Host metabolic alterations during inflammatory stress as related to nutritional status.

Malnutrition predisposes to infection, whereas infection can exacerbate malnutrition, resulting in hindered growth and development. This interplay between infection and nutrition suggests that host metabolism has a role in host defense during infection. Infection occasions profound alterations in host trace metal, nitrogen, and hormone metabolism and redistribution as a result of factors [leukocyte endogenous mediator (endogenous pyrogen)] released from stimulated phagocytes. Many of these alterations occur even in malnourished, protein-restricted, and zinc-deficient animals and persons, bespeaking the essential nature of these changes. Although these metabolic sequelae of infection appear to be of value to the host during acute illness, a metabolic deficit is often incurred which may persist long after resolution of clinical illness. Understanding host-parasite sequences will allow formulation of an integrated approach to the care of infected patients, combining the appropriate elements of nutrition with the best features of antimicrobial therapy.