Administration of Growth Hormone as an Adjunct to Nutritional Support in Critical Illness

Abstract

Erosion of lean body mass (LBM) is a usual metabolic consequence of critical illness. Despite provison of presumably adequate nutritional support, body compositional analysis demonstrates a net loss of body protein manifested by an accelerated rate of protein breakdown, negative nitrogen balance, and a reduction in skeletal muscle intracellular amino acid concentrations in severely ill patients (1, 2). Protein wasting interrelates with other metabolic responses to catabolic illness, including accelerated rates of lipolysis and gluconeogenesis, hypoxic tissue damage and antioxidant depletion, alterations in body fluid compartments, and reduced circulating levels of insulin-like growth factor I (IGF-I). A number of factors contribute to protein loss in intensive care unit (ICU) settings, including increased counterregulatory hormone and cytokine signals, recurrent infections and other catabolic insults, metabolic acidosis, and physical inactivity. The erosion of lean tissue (primarily skeletal muscle) undoubtedly serves an important adaptive function because amino acids, such as glutamine and alanine, are shunted from the periphery as substrates to be utilized for acute-phase protein synthesis, gluconeogenesis, and acid-base balance and to support immune cells and wound and tissue repair (1, 2).