HYPERGLYCEMIA IN PATIENTS WITH CRITICAL ILLNESS

2013 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Critical Illness ◽  
Growth Factor ◽  
High Risk ◽  
Key Words ◽  
Hormone Release ◽  
Increase Blood Glucose ◽  
Tnf Α ◽  
Key Words Blood

Blood glucose is normally stabled at the level of 70 – 130 mg/dL. Blood glucose is usually changed in case of illness, whether or not having previous diabetes. Hyperglycemia was usually seen in the critical illness patients. Blood glucose is increased in critical illnesses as the increasing in hormone release that make the increase of glucagon, epinephrine, norepinephrine, cortisol, growth hormone and insulin-like growth factor which help to increase blood glucose as well as the increasing in producing inflammatory intermediate factors and cytokines such as TNF-α, IL-1, IL-6. Hyperglycemia result in bad prognostic, nevertheless strict glycemia control causing high risk hypoglycemia. Resonable control of blood glucose in critical illness patients should be less than 8 - 9 mmol/L. Key words: Blood glucose, critical illness, hyperglycemia due to stress

scholarly journals Chronic pulsatile infusion of growth hormone to growth-restricted fetal sheep increases circulating fetal insulin-like growth factor-I levels but not fetal growth

2003 ◽  
Vol 177 (1) ◽  
pp. 83-92 ◽  
Author(s):  
MK Bauer ◽  
BB Breier ◽  
FH Bloomfield ◽  
EC Jensen ◽  
PD Gluckman ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Growth Factor ◽  
Fetal Growth ◽  
Fetal Blood ◽  
Gh Treatment ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Igf I ◽  
Blood Glucose Concentrations

Intra-uterine growth restriction (IUGR) is a major cause of perinatal mortality and morbidity. Postnatally, growth hormone (GH) increases growth, increases circulating insulin-like growth factor (IGF)-I levels, and alters metabolism. Our aim was to determine if GH infusion to IUGR fetal sheep would alter fetal growth and metabolism, and thus provide a potential intra-uterine treatment for the IUGR fetus. We studied three groups of fetuses: control, IUGR+ vehicle and IUGR+GH (n=5 all groups). IUGR was induced by repeated embolisation of the placental vascular bed between 110 and 116 days of gestation (term=145 days). GH (3.5 mg/kg/day) or vehicle was infused in a pulsatile manner from 117 to 127 days of gestation. Embolisation reduced fetal growth rate by 25% (P<0.01) and reduced the weight of the fetal liver (20%), kidney (23%) and thymus (31%; all P<0.05). GH treatment further reduced the weight of the fetal kidneys (32%) and small intestine (35%; both P<0.04), but restored the relative weight of the fetal thymus and liver (P<0.05). Embolisation decreased fetal plasma IGF-I concentrations (48%, P<0.001) and increased IGF binding protein 1 (IGFBP-1) concentrations (737%, P<0.002). GH treatment restored fetal plasma IGF-I concentrations to control levels, while levels in IUGR+vehicle fetuses stayed low (P<0.05 vs control). IGFBP-1 and IGFBP-2 concentrations were about sevenfold lower in amniotic fluid than in fetal plasma, but amniotic and plasma concentrations were closely correlated (r=0.75, P<0.0001 and r=0.55 P<0.0001 respectively). Embolisation transiently decreased fetal blood oxygen content (40%, P<0.002), and increased blood lactate concentrations (213%, P<0.04). Both returned to pre-embolisation levels after embolisation stopped, but blood glucose concentrations declined steadily in IUGR+vehicle fetuses. GH treatment maintained fetal blood glucose concentrations at control levels. Our study shows that GH infusion to the IUGR fetal sheep restores fetal IGF-I levels but does not improve fetal growth, and further reduces the fetal kidney and intestine weights. Thus, fetal GH therapy does not seem a promising treatment stratagem for the IUGR fetus.

scholarly journals Growth hormone-releasing peptide-2 infusion synchronizes growth hormone, thyrotrophin and prolactin release in prolonged critical illness

1999 ◽  
pp. 17-22 ◽  
Author(s):  
G Van den Berghe ◽  
P Wouters ◽  
CY Bowers ◽  
F de Zegher ◽  
R Bouillon ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Critical Illness ◽  
Cross Correlation ◽  
Pituitary Hormone ◽  
Hormone Release ◽  
Prolactin Release ◽  
Anterior Pituitary Hormone ◽  
Temporal Coupling ◽  
Pituitary Secretion ◽  
Design And Methods

OBJECTIVE: During prolonged critical illness, nocturnal pulsatile secretion of GH, TSH and prolactin (PRL) is uniformly reduced but remains responsive to the continuous infusion of GH secretagogues and TRH. Whether such (pertinent) secretagogues would synchronize pituitary secretion of GH, TSH and/or PRL is not known. DESIGN AND METHODS: We explored temporal coupling among GH, TSH and PRL release by calculating cross-correlation among GH, TSH and PRL serum concentration profiles in 86 time series obtained from prolonged critically ill patients by nocturnal blood sampling every 20 min for 9 h during 21-h infusions of either placebo (n=22), GHRH (1 microg/kg/h; n=10), GH-releasing peptide-2 (GHRP-2; 1 microg/kg/h; n=28), TRH (1 microg/kg/h; n=8) or combinations of these agonists (n=8). RESULTS: The normal synchrony among GH, TSH and PRL was absent during placebo delivery. Infusion of GHRP-2, but not GHRH or TRH, markedly synchronized serum profiles of GH, TSH and PRL (all P< or =0.007). After addition of GHRH and TRH to the infusion of GHRP-2, only the synchrony between GH and PRL was maintained (P=0.003 for GHRH + GHRP-2 and P=0.006 for TRH + GHRH + GHRP-2), and was more marked than with GHRP-2 infusion alone (P=0.0006 by ANOVA). CONCLUSIONS: The nocturnal GH, TSH and PRL secretory patterns during prolonged critical illness are herewith further characterized to include loss of synchrony among GH, TSH and PRL release. The synchronizing effect of an exogenous GHRP-2 drive, but not of GHRH or TRH, suggests that the presumed endogenous GHRP-like ligand may participate in the orchestration of coordinated anterior pituitary hormone release.

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