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The growth response during short-term growth hormone (GH) treatment was evaluated in eight prepubertal non-GH-deficient (non-GHD) children and compared with six prepubertal GH-deficient (GHD) patients. Standard doses of GH can improve growth rate in GHD and in some non-GHD patients. In neither group the growth response can be predicted by the acute increase in Thymidine Activity or Somatomedin-C levels. A diagnostic trial of GH treatment may be the only certain method of selecting the short non-GHD patients who may benefit from long-term GH therapy.

Twenty-five GH-deficient children were treated with GHRH (1-44), once daily sc for 6–24 months. At the 6th month of therapy, 40% of our patients showed a catch-up growth (responded), while the remaining 60% did not (nonre-sponders). No differences in auxological and biological variables at inclusion were found between the two groups. However, integrated GH secretion elicited by iv GHRH at inclusion was significantly (p<0.025) higher in responders than in non responded. During GHRH therapy, no significant increase in IGF 1/SmC was found in both groups. In all patients treatment was discontinued after 6–24 months, when its effect on growth rate failed. After a wash-out period of at least 6 months, patients were submitted to biosynthetic GH therapy. After 6 months of GH treatment a significant catch-up growth was found in both responder and non-responder children. Although the majority of GH-deficient children have hypothalamic rather than pituitary dysfunction, GHRH therapy is found to be less effective than GH treatment. Other methods of GHRH administration are worth investigating.

The effect of long-term human chorionic gonadotropin (HCG) therapy on the linear growth and biological growth parameters was studied in six thalassaemic boys aged 14.5–15.5 years old with hypogonadotropic hypogonadism. A significant (P<0.001) increase in growth velocity (from 3.3±0.3 to 7.6±0.6 cm/year) was found after 6–12 months of therapy, without acceleration of bone age. A striking improvement in pubertal development was observed. The treatment significantly increased growth hormone (GH) response to l-dopa administration (P<0.025) as well as sleep GH secretion (P<0.025). Serum growth factors, evaluated as thymidine activity during deep sleep, increased (P<0.001), but somatomedin C (Sm-C) levels did not. Prior to treatment, baseline and peak values of plasma growth hormone releasing hormone (GH-RH) following l-dopa were low. After HCG therapy, GH-RH response to l-dopa increased significantly (from 9.2±5.6 to 20.2±6.2 pg/ml; P<0.05), but remained (P<0.001) lower than in normal prepubertal children. This study suggests that in thalassaemia major an impaired GH-RH release can be observed, in addition to the described alteration in Sm-C generation.

The ability of GH to influence humoral and cell-mediated immunity was evaluated in 21 GH-deficient children, 1.8-17.7 yr, before and during therapy with biosynthetic GH (Somatonorm)(12U/mq)im injected three times weekly. Blood was collected prior to GH treatment (Gr. A), then following the 1stweek (Gr. B), then again at the 3rd-6thmonth (Gr. C), and finally at the 9th-12thmonthth of therapy. Cell-mediated immunity was assessed by quantititation of T lymphocyte subpopulations (T total, helper and suppressor cells) using monoclonal antibodies (OKT3, OKT4, OKT8). No variations in serum immunoglobulin levels were observed throught treatment period. Pretreatment OKT3, OKT4, OKT8 values (Gr. A) were within the normal range and did not change after the 1stweek of GH therapy (Gr. B). However, following 3–6 month GH treatment (Gr. C), OKT3 significantly increased (70.61 ± 1.84 vs 78.38±1.14, p < 0.001), OKT4 decreased (46.71±1.81 vs 40.23±2.09, p<0.01), OKT8 increased (25.00±1.44 vs 34.09±1.71, p<0.001) and OKT4/OKT8 ratios decreased (2.01±0.16 vs 1.34±0.10, p<0.001). At the 9th-12thmonth of therapy (Gr. D), the percentage of T cells was not significantly different from pretreatment values. Our data suggest some relationship between GH and thymic-dependent immune function.

The aim of this study was to evaluate with magnetic resonance imaging (MRI) the hypothalamic and pituitary structures in patients with idiopathic isolated growth hormone deficiency (GHD) or multiple pituitary hormone deficiencies (MPHD).MRI was performed in 16 patients with GHD (9 boys and 7 girls, aged 10.9 to 16.9 years) who developped a normal puberty and 15 patients with MPHD (13 boys and 2 girls, aged 11.3 to 25 years) including gonadotrophins deficiency.In 11/15 MPHD patients an ectopic, but normally active, neurohypophys was detected, while in the remaining 4 cases the high intensity signal of the neurohypophysis was absent. In the 16 patients with GHD, the signal of the neurohypophysis was normal.Moreover the pituitary height on MRI, ranging from 1 to 5 mm (2.80 ± SEM 0.34 mm) in MPHD was significantly lower (p< 0,0001) than in GHD patients (4.37 ± SEM 0.13 mm).These results suggest that MRI is useful in the investigation of idiopathic hypopituitarism : the finding of an ectopic or absent neurohypophysis together with a reduced height pituitary gland seem specific of MPHD.