Objective: The aims of this study were to clarify changes in total ghrelin within the somatotropic axis in severe burn subjects with or without inhalation injury as well as the responsiveness of GH, IGF-1, and IGFBP-3 to the different severity of burn injuries. Design: Twenty-three patients with severe burn injuries (>30% of 2nd degree burns or >10% of 3rd degree burns) were classified into 2 groups according to inhalation injury: group I with inhalation injury (n = 9) and group II without inhalation injury (n = 14). The evaluations of serum GH, IGF-1, IGFBP-3, and total ghrelin were done on post-burn injury days 3, 7, 14, 21, and 40. Cortisol levels were measured from 24-h urine collections on post-burn injury days 7 and 21. Results: In all subjects, the levels of GH fluctuated throughout the observation period whereas IGF-1 showed an initial decline with nadir on day 7 and a subsequent increase through day 40. The levels of IGFBP-3 and total ghrelin showed a progressive increase with nadir on day 3. Compared with the group II, the GH levels were increased in the group I on post-burn days 3, 7, and 14, of which day 7 showed statistical significance (p < 0.05). The levels of IGF-1 (days 7 and 21; p < 0.05) and IGFBP-3 (days 7, 14, 21, and 40; p < 0.05, p < 0.01, p < 0.05, p < 0.05, respectively) were lower in the group I than in the group II throughout the study period. On post-burn injury days 3, 7, 14, and 21, total ghrelin levels were lower in the group I than in the group II with statistical significance on post-burn day 7 (p < 0.001). Conclusions: Our present data show a concurrence of elevated GH levels and decreased IGF-I, IGFBP-3, and total ghrelin levels during the early burn injury period, in addition to more GH burst amplitude as well as greater falling of IGF-I, IGFBP-3 and total ghrelin levels proportional to the severity of burn injury. Further studies are needed to ascertain whether acyl- and desacyl-ghrelin instead of total ghrelin are completely independent of increased GH or other stress mediators, and whether GH-releasing hormone (GHRH) mainly stimulates the production and release of GH in acute critical conditions.
Bibliographical noteFunding Information:
This work was supported by a Grant (01-2007-12,13) from Hallym University Medical Center Research Fund.
All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism