Evidence map›Paper›PMID 18319312›Full record

SynthesisThe Journal of clinical endocrinology and metabolism2008

Generalized glucocorticoid resistance: clinical aspects, molecular mechanisms, and implications of a rare genetic disorder.

Evangelia Charmandari, Tomoshige Kino, Takamasa Ichijo, George P Chrousos

Open access · bronzeAbstract readSystematic Review
In one paragraph

Synthesis in The Journal of clinical endocrinology and metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 195 citations in OpenAlex.

  1. Review
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  10. Article
  11. Review
  12. Approach to the Patient: Diagnosis of Cushing Syndrome.The Journal of clinical endocrinology and metabolism · 2022
    Article
  13. Review
  14. Article
  15. Salt-Sensitive Hypertension in GRInternational journal of molecular sciences · 2021
    Article
  16. Review
  17. International journal of molecular medicine · 2021
    Article
  18. Article
  19. Article
  20. Article

4 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

4 authors at 2 institutions in 2 countries.

Evangelia CharmandariDivision of Endocrinology and Metabolism, Clinical Research Center, Biomedical Research Foundation of the Academy of Athens, 4 Soranou tou Efessiou Street, Athens, Greece. evangelia.charmandari@googlemail.com
Tomoshige Kino
Takamasa Ichijo
George P Chrousos
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institutes of Health · US

Funding

Molecular Mediators and Regulators of Glucocorticoid ActionsZIAHD008732 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 2009 to 2014
$5.1M
Vpr A Viral Coactivator Of Nuclear Receptors--MechanismsZ01HD008732 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI KINO, TOMOSHIGE · 2001 to 2008
$511k
Intramural NIH HHS
6 · The paper itself

Abstract

contextPrimary generalized glucocorticoid resistance is a rare genetic condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. We review the clinical aspects, molecular mechanisms, and implications of this disorder. EVIDENCE ACQUISITION: We conducted a systematic review of the published, peer-reviewed medical literature using MEDLINE (1975 through February 2008) to identify original articles and reviews on this topic. EVIDENCE SYNTHESIS: We have relied on the experience of a number of experts in the field, including our extensive personal experience.

conclusionsThe clinical spectrum of primary generalized glucocorticoid resistance is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue, and/or mineralocorticoid excess. The molecular basis of the condition has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction and reduce tissue sensitivity to glucocorticoids. A consequent increase in the activity of the hypothalamic-pituitary-adrenal axis compensates for the reduced sensitivity of peripheral tissues to glucocorticoids at the expense of ACTH hypersecretion-related pathology. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology.

Indexed as

Amino Acid SequenceDrug ResistanceGlucocorticoidsHumansMolecular Sequence DataMutationReceptors, GlucocorticoidResponse ElementsSignal TransductionGlucocorticoidsReceptors, Glucocorticoid

Identifiers

PMID18319312
PMCPMC2386273
OpenAlexW1991727114

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.