Evidence map›Paper›PMID 30592707›Full record

ArticleEndocrine connections2018

FGF-21 levels in polyuria-polydipsia syndrome.

Julie Refardt, Clara Odilia Sailer, Bettina Winzeler, Matthias Johannes Betz, Irina Chifu, Ingeborg Schnyder, Martin Fassnacht, Wiebke Fenske, Mirjam Christ-Crain

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In one paragraph

Article in Endocrine connections, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 87% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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 5 institutions in 2 countries.

Julie RefardtDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Clara Odilia SailerDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Bettina WinzelerDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Matthias Johannes BetzDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Irina ChifuDivision of Endocrinology and Diabetes, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany.
Ingeborg SchnyderDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Martin FassnachtDivision of Endocrinology and Diabetes, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany.
Wiebke FenskeDepartment of Endocrinology and Nephrology, University of Leipzig, Leipzig, Germany.
Mirjam Christ-CrainDepartments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
University Hospital of Basel · CHUniversity of Basel · CHIFB Adiposity Diseases · DEUniversitätsklinikum Würzburg · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathomechanism of primary polydipsia is poorly understood. Recent animal data reported a connection between fibroblast growth factor 21 (FGF-21) and elevated fluid intake independently of hormonal control by the hormone arginine-vasopressin (AVP) and osmotic stimulation. We therefore compared circulating FGF-21 levels in patients with primary polydipsia to patients with AVP deficiency (central diabetes insipidus) and healthy volunteers. In this prospective cohort study, we analyzed FGF-21 levels of 20 patients with primary polydipsia, 20 patients with central diabetes insipidus and 20 healthy volunteers before and after stimulation with hypertonic saline infusion targeting a plasma sodium level ≥150 mmol/L. The primary outcome was the difference in FGF-21 levels between the three groups. Baseline characteristics were similar between the groups except for patients with central diabetes insipidus being heavier. There was no difference in baseline FGF-21 levels between patients with primary polydipsia and healthy volunteers (122 pg/mL (52,277) vs 193 pg/mL (48,301), but higher levels in patients with central diabetes insipidus were observed (306 pg/mL (114,484); P = 0.037). However, this was not confirmed in a multivariate linear regression analysis after adjusting for age, sex, BMI and smoking status. Osmotic stimulation did not affect FGF-21 levels in either group (difference to baseline: primary polydipsia -23 pg/mL (-43, 22); central diabetes insipidus 17 pg/mL (-76, 88); healthy volunteers -6 pg/mL (-68, 22); P = 0.45). To conclude, FGF-21 levels are not increased in patients with primary polydipsia as compared to central diabetes insipidus or healthy volunteers. FGF-21 therefore does not seem to be causal of elevated fluid intake in these patients.

Indexed as

copeptindiabetes insipidusFGF21osmotic stimulationprimary polydipsia

Identifiers

PMID30592707
PMCPMC6311457
OpenAlexW2907597632

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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.