Evidence map›Paper›PMID 10206824›Full record

ReviewMetabolic brain disease1998

Astroglial dysfunction in hepatic encephalopathy.

M D Norenberg

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.0field-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

46 citing papers in PubMed, 169 citations in OpenAlex.

  1. Brain magnetic resonance spectroscopy in episodic hepatic encephalopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Trial
  2. Article
  3. Review
  4. Future Therapies of Hepatic Encephalopathy.Clinics in liver disease · 2024
    Review
  5. Review
  6. Article
  7. Hyperammonemia in Inherited Metabolic Diseases.Cellular and molecular neurobiology · 2022
    Review
  8. Article
  9. Review
  10. Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018
    Review
  11. Review
  12. Review
  13. Ammonia toxicity: from head to toe?Metabolic brain disease · 2017
    Review
  14. Review
  15. Factors associated with long-term survival in dogs undergoing liver lobectomy as treatment for liver tumors.The Canadian veterinary journal = La revue veterinaire canadienne · 2015
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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.

M D NorenbergDepartment of Pathology, University of Miami School of Medicine, FL 33101, USA. mnorenbe@mednet.med.miami.edu
University of Miami · US

Funding

TRAUMATIC BRAIN INJURY INDUCED SEIZURE & SYNAPTIC PLASTICITYP50NS030291 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GREEN, EDWARD J · 1991 to 2013
$14.8M
THE ASTROCYTE BENZODIAZEPINE RECEPTOR IN HEPATIC COMAR01DK038153 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI NORENBERG, MICHAEL DAVID · 1987 to 1994
–
NIDDK NIH HHS DK-38153NINDS NIH HHS NS-30291
6 · The paper itself

Abstract

While the pathogenesis of hepatic encephalopathy (HE) remains elusive, there is considerable evidence pointing to a key role of ammonia-induced dysfunction of astrocytes in this condition. Deficits in the ability of astrocytes to take up glutamate from the extracellular space may lead to abnormal glutamatergic neurotransmission. Furthermore, excessive stimulation of neuronal and glial glutamate receptors by elevated extracellular levels of glutamate may lead to excitotoxicity and greater glial dysfunction. Ammonia also causes upregulation of astroglial peripheral-type benzodiazepine receptors (PBRs) which is associated with increased production of neurosteroids. These neurosteroids have potent positive modulatory effects on the neuronal GABA(A) receptor which, combined with an ammonia-induced astroglial defect in GABA uptake, may result in enhanced GABAergic tone. Brain edema, associated with fulminant hepatic failure, may also result from astroglial abnormalities as the edema appears to be principally caused by swelling of these cells. Increased amounts of glutamine in astrocytes resulting from elevated brain ammonia levels may be a factor in this swelling. Other osmolytes such as glutathione may also be involved. Glial swelling may also result from NH4+ - and K+ -mediated membrane depolarization as well as by the actions of PBR agonists and neurosteroids. These findings show that an ammonia-induced gliopathy is a major factor in the pathogenesis of HE.

Indexed as

AmmoniaAnimalsAstrocytesBiological TransportGlutamic AcidHepatic EncephalopathyHumansReceptors, GABAReceptors, GlutamateAmmoniaGlutamic AcidReceptors, GABAReceptors, Glutamate

Identifiers

PMID10206824
OpenAlexW1608390320

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.