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In children with growth disorders, mean final height is associated to poor adherence to Growth Hormone therapy. The primary goal of this study is to identify patients who do not adhere to GH therapy and determine the influence of adherence in response to the treatment. The role of serum IGF-I and influence of socio-economic factors on the therapeutic adherence will also be evaluated.158 children under treatment with rhGH were included in the study. Age, gender, etiology, Tanner stage, duration of treatment, growth rate, IGF-I serum values, daily dose, and annual rhGH dose data were collected. Adherence to therapy was defined as moderate-to-poor when the patient had taken less than 92% of the prescribed medication. A subgroup of 106 patients completed a questionnaire to assess social and environmental effects.Moderate-to-poor adherence to rhGH treatment was determined in 33.5% of study patients. A decrease in adherence was associated to treatment duration (p=0.001). A significant correlation was determined between adherence and height velocity (p=0.002) and IGF-I (p0.0001) levels. Adherence rates were associated to the mother's educational level (p=0.007).Poor adherence to GH therapy was observed in one-third of study patients, resulting in suboptimal growth. IGF-I levels can be helpful to identify patients with poor adherence to GH medication. Physicians should pay special attention to certain characteristics of the patient and their environment, and encourage desirable therapeutic compliance.

We wanted to examine the relationship between initial growth response to recombinant human Growth Hormone (rhGH) treatment and body composition in children with growth hormone deficiency (GHD).Forty-two patients (21 boys and 21 girls) aged between 5.7-15.5 years (mean age: 10.8 ± 2.6 years) with isolated GHD. The auxological and laboratory data (GH and IGF-I levels) and results of bioelectrical impedance analyses were evaluated. Children with GHD were followed up for 12 months and categorized according to growth response to rhGH into good and poor responders (change in height of0.7 SDS or0.7 SDS over one year respectively). Mean doses of rhGH per kg of fat free mass (FFM) were calculated.Forty-eight percent of patients showed a good growth response to rhGH therapy. At study entry, mean age, height SDS, weight SDS, serum IGF-1 SDS, IGFBP-3 SDS, growth velocity prior to rhGH therapy, GH after clonidine and l-dopa were similar in the two groups. At baseline, BMI SDS and waist-hip ratio were significantly higher in good responders (p = 0.02 and p = 0.006, respectively). Good responders had lower percentages of FFM (73.4 ± 8.9 vs. 83.1 ± 5.9) and total body water (TBW) (56.5 ± 5.3 vs. 63.1 ± 4.4), compared to poor responders (p0.05). There were significant correlations between changes in height SDS over one year and baseline body composition in children with GHD on rhGH treatment (r = -0.617 for percentage of FFM, r = -0.629 for percentage of TBW, p0.001). A correlation between BMI SDS, waist-hip ratio, mean rhGH dose per FFM and growth response was observed only in prepubertal subjects.Baseline body composition data in children with GHD can be used to predict the growth response to rhGH treatment. A management strategy that involves titrating rhGH dose according to FFM as a means of optimizing the growth response to intervention requires further study.

Growth hormone (GH) has been implicated as an important factor in the growth regulation of several visceral organs including the gastrointestinal tract. Our aim was to study the effects of GH administration on colonic growth in dwarf rats with an isolated GH deficiency. Dwarf rats were treated with recombinant human growth hormone (rhGH; 2.0 mg/kg/day) for four weeks and compared with saline treated dwarf rats and rats with normal pituitary function. The colonic wall composition was measured by means of stereological techniques. RhGH treatment of the dwarf rats increased body weight by 80% and proximal and distal colon weight by 63% and 90%, when compared with placebo treated dwarf rats (P0.01). The weight of the proximal colonic mucosa increased by 83% (P0.01), submucosa by 78% (P0.05), and the muscularis propria by 51% (P0.001) in rhGH treated dwarf rats compared with dwarf controls. The weight of the distal colonic mucosa increased by 88% (P0.01), submucosa by 88% (P0.05) and the muscularis propria by 58% (P0.05) compared with dwarf controls. The growth of mucosa involved all mucosal layers, with a 73 and 92% increase in the proximal and distal colon luminal surface area respectively (P0.001, P0.01). The food consumption, expressed as g/day/100 g BW was 13% higher in dwarf rats receiving rhGH than in placebo treated rats (P0.05) and normal control rats (P0.05). When weights of the GI tract compartments are corrected for the increase in body weight the effects of GH treatment were small or non-significant. RhGH administration in GH deficient dwarf rats induces visceral growth with a pronounced increase in colonic luminal surface area and growth of all layers of the colonic wall. These findings confirm the important role of GH in the regulation of intestinal growth.

levels did not differ (patients vs. controls: 701±87 vs. 572±33mg/l, P =0.17), whereas bioactive IGF-I tended to be lower in patients (5.37±0.55 vs. 6.63±0.25mg/l, P < 0.06). Conclusion: The baseline findings of elevated free GH and low bioactive IGF-I support the concept of GH resistance in uremic hemodialysis patients. Using high dose rhGH treatment it was possible to obtain normal responses in total and bioactive IGF-I levels, showing that the GH resistance may be overcome. Nevertheless, our data imply that the response of bioactive IGF-I to GH is subnormal in hemodialysis patients.