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Procalcitonin increase after endotoxin injection in normal subjects
1Department of Medicine, Millard Fillmore Hospitals, State University of New York, Buffalo 14209.
The Journal of Clinical Endocrinology and Metabolism
|December 1, 1994
Summary
Endotoxin, a component of gram-negative bacteria, was found to induce systemic procalcitonin release in healthy volunteers. This study suggests endotoxin may mediate the procalcitonin increase observed in septicemia.
Area of Science:
- Biochemistry
- Immunology
- Critical Care Medicine
Background:
- Procalcitonin (PCT) levels are elevated in septicemia, particularly with gram-negative infections.
- Endotoxin, a lipopolysaccharide from gram-negative bacteria, is a key mediator of sepsis.
Purpose of the Study:
- To investigate the effect of endotoxin on procalcitonin concentrations in healthy human volunteers.
- To determine if endotoxin administration leads to a systemic increase in procalcitonin.
Main Methods:
- Healthy volunteers received intravenous endotoxin from Escherichia coli.
- Blood samples were collected serially for 24 hours post-injection.
- Procalcitonin, calcitonin, tumor necrosis factor-alpha, and interleukin-6 levels were measured.
Main Results:
- Procalcitonin was undetectable initially, becoming detectable at 4 hours and peaking at 6 hours post-endotoxin injection.
- Tumor necrosis factor-alpha and interleukin-6 levels increased following endotoxin administration.
- Calcitonin levels remained unchanged, showing no cross-reactivity with the procalcitonin assay.
Conclusions:
- Systemic release of procalcitonin is induced by endotoxin in humans.
- The observed increase in procalcitonin during septicemia may be mediated by endotoxin.
- Further research is needed to explore procalcitonin's role in inflammatory mechanisms.