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Franco Antoniazzi, Francesco Bertoldo, Giorgio Zamboni, Roberta Valentini, Stefania Sirpresi, Luciano Cavallo, Silvano Adami and Luciano Tato

Antoniazzi F, Bertoldo F, Zamboni G, Valentini R, Sirpresi S, Cavallo L, Adami S, Tatò L. Bone mineral metabolism in girls with precocious puberty during gonadotrophin-releasing hormone agonist treatment. Eur J Endocrinol 1995;133:412–7. ISSN 0804–4643

Bone mineral metabolism and mineralization before and during treatment were studied in 10 girls aged 6.9–8.4 years affected by central precocious puberty and treated with gonadotrophin-releasing hormone agonist (GnRHa) leuprolide acetate depot, in order to understand better the consequences of oestrogen deficiency and the reduction of growth hormone (GH)–insulin-like growth factor I (IGF-I) axis activity. Before and after 12 months of therapy, the patients underwent a clonidine stimulation test and a 4-day calcitriol osteoblast stimulation test. On day 0, day 5 and at 3-month intervals thereafter, serum calcium, phosphate, alkaline phosphatase, IGF-I, IGF binding protein 3 (IGFBP-3), GH, GH binding protein and osteocalcin levels were measured; urinary calcium, phosphate and hydroxyproline levels were evaluated in fasting spot samples. Trabecular and cortical bone mass variations, measured by dual X-ray absorptiometry in the lumbar spine and by dual photon absorptiometry in the radius, respectively were evaluated before the start and after 12 months of therapy. During treatment, a decrease of serum oestradiol levels from pubertal to prepubertal levels was observed. The GH peak following clonidine diminished significantly after 1 year. Growth hormone binding protein showed a slight increase, and IGF-I and IGFBP-3 decreased, although not significantly. Osteocalcin levels decreased significantly after 9 and 12 months of treatment, but they did not change significantly after calcitriol load, either before or after GnRHa therapy. Urinary hydroxyproline decreased significantly after 12 months. Before therapy, lumbar spine and radius bone mass were high for chronological age but appropriate for bone age; after 12 months of treatment, bone mass in the lumbar spine, but not in the radius, had decreased significantly. In our patients, regression of pubertal development was associated with a reduction of trabecular bone mass, which appears to be the primary consequence of GnRHa therapy and possibly related to decreased GH secretion.

Franco Antoniazzi, Clinica Pediatrica, Università di Verona, Policlinico Borgo Roma, 1-37134 Verona, Italy

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Claudio Maffeis, Roberto Franceschi, Paolo Moghetti, Marta Camilot, Silvana Lauriola and Luciano Tatò

Decreased levels of ghrelin have been measured in growing children during puberty. No data are available for girls with central precocious puberty (CPP).

Aims: To explore ghrelin changes before, during, and after GnRH analog treatment in girls with CPP.

Subjects and methods: A sample of 20 Caucasian girls (8.08 ± 0.65 years of age) with CPP was recruited. Height and weight, bone age, LH, FSH, 17β estradiol (E2), and ghrelin were measured before starting treatment with GnRH analog, 18 months after therapy began and again 6 months after therapy discontinuation.

Results: LH and E2 serum levels decreased significantly during treatment (2.45 ± 2.03 vs 0.67 ± 0.49 UI/l, P < 0.01 and 28.17 ± 9.7 vs 15 pmol/l, P < 0.01 respectively), returning to baseline levels after the discontinuation of therapy (4.75 ± 1.66 UI/l and 29.23 ± 6.99 pmol/l respectively). LH peaked following LHRH stimulation significantly (P < 0.01) decreased during treatment (24.45 ± 14.17 vs 1.3 ± 0.18 UI/l) and then increased after therapy discontinuation (12.58 ± 6.09, P < 0.01). Ghrelin decreased significantly (P < 0.05) during treatment (1849 ± 322 vs 1207 ± 637 pg/ml), and increased, though not significantly (P = 0.09) after therapy withdrawal (1567 ± 629 pg/ml).

