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Hepatic encephalopathy: An update of pathophysiologic mechanisms
Hazell AS, Butterworth RF.. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 1999-11-01
Topic: Brain proteins, microglia and lab models
Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs in both acute and chronic liver failure. Although the precise pathophysiologic mechanisms responsible for HE are not completely understood, a deficit in neurotransmission rather than a primary deficit in cerebral energy metabolism appears to be involved. The neural cell most vulnerable to liver failure is the astrocyte.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Hazell, A. S., & Butterworth, R. F. (1999). Hepatic encephalopathy: An update of pathophysiologic mechanisms. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.). https://doi.org/10.1046/j.1525-1373.1999.d01-120.x
Vancouver
Hazell AS, Butterworth RF. Hepatic encephalopathy: An update of pathophysiologic mechanisms. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.). 1999. doi:10.1046/j.1525-1373.1999.d01-120.x. PMID: 10564534.
BibTeX
@article{hazell1999-10564534,
author = {Hazell, A. S. and Butterworth, R. F.},
title = {{Hepatic encephalopathy: An update of pathophysiologic mechanisms}},
journal = {Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)},
year = {1999},
doi = {10.1046/j.1525-1373.1999.d01-120.x},
pmid = {10564534},
url = {https://doi.org/10.1046/j.1525-1373.1999.d01-120.x}
}
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Key findings
- Although the precise pathophysiologic mechanisms responsible for HE are not completely understood, a deficit in neurotransmission rather than a primary deficit in cerebral energy metabolism appears to be involved.
- The neural cell most vulnerable to liver failure is the astrocyte.
- In acute liver failure, the astrocyte undergoes swelling resulting in increased intracranial pressure; in chronic liver failure, the astrocyte undergoes characteristic changes known as Alzheimer type II astrocytosis.
- In portal-systemic encephalopathy resulting from chronic liver failure, astrocytes manifest altered expression of several key proteins and enzymes including monoamine oxidase B, glutamine synthetase, and the so-called peripheral-type benzodiazepine receptors.
Why it matters
This review concerns hepatic encephalopathy, a neuropsychiatric disorder of liver failure, in which the astrocyte is the most vulnerable neural cell. It is not about Alzheimer's disease treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 40/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)) |
| Journal's citation record | 0 / 4 | Proceedings of The Society for Experimental Biology and Medicine: journal h-index 68 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 1999 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 301 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 10.4 citations a year over 29 year(s) since 1999 |
| Impact for its field and year | 3 / 6 | Cited 7.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Roger F. Butterworth: h-index 81 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Université de Montréal: institution h-index 1,020 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 10564534) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 40 / 100 | — |
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