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. 2013 Mar 20;4:34. doi: 10.3389/fendo.2013.00034

Table 2.

Alterations during transition phase in CO-GHD patients.

Author N (age, years) Body composition IGF-I BMD Muscle QoL Serum lipids Carbohydrate metabolism Other parameters
Johannsson et al. (1999) 56 (16–20) ↓ LBM and ↑ BF both in severe GH deficiency patients and in those having sufficient endogenous GH secretion (more marked than in controls), ↑ of truncal fat in GHD subjects ↓IGF1 after 2 year off-therapy in subjects with severe GHD NA NA NA ↓ HDL-c and ↓ TG in GHD group ↓ Serum insulin both in severe GH deficiency patients and in those having sufficient endogenous GH secretion No changes in FT4 and FT3 concentrations ↓ SBP in patients having sufficient GH secretion
Nørrelund et al. (2000) 18 (20 ± 1) ↑ TBF in placebo group; ↑ FFM when GH therapy is restarted in placebo group NA NA NA NA ↓ Rates of lipid oxidation in placebo group ↑ IS in placebo group; ↓ IS when GH therapy is restarted
Vahl et al. (2000) 19 (20.2 ± 0.65) TBF and WC ↑ in placebo group ↓ In placebo group NA No significant changes Placebo group have lower total score ↑ HDL-c in the GH group ↓ Fasting glucose in the placebo group ↓ Of FT3 in placebo group
Lanes et al. (2001) 19 (Ut: 14.2 ± 2.8; T: 14.4 ± 2.6) NA NA NA NA NA LDL-C and lipoprotein(a) > in untreated patients compared to controls NA No differences in mass and cardiac function between groups
Colao et al. (2002) 20 (17–20) NA ↓ in GHD subjects after 6 months off-therapy NA NA NA ↑ TG, ↑ LDL, ↑ total/HDL cholesterol ratio in GHD patients after stop therapy No changes ↓ LVM, ↑ fibrinogen levels,↓ E/A in GHD subjects off-therapy
Attanasio et al. (2002) 127 (CO: 20.9 ± 2.4; AO: 25.2 ± 3) CO-GHD patients have <BMI, <LBM, <FM than AO-GHD IGF1 is < in CO-GHD than AO-GHD CO-GHD show < BMC NA NA NA NA
Drake et al. (2003) 24 (17 ± 1.4) NA NA ↑ BMC and mean lumbar BMD in ongoing GH subjects NA NA NA NA
Shalet et al. (2003) 149 (AD: 19.4 ± 2.7; PD: 19.6 ± 2.8) NA A dose-dependent ↑ Total BMC ↑ in treated groups, predominantly at the lumbar spine NA NA NA NA ↑ Bone-specific alkaline phosphatase in GH-treated group
Underwood et al. (2003) 64 (23.8 ± 4.2) ↑ FM in placebo group; ↓ FM in GH-treated group ↑ In high GH dose treated group-dose Dose-related ↑ spine BMD NA No significant effects among groups ↓ LDL in high GH dose treated group NA No changes in cardiac structure or function
Attanasio et al. (2004) 139 (AD: 19.4 ± 2.7; PD: 19.6 ± 2.8) ↑ LBM in GH-treated patients, ↓ fat mass No differences among groups NA NA NA ↑ Total C and LDL/HDL ratio in non GH-treated patients; ↓ LDL/HDL-C in pediatric dose subjects NA
Carroll et al. (2004) 24 (17 ± 0.3) ↑ LBM in GH-treated patients ↓ IGF1 in patients off-therapy NA NA NA No differences between two groups ↑ Is after GH cessation
Mauras et al. (2005) 58 (15.8 ± 1.8) No differences between groups Less reduction in GH-treated group (no significative) No differences between groups No differences between groups No differences between groups No differences between groups No differences between groups
Koltowska-Häggström et al. (2010) 313 (IGHD: 17.5 ± 1.84; NON-IGHD: 17.1 ± 1.91) NA ↑ After 1 year of GH treatment NA NA A longer GH gap is associated with a poorer QoL A longer duration of GH interruption was associated with a worse lipid profile in non-IGHD patients NA
Bazarra-Castro et al. (2012) 75 (<25) ↑ BMI during GH therapy pause NA NA NA NA NA NA

LBM, lean body mass; BF, body fat; TG, triglycerides; SBP, systolic blood pressure; TBF, total body fat; FFM, fat-free mass; IS, insulin sensitivity; WC, waist circumference; LVM, left ventricular mass; E/A, early-to-late mitral flow velocity ratio; BMI, body mass index; LBM, lean body mass; FM, fat mass; BMC, bone mineral content; BMD, bone mineral density; QoL, quality of life; Ut, untreated group; T, treated group; CO, childhood-onset GHD; AO, adult onset GHD; AD, adult dose; PD, pediatric dose; IGHD, idiopathic GHD; NON-IGHD, non-idiopathic GHD.