The effects of growth hormone administration on the markers of cardiovascular disease in growth hormone deficient adults / 대한내과학회지

ABSTRACT

BACKGROUND: Subjects with growth hormone-deficiency (GHD) have increased cardiovascular mortality, and growth hormone (GH) replacement may modulate cardiovascular disease risk. Therefore, we evaluated the effects of GH administration on the markers of cardiovascular disease in subjects with GHD. METHODS: 37 subjects (12 men and 25 women) with GHD and 65 normal subjects were enrolled in this study. GH or placebo were given for 3 months at a dose adjusted for normal serum insulin-like growth factor-I (IGF-I) level. Height, weight, waist circumference, hip circumference, lean body mass, fat mass, blood pressure, fasting blood glucose, IGF-I, lipid profile, uric acid, C-reactive protein (CRP), plaminogen activator inhibitor-1 (PAI-1), apolipoprotein AI, and quality of life-assessment of growth hormone deficiency in adults (QoL-AGHDA) were measured at baseline and month 3. RESULTS: Subjects with GHD showed higher levels of triglyceride, CRP, and PAI-1, but lower level of fasting glucose than normal subjects. Fat mass, CRP, and PAI-1 levels decreased in GH recipients (fat mass; 21.9+/-6.6 to 21.3+/-6.7%, p<0.05, CRP; 2.73+/-2.11 to 1.47+/-1.29 mg/L, p<0.001, PAI-1; 48.9+/-33.2 to 31.6+/-28.5 ng/mL, p<0.05). Fasting blood glucose and total cholesterol levels increased in GH recipients (fasting blood glucose; 4.58+/-0.46 to 4.81+/-0.36 mmol/L, p<0.05, total cholesterol; 5.36+/-1.31 to 6.17+/-1.12 mmol/L, p<0.01). Placebo recipients showed decrease in waist-hip ratio (0.93+/-0.05 to 0.92+/-0.04, p<0.05) and increase in fasting blood glucsoe (4.63+/-0.38 to 4.89+/-0.45 mmol/L, p<0.05) and uric acid (319.6+/-89.2 to 335.6+/-89.2 micro mol/L, p<0.05). QoL-AGHDA score improved in both groups (GH recipients; 10.0+/-6.0 to 7.4+/-5.5, p<0.01, placebo recipients; 9.8+/-4.4 to 6.7+/-3.4, p<0.05). CONCLUSION: Our results demonstrated favourable effects of GH on cardiovascular disease through modulating CRP and PAI-1 plasma level in subjects with GHD.