Bone Abstracts

Aim: To determine the response to treatment, clinical and instrumental features in children with partial GH deficiency (pGHD) and severe GHD (sGHD).

Methods: We examined retrospectively 30 children with isolated GHD (stage on Tanner 1) in the Endocrinological department of University hospital (Minsk) over 2004–2012 years. Group 1 (G1) – children with pGHD (n=5) mean±S.D., age 6.3±1.4 years; group 2 (G2) – sGHD (n=25), 4.8±0.9 years (P=0.4). Children in both groups were treated with GH more than 3 years. Stimulating GH levels, height on the moment of diagnosis (H); bone X-ray with the calculation years of delay relative to chronological age on diagnosis (D1), 1 year (D2), 2 years (D3), and 3 years (D4) of treatment; magnetic resonance imaging (MRI) were analyzed. The results were processed using SPSS 17.

Results: The maximum GH levels (IU/l) in clonidine sample G1 was 14.8±0.5, G2 6.2±0.6 (P=0.6), insulin sample 5.7±1.5 and 5.6±0.4 (P=0.8). G1 was treated with GH in the average dose 0.75±0.3 mg/day, G2 0.7±0.3 (P=0.5). H G2 3rd percentile was in 5 (100%) children; G1 <3 percentile was in 13(52%), 3rd 9(36%), and 10th 3(12%) children.

Six (24%) children in G2 had been confirmed pituitary pathology by MPI (two microadenoma and four pituitary hypoplasia), G1 microadenoma in one patient.

Maturation by X-ray was delayed in both groups, the dynamics G2: D1 3.1±1.7, D2 2.4±1.2, D3 2.1±0.4 (p(D1–D2)=0.2), (p(D2–D3)=0.3), and (p(D1–D3)=0.4); G1: D1 2±1.4, D2 1.5±0.5, D3 1±0.5 (p(D1–D2)=0.1), (p(D2–D3)=0.01), and (p(D1–D3)=0.01).

Conclusions: We didn’t notice the reliable differences of bone age retardation in children with sGHD at the age of diagnosis and all years of treatment. There were the reliable reducing of bone age retardation in group with pGHD between the beginning of the treatment, 2nd (P=0.01) and 1st years (P=0.01).