Evidence map›Paper›PMID 25329583›Full record

Trial reportPloS one2014

Blood levels of S-100 calcium-binding protein B, high-sensitivity C-reactive protein, and interleukin-6 for changes in depressive symptom severity after coronary artery bypass grafting: prospective cohort nested within a randomized, controlled trial.

Daniel M Pearlman, Jeremiah R Brown, Todd A MacKenzie, Felix Hernandez, Souhel Najjar

Open access · goldAbstract readMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Role of Interleukin-6 in Depressive Disorder.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Review
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

5 authors at 3 institutions in 1 country.

Daniel M PearlmanNeuroinflammation Research Group, Epilepsy Center Division, Department of Neurology, NYU School of Medicine, New York, New York, United States of America; The Dartmouth Institute for Health Policy and Clinical Practice, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Jeremiah R BrownThe Dartmouth Institute for Health Policy and Clinical Practice, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America; Section of Epidemiology and Biostatistics, Department of Community and Family Medicine, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America; Section of Cardiology, Department of Medicine, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Todd A MacKenzieThe Dartmouth Institute for Health Policy and Clinical Practice, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America; Section of Epidemiology and Biostatistics, Department of Community and Family Medicine, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America; Section of Cardiology, Department of Medicine, Audrey and Theodor Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Felix HernandezCardiothoracic Surgery, Eastern Maine Medical Center, Bangor, Maine, United States of America.
Souhel NajjarNeuroinflammation Research Group, Epilepsy Center Division, Department of Neurology, NYU School of Medicine, New York, New York, United States of America.
Dartmouth Institute for Health Policy and Clinical Practice · USDartmouth College · USEastern Maine Medical Center · US

Funding

AHRQ HHS K01 HS018443
6 · The paper itself

Abstract

backgroundCross-sectional and retrospective studies have associated major depressive disorder with glial activation and injury as well as blood-brain barrier disruption, but these associations have not been assessed prospectively. Here, we aimed to determine the relationship between changes in depressive symptom severity and in blood levels of S-100 calcium-binding protein B (S-100B), high-sensitivity C-reactive protein, and interleukin-6 following an inflammatory challenge.

methodsFifty unselected participants were recruited from a randomized, controlled trial comparing coronary artery bypass grafting procedures performed with versus without cardiopulmonary bypass for the risk of neurocognitive decline. Depressive symptom severity was measured at baseline, discharge, and six-month follow-up using the Beck Depression Inventory II (BDI-II). The primary outcome of the present biomarker study was acute change in depressive symptom severity, defined as the intra-subject difference between baseline and discharge BDI-II scores. Blood biomarker levels were determined at baseline and 2 days postoperative.

resultsChanges in S-100B levels correlated positively with acute changes in depressive symptom severity (Spearman ρ, 0.62; P = 0.0004) and accounted for about one-fourth of their observed variance (R2, 0.23; P = 0.0105). This association remained statistically significant after adjusting for baseline S-100B levels, age, weight, body-mass index, or β-blocker use, but not baseline BDI-II scores (P = 0.064). There was no statistically significant association between the primary outcome and baseline S-100B levels, baseline high-sensitivity C-reactive protein or interleukin-6 levels, or changes in high-sensitivity C-reactive protein or interleukin-6 levels. Among most participants, levels of all three biomarkers were normal at baseline and markedly elevated at 2 days postoperative.

conclusionsAcute changes in depressive symptom severity were specifically associated with incremental changes in S-100B blood levels, largely independent of covariates associated with either. These findings support the hypothesis that glial activation and injury and blood-brain barrier disruption can be mechanistically linked to acute exacerbation of depressive symptoms in some individuals.

Indexed as

Severity of Illness IndexAdultAgedAged, 80 and overBiomarkersCoronary Artery BypassC-Reactive ProteinDepressionFemaleHumansInterleukin-6MaleMiddle AgedPostoperative ComplicationsProspective StudiesS100 Calcium Binding Protein beta SubunitBiomarkersC-Reactive ProteinIL6 protein, humanInterleukin-6S100B protein, humanS100 Calcium Binding Protein beta Subunit

Identifiers

PMID25329583
PMCPMC4203837
OpenAlexW2069353795

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.