A lipid A analog, E5531, blocks the endotoxin response in human volunteers with experimental endotoxemia
Critical Care Medicine, ISSN: 0090-3493, Vol: 28, Issue: 8, Page: 2713-2720
2000
- 81Citations
- 28Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations81
- Citation Indexes81
- 81
- CrossRef63
- Captures28
- Readers28
- 28
Article Description
Background: Endotoxin (lipopolysaccharide [LPS]) has been associated with sepsis and the high mortality rate seen in septic shock. The administration of a small amount of LPS to healthy subjects produces a mild syndrome qualitatively similar to that seen in clinical sepsis. We used this model to test the efficacy of an endotoxin antagonist, E5531, in blocking this LPS-induced syndrome. Methods: In a placebo-controlled, double-blind study, we randomly assigned 32 healthy volunteers to four sequential groups (100, 250, 500, or 1000 μg of E5531). Each group of eight subjects (six assigned to E5531, two assigned to placebo) received a 30-min intravenous infusion of study drug. LPS (4 ng/kg) was administered to all subjects as an intravenous bolus in the contralateral arm at the midpoint of the infusion. Symptoms, signs, laboratory values, and hemodynamics (by echocardiogram) were evaluated at prospectively defined times. Results: In subjects receiving placebo, LPS caused headache, nausea, chills, and myalgias. E5531 led to a dose-dependent decrease in these symptoms that was statistically significant (p < .05) except for myalgias. The signs of endotoxemia (fever, tachycardia, and hypotension) were consistently inhibited at the three higher doses (250, 500, and 1000 μg, p < .05). Tumor necrosis factor-α and interleukin-6 blood levels were both lower in those who received E5531 (p < .0001). The C-reactive protein level and white blood cell count response were decreased at all doses (p < .0001). The hyperdynamic cardiovascular state (high cardiac index and low systemic vascular resistance) associated with endotoxin challenge was significantly inhibited at the higher doses of E5531. Conclusions: E5531 blocks the symptoms and signs and cytokine, white blood cell count, C-reactive, protein, and cardiovascular response seen in experimental endotoxemia. This agent is a potent inhibitor of endotoxin challenge in humans and may be of benefit in the prevention or treatment of sepsis and septic shock.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0033847364&origin=inward; http://dx.doi.org/10.1097/00003246-200008000-00005; http://www.ncbi.nlm.nih.gov/pubmed/10966240; http://journals.lww.com/00003246-200008000-00005; https://dx.doi.org/10.1097/00003246-200008000-00005; https://journals.lww.com/ccmjournal/Abstract/2000/08000/A_lipid_A_analog,_E5531,_blocks_the_endotoxin.5.aspx
Ovid Technologies (Wolters Kluwer Health)
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