Evidence map›Paper›PMID 39848955›Full record

ReviewNature reviews. Disease primers2025

Cushing syndrome.

Lynnette K Nieman, Frederic Castinetti, John Newell-Price, Elena Valassi, Jacques Drouin, Yutaka Takahashi, André Lacroix

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Disease primers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Cancer incidence in endogenous hypercortisolism.Journal of endocrinological investigation · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. The value of targeting CXCR4 withEuropean journal of nuclear medicine and molecular imaging · 2026
    Article
  16. Article
  17. Article
  18. Neutralization of acyl-CoA-binding protein attenuates glucocorticoid-mediated suppression of cancer immunosurveillance.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Article
  20. Article
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

7 authors.

Lynnette K NiemanSection on Translational Endocrinology, Diabetes, Endocrine and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, MD, USA. NiemanL@nih.gov.ORCID http://orcid.org/0000-0003-0534-8025
Frederic CastinettiAix Marseille Univ, INSERM, UMR1251, Marseille Medical Genetics, Institut MarMaRa, Marseille, France.ORCID http://orcid.org/0000-0002-1808-8800
John Newell-PriceSchool of Medicine & Population Health, University of Sheffield, Sheffield, UK.ORCID http://orcid.org/0000-0002-0835-5493
Elena ValassiEndocrinology Department, Germans Trias i Pujol Hospital and Research Institute, CIBERER Unit 747, Badalona, Spain.ORCID http://orcid.org/0000-0002-3864-0105
Jacques DrouinLaboratoire de génétique moléculaire, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada.
Yutaka TakahashiDepartment of Diabetes and Endocrinology, Nara Medical University, Kashihara, Nara, Japan.ORCID http://orcid.org/0000-0002-1337-9246
André LacroixEndocrine Division, Department of Medicine, Centre hospitalier de l'Université de Montréal (CHUM), Montreal, Québec, Canada.ORCID http://orcid.org/0000-0003-4137-3025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cushing syndrome (CS) is a constellation of signs and symptoms caused by excessive exposure to exogenous or endogenous glucocorticoid hormones. Endogenous CS is caused by increased cortisol production by one or both adrenal glands (adrenal CS) or by elevated adrenocorticotropic hormone (ACTH) secretion from a pituitary tumour (Cushing disease (CD)) or non-pituitary tumour (ectopic ACTH secretion), which stimulates excessive cortisol production. CS is associated with severe multisystem morbidity, including impaired cardiovascular and metabolic function, infections and neuropsychiatric disorders, which notably reduce quality of life. Mortality is increased owing to pulmonary emboli, infection, myocardial infarction and cerebrovascular accidents. The clinical presentation is variable and because some CS signs and symptoms are common in the general population, the diagnosis might not be considered until many features have accumulated. Guidelines recommend screening patients with suspected CS with 24-h urine cortisol, bedtime salivary cortisol and/or 1 mg dexamethasone suppression test. Subsequently, determining the aetiology of CS is important as it affects management. The first-line therapy for all aetiologies of endogenous CS is surgical resection of the causal tissue, including corticotroph adenoma or ectopic tumour for ACTH-dependent CS or unilateral or bilateral adrenalectomy for adrenal CS. Second-line therapies include steroidogenesis inhibitors for any cause of CS, pituitary radiation (with or without steroidogenesis inhibitors) for CD, and bilateral adrenalectomy for ACTH-dependent causes of CS.

Indexed as

Cushing SyndromeAdrenocorticotropic HormoneHumansHydrocortisoneAdrenocorticotropic HormoneHydrocortisone

Identifiers

PMID39848955

What OpenQuestion holds

Textmetadata
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.