Evidence map›Paper›PMID 34849663›Full record

ReviewEndocrine reviews2022

Molecular Derangements and the Diagnosis of ACTH-Dependent Cushing's Syndrome.

Lynnette K Nieman

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Gut Microbiota-Driven Pathways Linking Chronic Stress to Tumor Progression.International journal of biological sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Cushing syndrome.Nature reviews. Disease primers · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Approach to the Patient: Diagnosis of Cushing Syndrome.The Journal of clinical endocrinology and metabolism · 2022
    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

1 author at 1 institution in 1 country.

Lynnette K NiemanDiabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0003-0534-8025
National Institutes of Health · US

Funding

The differential diagnosis and treatment of Cushing's syndromeZIADK075122 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI NIEMAN, LYNNETTE · 2016 to 2025
$4.0M
The Physiology Of HypercortisolismZIADK075121 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI NIEMAN, LYNNETTE · 2016 to 2024
$1.7M
Intramural NIH HHS ZIA DK075121
6 · The paper itself

Abstract

Endogenous Cushing's syndrome (CS) is associated with morbidities (diabetes, hypertension, clotting disorders) and shortens life because of infections, pulmonary thromboembolism, and cardiovascular disease. Its clinical presentation is immensely variable, and diagnosis and treatment are often delayed. Thus, there are many opportunities for basic and clinical research leading to better tests, faster diagnosis, and optimized medical treatments. This review focuses on CS caused by excessive adrenocorticotropin (ACTH) production. It describes current concepts of the regulation of ACTH synthesis and secretion by normal corticotropes and mechanisms by which dysregulation occurs in corticotrope (termed "Cushing's disease") and noncorticotrope (so-called ectopic) ACTH-producing tumors. ACTH causes adrenal gland synthesis and pulsatile release of cortisol; the excess ACTH in these forms of CS leads to the hypercortisolism of endogenous CS. Again, the differences between healthy individuals and those with CS are highlighted. The clinical presentations and their use in the interpretation of CS screening tests are described. The tests used for screening and differential diagnosis of CS are presented, along with their relationship to cortisol dynamics, pathophysiology, and negative glucocorticoid feedback regulation in the two forms of ACTH-dependent CS. Finally, several gaps in current understanding are highlighted in the hope of stimulating additional research into this challenging disorder.

Indexed as

Cushing SyndromeAdrenal GlandsAdrenocorticotropic HormoneDiagnosis, DifferentialGlucocorticoidsHumansHydrocortisoneAdrenocorticotropic HormoneGlucocorticoidsHydrocortisone

Identifiers

PMID34849663
PMCPMC9512149
OpenAlexW3215011458

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.