Evidence map›Paper›PMID 30753168›Full record

ArticleJCI insight2019

A unique androgen excess signature in idiopathic intracranial hypertension is linked to cerebrospinal fluid dynamics.

Michael W O'Reilly, Connar Sj Westgate, Catherine Hornby, Hannah Botfield, Angela E Taylor, Keira Markey, James L Mitchell, William J Scotton, Susan P Mollan, Andreas Yiangou and 9 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
10.3field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 128 citations in OpenAlex.

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18 more citing papers are in PubMed but not listed here.

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

19 authors at 5 institutions in 2 countries.

Michael W O'ReillyInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Connar Sj WestgateInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Catherine HornbyInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Hannah BotfieldInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Angela E TaylorInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Keira MarkeyInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
James L MitchellInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
William J ScottonInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Susan P MollanBirmingham Neuro-Ophthalmology Unit, Ophthalmology Department, University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom.
Andreas YiangouInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Carl JenkinsonInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Lorna C GilliganInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Mark SherlockDepartment of Endocrinology and Diabetes Mellitus, Tallaght Hospital, Tallaght, Dublin, Ireland.
James GibneyDepartment of Endocrinology and Diabetes Mellitus, Tallaght Hospital, Tallaght, Dublin, Ireland.
Jeremy W TomlinsonOxford Centre for Diabetes, Endocrinology and Metabolism, National Institute of Health Research (NIHR) Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, United Kingdom.
Gareth G LaveryInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
David J HodsonInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Wiebke ArltInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Alexandra J SinclairInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
The Edgbaston Hospital · GBUniversity of Birmingham · GBTallaght University Hospital · IEChurchill Hospital · GBUniversity Hospitals Birmingham NHS Foundation Trust · GB

Funding

Department of Health NIHR-CS-011-028Medical Research Council G0601430Medical Research Council MR/K015184/1Medical Research Council MR/N00275X/1Medical Research Council MR/P011462/1Medical Research Council MR/S025618/1Wellcome Trust 099909
6 · The paper itself

Abstract

Idiopathic intracranial hypertension (IIH) is a condition of unknown etiology, characterized by elevated intracranial pressure frequently manifesting with chronic headaches and visual loss. Similar to polycystic ovary syndrome (PCOS), IIH predominantly affects obese women of reproductive age. In this study, we comprehensively examined the systemic and cerebrospinal fluid (CSF) androgen metabolome in women with IIH in comparison with sex-, BMI-, and age-matched control groups with either simple obesity or PCOS (i.e., obesity and androgen excess). Women with IIH showed a pattern of androgen excess distinct to that observed in PCOS and simple obesity, with increased serum testosterone and increased CSF testosterone and androstenedione. Human choroid plexus expressed the androgen receptor, alongside the androgen-activating enzyme aldoketoreductase type 1C3. We show that in a rat choroid plexus cell line, testosterone significantly enhanced the activity of Na+/K+-ATPase, a surrogate of CSF secretion. We demonstrate that IIH patients have a unique signature of androgen excess and provide evidence that androgens can modulate CSF secretion via the choroid plexus. These findings implicate androgen excess as a potential causal driver and therapeutic target in IIH.

Indexed as

HydrodynamicsAdultAndrogensAnimalsFemaleHumansIntracranial HypertensionObesityPolycystic Ovary SyndromePseudotumor CerebriRatsTestosteroneAndrogensTestosteroneEndocrinologyNeurological disordersNeuroscience

Identifiers

PMID30753168
PMCPMC6483000
OpenAlexW2914690162

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.