ADJUVANT RECOMBINANT HUMAN GROWTH-HORMONE DOES NOT AUGMENT ENDOGENOUSGLUCOSE-PRODUCTION IN TOTAL PARENTERAL NUTRITION-FED MULTIPLE TRAUMA PATIENTS

Hyperglycemia and insulin resistance are well-known, consistent respon ses to severe injury. The purpose of this study was to investigate the mechanism for the further exaggerated hyperglycemia due to adjuvant r ecombinant human growth hormone (rhGH) treatment in multiple trauma pa tients. We have measured in 20 adult severely injured, highly cataboli c, hypermetabolic, multiple trauma patients, the glucose kinetics (app earance, clearance, oxidation, and recycling) once in the basal state (study I), 48 to 60 hours after injury but before starting nutritional therapy, and again (study II) after 7 days of intravenous nutrition ( 1.1 times resting energy expenditure, 250 mg nitrogen [N]/kg/d) with o r without adjuvant rhGH. Group H (n = 10) randomly received daily (8 n M) rhGH (0.15 mg/kg/d) and group C (n = to) received the vehicle of in fusion. Adjuvant rhGH treatment in intravenously fed trauma patients ( 1) increases plasma insulin-like growth factor-1 (IGF-1) and insulin c oncentrations, (2) improves N balance, and (3) exaggerates the hypergl ycemic response without affecting endogenous glucose output, glucose o xidation, or recycling. The mechanism for the hyperglycemic hyperinsul inemia in trauma may be due to a defective nonoxidative glucose dispos al, as well as inhibition of glucose transport activity into tissue ce lls. Copyright (C) 1996 by W.B. Saunders Company