AN ALTERED RESPONSE BY PERIPHERAL LEUKOCYTES TO SYNTHESIZE OR RELEASE LEUKOCYTE ENDOGENOUS MEDIATOR IN CRITICALLY ILL, PROTEIN-MALNOURISHED PATIENTS
- 1 January 1982
- journal article
- research article
- Vol. 100 (6) , 844-857
Abstract
LEM [leukocyte endogenous mediator] 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 was demonstrated. Blood leukocytes from 15 protein-malnourished patients (serum albumin < 2.5 g/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 > 52% (the minimum value obtained when LEM from 10 human volunteers was injected into the rats). With this criterion, 8 patients were responders and only 1 died during their hospital stay, whereas 5 of 7 nonresponders expired (P < 0.05). On day 0, prior to i.v. nutritional support, there was no difference in the capacity to produce LEM between responding and nonresponding patients. 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 < 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 < 0.005). Apparently, 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.This publication has 8 references indexed in Scilit:
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