Endotoxin levels measured by a chromogenic assay in portal, hepatic and peripheral venous blood in patients with cirrhosis
Open accessAbstract
Endotoxin concentrations were measured in the portal, hepatic and peripheral venous blood of two groups of patients with cirrhosis using a limulus-based chromogenic assay. The high sensitivity of chromogenic detection allowed measurement of endotoxin as low as 10 to 15 pg per ml, an order of magnitude greater than previously possible by gelation studies. Group 1 consisted of 56 patients with cirrhosis undergoing angiographic evaluation. In this group, there was wide variability in hepatic venous concentration [ 73 ± 110 pg per ml (mean ± S.D.)] and peripheral venous concentration [31 ± 58 pg per ml]. However, paired t test showed peripheral venous concentration was significantly (p < 0.001) lower than hepatic venous concentration. Neither hepatic or peripheral venous endotoxin levels correlated significantly with a variety of clinical, biochemical or radiological parameters. Group 2 consisted of 21 patients with cirrhosis undergoing shunt surgery. Endotoxin levels again showed a wide range, with portal venous concentration (142 ± 167 pg per ml) and simultaneous peripheral venous concentration (82 ± 150 pg per ml). Paired t test in this group showed a significant (p < 0.001) portal to peripheral venous gradient. This study showed the feasibility of measuring endotoxin in plasma to low concentrations by a chromogenic assay technique. It supports the concept of relatively high levels of endotoxin in the portal circulation. In the presence of liver disease, systemic endotoxemia occurs, which is augmented by stressful situations.
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Most endotoxin enters the body via the gut and hepatic portal vein, and most of this endotoxin is cleared by the liver.
“Most endotoxin enters the body via the gut and hepatic portal vein, and most of this endotoxin is cleared by the liver [41].”
From The endotoxin hypothesis of neurodegeneration (2019) · cites this paper as [41]
Serious liver disease increases peripheral blood endotoxin to potentially toxic levels (60-80 pg/ml in cirrhosis).
“So, serious liver disease increases peripheral blood endotoxin to potentially toxic levels (60–80 pg/ml in cirrhosis) [11, 41].”
From The endotoxin hypothesis of neurodegeneration (2019) · cites this paper as [41]
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- Authors
- Lumsden, A. B., Henderson, M. J., & Kutner, M. H.
- Affiliations
- Emory University (US)
- Venue
- Hepatology
- Published
- 1988-03
- Volume
- 8
- Issue
- 2
- Pages
- 232-236
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W1972486471
- Cited by
- 427
- References
- 43
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 4 · 2023: 11 · 2022: 10 · 2021: 8 · 2020: 12 · 2019: 7 · 2018: 11 · 2017: 11 · 2016: 19 · 2015: 15 · 2014: 8 · 2013: 11 · 2012: 14
- FWCI
- 8.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Center for Research Resources (5M01 RR 00039, M01RR000039)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- endotoxin, liver cirrhosis, portal blood, hepatic venous blood, peripheral venous blood
- MeSH terms
- Chromogenic Compounds, Endotoxins, Escherichia coli, Esophageal and Gastric Varices, Hemorrhage, Humans, Intraoperative Period, Liver Circulation, Liver Cirrhosis, Osmolar Concentration, Postoperative Period, Veins
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