Evidence map›Paper›PMID 36074938›Full record

ArticleEuropean journal of endocrinology2022

11-Oxygenated C19 steroids are the predominant androgens responsible for hyperandrogenemia in Cushing's disease.

Hanna F Nowotny, Leah Braun, Frederick Vogel, Martin Bidlingmaier, Martin Reincke, Lea Tschaidse, Matthias K Auer, Christian Lottspeich, Stefan A Wudy, Michaela F Hartmann and 5 more

Open access · hybridAbstract read
In one paragraph

Article in European journal of endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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  3. Approach to the patient: investigation of postmenopausal androgen excess.The Journal of clinical endocrinology and metabolism · 2026
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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

15 authors at 3 institutions in 2 countries.

Hanna F NowotnyMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.ORCID 0000-0003-3791-9929
Leah BraunMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.
Frederick VogelMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.ORCID 0000-0001-8821-8968
Martin BidlingmaierMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.
Martin ReinckeMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.ORCID 0000-0002-9817-9875
Lea TschaidseMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.
Matthias K AuerMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.ORCID 0000-0001-7153-8332
Christian LottspeichMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.
Stefan A WudyDivision of Pediatric Endocrinology & Diabetology, Laboratory for Translational Hormone Analysis in Pediatric Endocrinology, Steroid Research & Mass Spectrometry Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University, Giessen, Germany.
Michaela F HartmannDivision of Pediatric Endocrinology & Diabetology, Laboratory for Translational Hormone Analysis in Pediatric Endocrinology, Steroid Research & Mass Spectrometry Unit, Center of Child and Adolescent Medicine, Justus-Liebig-University, Giessen, Germany.
James HawleyDepartment of Clinical Biochemistry, Manchester University Foundation NHS Trust, Manchester Academic Health Sciences Centre, Manchester, UK.
Joanne E AdawayDepartment of Clinical Biochemistry, Manchester University Foundation NHS Trust, Manchester Academic Health Sciences Centre, Manchester, UK.
Brian KeevilDepartment of Clinical Biochemistry, Manchester University Foundation NHS Trust, Manchester Academic Health Sciences Centre, Manchester, UK.
Katharina SchilbachMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.
Nicole ReischMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, LMU München, Munich, Germany.ORCID 0000-0002-7469-6069
LMU Klinikum · DEManchester Academic Health Science Centre · GBJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Symptoms of hyperandrogenism are common in patients with Cushing's disease (CD), yet they are not sufficiently explained by androgen concentrations. In this study, we analyzed the contribution of 11-oxygenated C19 steroids (11oxC19) to hyperandrogenemia in female patients with CD. Methods: We assessed saliva day profiles in females with CD pre (n = 23) and post (n = 13) successful transsphenoidal surgery, 26 female controls, 5 females with CD treated with metyrapone and 5 treated with osilodrostat for cortisol, cortisone, androstenedione (A4), 11-hydroxyandrostenedione (11OHA4), testosterone (TS), 11-ketotestosterone (11KT), as well as metabolites of classic and 11-oxygenated androgens in 24-h urine. In addition, morning baseline levels of gonadotropins and estradiol, sex hormone-binding globulin, cortisol and dehydroepiandrosterone sulfate (DHEAS) in serum and adrenocorticotrophic hormone in plasma in patients and controls were investigated. Results: Treatment-naïve females with CD showed a significantly elevated area under the curve of 11OHA4 and 11KT in saliva throughout the day compared to controls (11OHA4 mean rank difference (mrd) 18.13, P = 0.0002; 11KT mrd 17.42; P = 0.0005), whereas A4, TS and DHEAS were comparable to controls. Gonadotropin concentrations were normal in all patients with CD. After transsphenoidal surgery, 11oxC19 and their metabolites dropped significantly in saliva (11OHA4 P < 0.0001; 11KT P = 0.0010) and urine (11-oxo-androsterone P = 0.0011; 11-hydroxy-androsterone P < 0.0001), treatment with osilodrostat and metyrapone efficaciously blocked 11oxC19 synthesis. Conclusion: Hyperandrogenemia in CD is predominantly caused by excess of 11oxC19 steroids.

Indexed as

CortisoneHyperandrogenismPituitary ACTH HypersecretionPolycystic Ovary SyndromeAdrenocorticotropic HormoneAndrogensAndrostenedioneAndrosteroneDehydroepiandrosterone SulfateEstradiolFemaleHumansHydrocortisoneMetyraponeSex Hormone-Binding GlobulinSteroidsAdrenocorticotropic HormoneAndrogensAndrostenedioneAndrosteroneCortisoneDehydroepiandrosterone SulfateEstradiolHydrocortisoneMetyraponeSex Hormone-Binding GlobulinSteroidsTestosterone

Identifiers

PMID36074938
PMCPMC9578081
OpenAlexW4295087970

What OpenQuestion holds

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LicenceCC BY
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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.