Evidence map›Paper›PMID 28795329›Full record

ArticleEndocrine2017

Copeptin as a marker of an altered CRH axis in pituitary disease.

Krzysztof C Lewandowski, Andrzej Lewiński, Elżbieta Skowrońska-Jóźwiak, Katarzyna Malicka, Wojciech Horzelski, Georg Brabant

Open access · hybridAbstract read
In one paragraph

Article in Endocrine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Copeptin: a novel prognostic biomarker in trauma: a review article.Journal of health, population, and nutrition · 2023
    Review
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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

6 authors at 4 institutions in 2 countries.

Krzysztof C LewandowskiDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland.
Andrzej LewińskiDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland.
Elżbieta Skowrońska-JóźwiakDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland.
Katarzyna MalickaPolish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Wojciech HorzelskiFaculty of Mathematics and Computer Science, University of Lodz, Lodz, Poland.
Georg BrabantExperimental and Clinical Endocrinology Med Clinic I, University of Luebeck, Ratzeburger Allee 160, 23538, Lübeck, Germany. georg.brabant@uksh.de.ORCID http://orcid.org/0000-0001-8532-7632
Medical University of Lodz · PLPolish Mother’s Memorial Hospital Research Institute · PLUniversity of Łódź · PLUniversity of Lübeck · DE

Funding

This study was partially supported by the statutory funds from the Medical University of Lodz, Poland No. 503/1-107-03/503-01
6 · The paper itself

Abstract

backgroundCopeptin (pre-proAVP) secreted in equimolar amounts with vasopressin closely reflects vasopressin release. Copeptin has been shown to subtly mirror stress potentially mediated via corticotrophin-releasing hormone. To further test a potential direct interaction of corticotrophin-releasing hormone with copeptin release, which could augment vasopressin effects on pituitary function, we investigated copeptin response to corticotrophin-releasing hormone. PATIENTS AND

methodsCortisol, adrenocorticotropin and copeptin were measured in 18 healthy controls and 29 subjects with a history of pituitary disease during standard corticotrophin-releasing hormone test.

resultsPatients with previous pituitary disease were subdivided in a group passing the test (P1, n = 20) and failing (P2, n = 9). The overall copeptin response was higher in controls than in subjects with pituitary disease (area under the curve, p = 0.04 for P1 + P2) with a maximum increase in controls from 3.84 ± 2.86 to 12.65 ± 24.87 pmol/L at 30 min, p < 0.05. In contrast, both groups of pituitary patients lacked a significant copeptin response to corticotrophin-releasing hormone, and even in P1, where adrenocorticotropin concentrations increased fourfold (mean, 21.48 vs. 91.53 pg/mL, p < 0.01), copeptin did not respond (e.g., 4.35 ± 5.81 vs. 5.36 ± 6.79 pmol/L, at 30 min, p = ns).

conclusionsCorticotrophin-releasing hormone is able to stimulate copeptin release in healthy controls suggesting a direct interaction of corticotrophin-releasing hormone and vasopressin/vasopressin. Interestingly, this relation is altered already in the group of pituitary patients who pass the standard corticotrophin-releasing hormone test indicating (1) the corticotrophin-releasing hormone-adrenocorticotropin-cortisol response is largely independent from the vasopressin system, but (2) the corticotrophin-releasing hormone-vasopressin interaction reflected by copeptin may be much more sensitive to reveal subtle alterations in the regulation of pituitary function.

Indexed as

Signal TransductionAdrenal CortexAdrenocorticotropic HormoneAdultBiomarkersCorticotropin-Releasing HormoneCRF Receptor, Type 1FemaleGlycopeptidesHumansHydrocortisoneHypothalamo-Hypophyseal SystemImmunoassayKineticsMaleMiddle AgedAdrenocorticotropic HormoneBiomarkerscopeptinsCorticotropin-Releasing HormoneCRF Receptor, Type 1GlycopeptidesHydrocortisoneReceptors, Corticotropin-Releasing HormoneRecombinant ProteinsCopeptinCRH testDiabetes insipidusPituitary

Identifiers

PMID28795329
PMCPMC5573756
OpenAlexW2735856590

What OpenQuestion holds

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Registered trials

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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.