Goals of nutritional support in acute infections

Defense mechanisms employed by the host to fight infection are highly dependent on adequate protein synthesis to support phagocytic and lymphoid cell activity as well as immunoglobulin production. Interleukin I is a small, not yet fully characterized protein produced by macrophages which appears to initiate most of the nonspecific metabolic changes observed during infection. These alterations include: increase in the synthesis of visceral proteins, white blood cells, and acute phase globulins; enhanced somatic protein breakdown; sequestering of serum iron and zinc in the liver; and induction of fever. The ability of leukocytes to produce interleukin I is impaired in patients with visceral protein depletion or kwashiorkor-like, hypoalbuminemic malnutrition and can be restored in the healthy unstressed patient within approximately three to five days by feeding. Similarly, in the stressed patient, adequate protein and caloric intake improves the ability to produce interleukin I, which may improve survival. Other defects in host defense in advanced stages of protein malnutrition include lymphopenia, impaired phagocytosis, and deficiencies in fibronectin, immunoglobulins, and complement levels. Thus, the goal of nutritional support is to maintain sufficient amounts of amino acids for visceral protein synthesis required for adequate host defense.