An altered response by peripheral leukocytes to synthesize or release leukocyte endogenous mediator in critically ill, protein-malnourished patients.
LEM derived from fixed and circulating macrophages is involved in certain aspects of the metabolic response to infection. A reduction in the synthesis or release of LEM from leukocytes of nonstressed, protein-malnourished patients has been demonstrated. In this study, blood leukocytes from 15 protein-malnourished patients (serum albumin less than 2.5 gm/dl) who were critically ill were assayed for their in vitro capacity to produce LEM. Samples were taken before (day 0) and 3 or 7 days after the institution of parenteral nutrition. Hospitalized patients were judged capable of producing LEM (responders) if the percentage of polymorphonuclear leukocytes in the blood of the rats injected with their LEM was greater than 52% ( the minimum value obtained when LEM from 10 human volunteers was injected into the rats). With this criterion, eight patients were responders and only one died during their hospital stay, whereas five of seven nonresponders expired (p less than 0.05). On day 0, prior to intravenous nutritional support, there was no difference in the capacity to produce LEM between responding and nonresponding patients. However, those patients whose leukocytes were capable of responding received significantly greater quantities of dietary protein and calories over the 7-day study period than nonresponders (p less than 0.05). There was a correlation between the polymorphonuclear leukocyte response to LEM in rats and the patients' dietary protein intake (r = 0.719, p less than 0.005). these findings suggest that an appreciable fraction of severely ill, protein-malnourished patients have a reduced capacity to synthesize LEM, as judged by bioassay and an increased risk of mortality. The in vitro capacity to produce LEM in a critically ill population appears to be associated with the dietary intake of the patient.
D000818:Animals; D004734:Energy Metabolism / Q000187:drug effects; D005334:Fever / Q000139:chemically induced; D006801:Humans; D007275:Injections, Intravenous; D007375:Interleukin-1; D007962:Leukocytes / Q000378:metabolism*; D007964:Leukocytosis; D009747:Nutritional Physiological Phenomena; D014176:Protein Biosynthesis; D011502:Protein-Energy Malnutrition / Q000378:metabolism*; D011506:Proteins / Q000008:administration & dosage; D051381:Rats; D012709:Serum Albumin / Q000032:analysis; D015032:Zinc / Q000097:blood
D007375:Interleukin-1; D011506:Proteins; D012709:Serum Albumin; C008270:leukocyte endogenous mediator; D015032:Zinc