[Hepatic coma].

E Walter

Home/Archive/PubMed

PubMed · 7914030

[Hepatic coma].

E Walter

View original source ↗Export metadata ↓

Abstract

The term "hepatic encephalopathy" describes the neuropsychiatric signs and symptoms of patients with acute or chronic liver disease, irrespective of the presence or absence of liver cirrhosis. Cerebral edema, the pathophysiology and treatment of which being quite different from hepatic encephalopathy, is the leading cause of death in patients with acute liver failure. Lactulose (orally or as enema) is one of the cornerstones of the treatment of hepatic encephalopathy; most important for the management of patients with cerebral edema is close monitoring (including intracranial pressure monitoring) of the patients and rapid reduction of intracranial pressure (e.g. with mannitol). The pathophysiologic and therapeutic concepts in the care of patients with hepatic encephalopathy and cerebral edema are described.

Explore related subjects

Blood-Brain Barrier Brain Edema Combined Modality Therapy Hepatic Encephalopathy Humans Liver Cirrhosis Neurotoxins Neurotransmitter Agents English Abstract Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

E Walter. 1994-07-02. [Hepatic coma].. https://pubmed.ncbi.nlm.nih.gov/7914030/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Protective effects of liver-derived apolipoprotein A1 against heat stress-induced hypothalamic lipid metabolism and blood-brain barrier integrity.

Heat stress (HS), a prevalent occupational and environmental hazard, has increasingly been recognized as a major contributor to multiple physiological disorders. The hypothalamus, a key regulator of thermoregulation and endocrine signaling, is especially susceptible to metabolic and inflammatory disturbances induced by HS. This study investigates the interplay among lipid metabolism, blood-brain barrier (BBB) integrity, and neuroinflammation in the hypothalamus under HS conditions, with a specific focus on apolipoprotein A1 (APOA1) as a potential protective factor. To achieve this, we integrated proteomic and lipidomic analyses with experimental validation in porcine and murine models. Proteomic analysis identified 266 differentially expressed proteins (DEPs) in the hypothalamus following HS, with significant enrichment in lipid metabolism pathways-especially glycerophospholipid (GP) metabolism-in which APOA1 displayed a marked increase. Lipidomic profiling further revealed HS-induced disruptions in phosphatidylcholine (PC), phosphatidylethanolamine (PE), and cardiolipin (CL) metabolism. Additionally, blood-brain barrier integrity was compromised, as evidenced by increased perivascular IgG extravasation, reduced pericyte coverage, and decreased expression of tight junction proteins ZO-1 and Occludin. HS also triggered pronounced neuroinflammation, characterized by elevated levels of iNOS, GFAP, and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). Notably, administration of D-4F, an APOA1 mimetic peptide, alleviated blood-brain barrier damage, reduced neuroinflammation, and preserved synaptic integrity, thereby suggesting a neuroprotective role for APOA1 in HS-induced hypothalamic dysfunction. These findings underscore the critical role of lipid metabolism in maintaining hypothalamic homeostasis under HS conditions and position APOA1 as a key regulator with potential therapeutic implications for mitigating HS-related neuroinflammatory and metabolic disturbances.

Blood-Brain Barrier↗

PubMed1995

[Environmental poisons and the nervous system].

The neurons are extremely vulnerable to changes in the local chemical environment, and the nervous system has therefore been given special priority and protection compared with other organ systems. Neurotoxic syndromes may occur when these biochemical conditions are disturbed. The brain is particularly vulnerable to hypoxia, and exposure to toxins that interfere with the intake, transport and utilization of oxygen provoke rapid and major neuronal damage. Compounds crossing the blood-brain barrier may induce both general and extremely localized neurotoxic effects. Today, dramatic and acute neurotoxic manifestations seldom occur in our part of the world. The focus of attention is now directed at the consequences of long-term and low-level exposure. This review presents a general description of some neurotoxic mechanisms, and the clinical effects of a few hazardous substances, ie metals, pesticides, organic solvents.

Blood-Brain Barrier↗

PubMed1995

HIV-1 infection of human brain-derived microvascular endothelial cells in vitro.

We examined the ability of human immunodeficiency virus (HIV) type 1 (HIV-1) to infect in vitro, primary brain-derived human microvascular endothelial cells (HMEC) that constitute the blood-brain barrier (BBB). Immunofluorescence (IFA) and antigen capture assays failed to demonstrate p24 antigen from HIV inoculated endothelial cells and supernatants did not contain detectable levels of reverse transcriptase (RT). HIV could be rescued by cocultivation of infected HMEC with a susceptible T-lymphocyte line (CEM-SS), which were then shown to form syncytia and produce RT activity and p24 Ag (IFA, antigen captive assay). Polymerase chain reaction (PCR) was successfully used to amplify HIV-specific gag and env gene sequences from HMEC. CD4 expression was not identified on these cells by IFA. These results suggest that HIV infection of BBB endothelium occurs, but that viral replication is minimal. Infection of the BBB by HIV may give the virus a foothold in the CNS and suggests that the brain might be infected directly and may not be limited to just the passage of infected mononuclear cells.

Blood-Brain Barrier↗