ESPE Abstracts

Background: GH has several effects on lipid and glucose homeostasis. In adults GH deficiency (GHD) has been associated to increased mortality for cardiovascular disease (CVD). In childhood few studies have investigated the effect of GHD and recombinant human GH (rhGH) therapy on metabolic parameters that may increase the risk of CVD.

Objective and hypotheses: To assess changes of lipid profile, insulin-resistance indexes, and CVD risk in children and adolescents with GHD before, during, and after rhGH therapy.

Method: Forty-six subjects (11.3±2.28 years old; 25 boys) with GHD were studied. All patients underwent to fasting blood samples in order to assess glycemia (G), insulin (I), total cholesterol, LDL, HDL, triglycerides, and IGF1. Moreover, G/I ratio, HOMA-IR, and atherogenic index (AI) were calculated. All data were collected at diagnosis (T₀), during rhGH therapy (T₁ 1-year, rhGH dose 0.034±0.003 mg/kg per day; T₂ 2-year, rhGH 0.030±0.003 mg/kg per day; T₃ stop-therapy, and rhGH 0.028±0.004 mg/kg per day), and at 1-year off-therapy (T₄). Longitudinal data were analyzed using Friedman ANOVA and are reported as mean±S.D.

Results: We demonstrated a significant increased of insulin levels (T₀ 6.65±4.17, T₁ 13.4±5.19, T₂ 10.2±2.55, T₃ 16.1±6.76, T₄ 9.07±4.05 μIU/ml; χ²=36.8, P<0.0001) and HOMA-IR (1.41±0.88, 2.91±1.27, 2.20±0.61, 3.65±1.88, and 1.91±0.91; χ²=34.0, P<0.0001). A significant decreased of G/I ratio (18.1±10.7, 7.27±2.44, 9.40±3.88, 6.50±2.92, and 11.9±7.31; χ²=34.4, P<0.0001) and HDL levels (61.6±15.3, 62.1±15.2, 65.2±10.1, 56.0±17.7, and 52.8±16.6 mg/dl; χ²=13.3, P=0.0100) was also found. AI was not significantly changed (2.77±0.52, 2.73±0.48, 2.69±0.43, 3.00±0.78, and 3.12±0.74; χ²=4.69, P=0.3208)

Conclusion: GHD was not associated with impaired lipidic and glycemic metabolism. During rhGH treatment we demonstrated a significant worsening of insulin-resistance indexes and HDL values despite they were always in the normal range. No change of AI was found. GHD and rhGH therapy seem not to impair CVD metabolic risk factors.