cells. Application of ADM to ECs elicited protective effects on vascular barrier function, suggesting a feedback protective mechanism in SCLS.

conclusionsSince ADM has established hypotensive effects, differentiating between these dual actions of ADM is crucial for therapeutic applications aimed at more common diseases associated with increased ADM levels.

Indexed as

Acute DiseaseAdrenomedullinAgedBiomarkersCapillary Leak SyndromeCase-Control StudiesCells, CulturedEndothelium, VascularFemaleGene Expression ProfilingGene Expression RegulationHumansLeukocytes, MononuclearMaleMiddle AgedMonocytesADM protein, humanAdrenomedullinBiomarkersadrenomedullinangiogenesisendotheliumvascular leak

Identifiers

PMID29360169
PMCPMC6312640
OpenAlexW2790554811

What OpenQuestion holds

Textmetadata
LicenceTDM
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.