Does the route of feeding modify the inflammatory response?
OBJECTIVE
The authors compared the responses to endotoxin in enterally and parenterally fed human volunteers.


BACKGROUND
Recent investigations have reported that the response to endotoxin in humans is greater in individuals who receive parenteral nutrition rather than enteral feeding. It was proposed that this difference was related to gut barrier dysfunction during intravenous nutrition. To evaluate this hypothesis, the authors analyzed the responses of human subjects to an intravenously administered bolus of endotoxin after enteral or parenteral nutrition.


METHODS
Fifteen randomly selected healthy volunteers were studied during two separate investigations; ten studies were performed in ten subjects who received enteral nutrition, and nine studies were carried out in five additional subjects who received parenteral nutrition. After 2 days of enteral feedings or 7 days of parenteral feedings, endotoxin was administered by intravenous injection; temperature, symptom score, and duration then were measured serially. Blood samples were obtained for leukocyte and platelet count, and plasma concentrations of corticotrophin, cortisol, epinephrine, norepinephrine, tumor necrosis factor, and interleukin-6. Mononuclear cell response to phytohemagglutinin was determined at 0, 4, and 24 hours.


RESULTS
In the parenteral group, a diminished response was observed in platelet count and plasma interleukin-6 levels compared with volunteers who received enteral nutrition. The duration of symptoms tended to be reduced in the parenterally fed group, although this did not achieve significance. Other responses were not significantly different between the two groups.


CONCLUSIONS
The responses to endotoxin in human subjects who received parenteral nutrition were similar compared with subjects who received enteral nutrition, although platelet count and plasma interleukin-6 concentration were diminished.
Santos
A A
AA
Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts.
Rodrick
M L
ML
Jacobs
D O
DO
Dinarello
C A
CA
Wolff
S M
SM
Mannick
J A
JA
Wilmore
D W
DW
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000596:Amino Acids / Q000008:administration & dosage; D001831:Body Temperature / Q000502:physiology; D004731:Endotoxins / Q000008:administration & dosage / Q000009:adverse effects*; D004750:Enteral Nutrition; D004926:Escherichia coli; D005217:Fat Emulsions, Intravenous / Q000008:administration & dosage; D005526:Food, Formulated; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D007275:Injections, Intravenous; D015850:Interleukin-6 / Q000097:blood; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008070:Lipopolysaccharides / Q000009:adverse effects; D008297:Male; D010288:Parenteral Nutrition; D010976:Platelet Count; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000596:Amino Acids; D004731:Endotoxins; D005217:Fat Emulsions, Intravenous; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000324:Adrenocorticotropic Hormone; D005947:Glucose