Evidence map›Paper›PMID 24715566›Full record

ReviewComprehensive Physiology2014

Physiological basis for the etiology, diagnosis, and treatment of adrenal disorders: Cushing's syndrome, adrenal insufficiency, and congenital adrenal hyperplasia.

Hershel Raff, Susmeeta T Sharma, Lynnette K Nieman

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Comprehensive Physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00005664 (Evaluation of Patients With Endocrine-Related Conditions), which is not on this map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
–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.

NCT00005664 terminatednot on this map

Evaluation of Patients With Endocrine-Related Conditions

TypeobservationalSponsorEunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)Ran2000 to 2019Enrolled1,588ConditionsAdrenal Insufficiency, Pituitary Neoplasm, Obesity
3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 142 citations in OpenAlex.

  1. Pooled it
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  3. Trial
  4. Trial
  5. Article
  6. Ketamine Reverses Chronic Stress-Induced Behavioral Changes via the Expression of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  9. Review
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  12. Iatrogenic adrenal insufficiency in adults.Nature reviews. Endocrinology · 2024
    Review
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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

3 authors at 2 institutions in 1 country.

Hershel RaffEndocrine Research Laboratory, Aurora St. Luke's Medical Center, Aurora Research Institute and Departments of Medicine, Surgery, and Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Susmeeta T Sharma
Lynnette K Nieman
Medical College of Wisconsin · USNational Institutes of Health · US

Funding

The Physiology Of HypercortisolismZIAHD000638 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI NIEMAN, LYNNETTE · 2009 to 2015
$3.0M
The physiology of adrenal insufficiencyZIAHD008831 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI NIEMAN, LYNNETTE · 2009 to 2015
$1.0M
The physiology of adrenal insufficiencyZ01HD008831 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI NIEMAN, LYNNETTE K · 2007 to 2008
$542k
THE PHYSIOLOGY OF HYPERCORTISOLISMZ01HD000638 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI NIEMAN, LYNNETTE K · 1994 to 2008
$357k
Intramural NIH HHS Z01 HD000638Intramural NIH HHS Z01 HD008831
6 · The paper itself

Abstract

The hypothalamic-pituitary-adrenal (HPA) axis is a classic neuroendocrine system. One of the best ways to understand the HPA axis is to appreciate its dynamics in the variety of diseases and syndromes that affect it. Excess glucocorticoid activity can be due to endogenous cortisol overproduction (spontaneous Cushing's syndrome) or exogenous glucocorticoid therapy (iatrogenic Cushing's syndrome). Endogenous Cushing's syndrome can be subdivided into ACTH-dependent and ACTH-independent, the latter of which is usually due to autonomous adrenal overproduction. The former can be due to a pituitary corticotroph tumor (usually benign) or ectopic ACTH production from tumors outside the pituitary; both of these tumor types overexpress the proopiomelanocortin gene. The converse of Cushing's syndrome is the lack of normal cortisol secretion and is usually due to adrenal destruction (primary adrenal insufficiency) or hypopituitarism (secondary adrenal insufficiency). Secondary adrenal insufficiency can also result from a rapid discontinuation of long-term, pharmacological glucocorticoid therapy because of HPA axis suppression and adrenal atrophy. Finally, mutations in the steroidogenic enzymes of the adrenal cortex can lead to congenital adrenal hyperplasia and an increase in precursor steroids, particularly androgens. When present in utero, this can lead to masculinization of a female fetus. An understanding of the dynamics of the HPA axis is necessary to master the diagnosis and differential diagnosis of pituitary-adrenal diseases. Furthermore, understanding the pathophysiology of the HPA axis gives great insight into its normal control.

Indexed as

Adrenal Hyperplasia, CongenitalAdrenal InsufficiencyCushing SyndromeHumansHypothalamo-Hypophyseal SystemPituitary-Adrenal System

Identifiers

PMID24715566
PMCPMC4215264
OpenAlexW1519533122

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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.