Conclusions: Contrary to what is expected in physiologic puberty, where ghrelin is progressively reduced, the prepubertal hormone milieau induced by GnRHa treatment in patients suffering from central precocious puberty (CPP) did not promote an increase in ghrelin circulating levels. Therefore, in CPP, ghrelin secretion seems to be independent from pubertal development per se. Concomitant estrogen suppression during treatment may play a potential role in the regulation of ghrelin secretion in these girls.

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Franco Antoniazzi, Elena Monti, Giacomo Venturi, Roberto Franceschi, Francesco Doro, Davide Gatti, Giorgio Zamboni and Luciano Tatò


To verify the effects of bisphosphonates (Bps) in combination with recombinant human GH (rGH) in pediatric osteogenesis imperfecta (OI) patients; we focused on possible improvement of bone mineral density (BMD), projected bone areas, growth velocity, and fractures risk.


A randomized controlled 1-year clinical trial on 30 prepubertal children (M:F=14:16) affected by OI (type I, IV, and III) being treated with neridronate.


Following an observational period of 12 months during ongoing neridronate treatment, the patients were randomly divided into two groups: 15 were treated for 12 months with rGH and neridronate (group Bp+rGH) and 15 continued neridronate alone (group Bp). We evaluated auxological parameters, number of fractures, bone age (BA), bone metabolic parameters, and bone mass measurements (at lumbar spine and radius by dual-energy X-ray absorptiometry).


The mean variation in percentage of BMD (Δ%BMD) – at lumbar spine (L2–L4), at distal and ultradistal radius – and the projected area of lumbar spine increased significantly in group Bp+rGH (P<0.05). Growth velocity was significantly higher during rGH treatment in group Bp+rGH versus group Bp and versus pretreatment (P<0.05), with no difference in increase in BA or fracture risk rate. Patients with quantitative (-qt) collagen synthesis defects had a higher, although not significant, response to rGH in terms of growth velocity and BMD.


In OI patients, the combined rGH–Bp treatment may give better results than Bp treatment alone, in terms of BMD, lumbar spine projected area and growth velocity, particularly in patients with quantitative defects.

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Claudio Maffeis, Riccardo C Bonadonna, Alessandro Consolaro, Roberto Vettor, Claudia Banzato, Davide Silvagni, Giovanna Bogoni, Maristella Pellegrino and Luciano Tatò

Objective: To explore the changes of ghrelin circulating levels induced by a mixed meal and their relationship with postprandial substrate oxidation rates in overweight and obese children with different levels of insulin sensitivity.

Methods: A group of ten boys (age 9–12 years) with different levels of overweight (standard deviation score of body mass index: 1.6–3.2) was recruited. Body composition was measured by dual-energy X-ray absorptiometry. Insulin sensitivity was assessed by a frequently sampled i.v. glucose tolerance test. Pre-prandial and postprandial (3 h) substrate oxidation was measured by indirect calorimetry. The energy content of the test meal (16% protein, 36% carbohydrate and 48% fat) was 40% of pre-prandial energy expenditure (kJ/day).

Results: Pre-prandial serum concentration of total ghrelin was 701.4±66.9 pg/ml (S.E.M.). The test meal induced a rapid decrease in ghrelin levels and maximal decrease was 27.3±2.7% below baseline. Meal intake induced a progressive increase of the carbohydrate oxidation rate for 45 min after food ingestion, followed by a slow decrease without returning to pre-prandial values. Postprandial cumulative carbohydrate oxidation was 16.9±0.8 g/3 h. Insulin sensitivity and postprandial maximal decrease of ghrelin concentration showed a significant correlation (r = 0.803, P < 0.01). Moreover, the postprandial carbohydrate oxidation rate correlated with the area under the curve for both insulin (r = 0.673, P < 0.03) and ghrelin (r = −0.661, P < 0.04).

Conclusions: A relevant association between postprandial insulin-mediated glucose metabolism and ghrelin secretion in children with different levels of overweight was found. It is possible that the maintenance of an adequate level of insulin sensitivity and glucose oxidation may affect appetite regulation by favoring a more efficient postprandial ghrelin reduction.