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Biomedical subjects

Giuseppe Saggese

Publications and source records attributed to Giuseppe Saggese.

11 recordsLinked to original sources
PubMed2004

Relationships of serum leptin levels with biochemical markers of bone turnover and with growth factors in normal weight and overweight children.

OBJECTIVE: To examine the hypothesis of an influence of leptin on growth factors and on biochemical markers of bone turnover of prepubertal overweight children. DESIGN AND METHODS: 395 prepubertal children, 6-13 years of age, were selected and the relationships between circulating serum levels of leptin and insulin-like growth factor I (IGF-I), insulin growth factor binding protein-3 (IGFBP-3) and some biochemical markers of bone turnover (osteocalcin, OC; carboxyterminal propeptide of type I procollagen, PICP, and carboxyterminal propeptide of type I collagen, ICTP) were analyzed. The subjects were subdivided into normal weight (NW, n = 163) and weight excess (WE, n = 232) subjects. RESULTS AND CONCLUSIONS: Significant differences between the two groups were found for leptin (p < 0.01), IGF-I (p < 0.01) and IGFBP-3 (p < 0.01), with higher values in WEs, and for OC (p < 0.01) with higher values in NWs. A significant reduction of leptin (p < 0.01) and IGFBP-3 (p < 0.01) serum values and an increase of those of OC (p < 0.01) and PICP (p < 0.05), but not of ICTP, were registered in 103 WEs who showed a drop in weight excess during a weight-excess reduction program. No variations were observed in 26 non-responsive subjects. In a multivariate analysis in which leptin, corrected by BMI and sex, was the independent variable, a significant negative correlation was found with PICP (beta = -0.235, p < 0.01), IGF-I (beta = -0.180, p < 0.01) and height velocity (beta = -0.155, p < 0.01). There was no correlation with OC, ICTP and IGFBP-3. The results demonstrate that nutritional status and leptin levels are involved in the regulation of growth factors and biochemical markers of bone formation.

Anthropometry↗
PubMed2004

Longitudinal changes of lumbar bone mineral density (BMD) in patients with GH deficiency after discontinuation of treatment at final height; timing and peak values for lumbar BMD.

OBJECTIVE: GH treatment has an important role in the acquisition of bone mass in children and adolescents with GH deficiency (GHD). However, there is no information concerning the timing and value of peak bone mass in treated patients with GHD. In adolescents with GHD we longitudinally measured lumbar bone mineral density (BMD) after discontinuation of GH treatment at final height until they achieved lumbar peak BMD (pBMD). Moreover, the changes of lumbar BMD after the attainment of the peak were assessed for a period of 2 years. The results of patients were compared with those obtained in age- and sex-matched healthy controls. PATIENTS AND MEASUREMENTS: Lumbar BMDarea [bone mineral content (BMC) corrected by the vertebral surface area scanned] and lumbar BMDvolume (BMC corrected by vertebral volume estimated by a mathematical model), by dual energy X-ray absorptiometry, were assessed in 16 patients (nine males, seven females; aged 14.9-18.8 years) with isolated GHD and 157 healthy subjects (78 males, aged 16.2-24.9 years; 79 females, aged 14.1-22.8 years) as controls. In patients, lumbar BMDarea and lumbar BMDvolume were measured at final height and approximately every year up to 21-24 years and 19-22 years in males and females, respectively; BMD values of the patients were plotted on the reference curves for age and sex obtained in controls. RESULTS: At final height, seven male (78%) and five female (71%) patients had a value for lumbar BMDarea below 2SD of normal mean, whereas all patients had a value of lumbar BMDvolume between 0 and -2SD of normal mean. In patients, lumbar pBMDarea and lumbar pBMDvolume were achieved approximately 1-3 years after final height. The timing of lumbar pBMDarea and lumbar pBMDvolume was significantly (P < 0.0001) delayed in patients in comparison with controls (pBMDarea: males, 19.8 +/- 0.6 years and 18.4 +/- 0.6 years; females, 18.0 +/- 0.3 years and 16.7 +/- 0.6 years, respectively; pBMDvolume: males, 19.8 +/- 0.7 years and 18.6 +/- 0.6 years; females, 18.0 +/- 0.4 years and 16.7 +/- 0.6 years, respectively). In addition, mean values for lumbar pBMDarea and lumbar pBMDvolume were significantly (P < 0.01 to P < 0.0001) reduced in patients compared with controls (pBMDarea: males, 1.129 +/- 0.055 g/cm2 and 1.225 +/- 0.048 g/cm2; females, 1.122 +/- 0.053 g/cm2 and 1.227 +/- 0.060 g/cm2, respectively; pBMDvolume: males, 0.326 +/- 0.010 g/cm3 and 0.352 +/- 0.036 g/cm3; females, 0.348 +/- 0.010 g/cm3 and 0.388 +/- 0.039 g/cm3, respectively). In patients, mean values of lumbar BMDvolume declined significantly (P < 0.03 to P < 0.01) 2 years after its peak. At any rate, mean values of lumbar BMDarea and lumbar BMDvolume of patients one and two years after their peak remained significantly lower (P < 0.01 to P < 0.0001) than those of controls. CONCLUSIONS: The results show that treated adolescents with GHD have an increase of lumbar BMDarea and lumbar BMDvolume after discontinuation of GH treatment at final height, but they have delayed timing and reduced mean values of lumbar pBMDarea and lumbar pBMDvolume in comparison with controls. In patients, mean values of lumbar BMDvolume declined 2 years after its peak. Although the number of the patients was small, the results seem to indicate that GH has a role in the acquisition of lumbar BMD after final height in patients with GHD, suggesting that GH treatment should be continued up to the achievement of lumbar pBMD.

Absorptiometry, Photon↗
PubMed2003

Assessment of bone quality by quantitative ultrasound of proximal phalanges of the hand and fracture rate in children and adolescents with bone and mineral disorders.

Bone quality by quantitative ultrasound and fracture rate were assessed in 135 (64 males) children and adolescents aged 3-21 y with bone and mineral disorders such as chronic anticonvulsants or glucocorticoids treatment, juvenile rheumatoid arthritis, celiac disease, paucity of intrahepatic bile ducts, autoimmune hepatitis, genetic diseases, idiopathic juvenile osteoporosis, disuse osteoporosis, beta-thalassemia major, survivors of acute lymphoblastic leukemia, liver transplantation, calcium deficiency, and nutritional or X-linked hypophosphatemic rickets. Amplitude-dependent speed of sound through the distal end of the first phalangeal diaphysis of the last four fingers of the hand was measured by an ultrasound device. In the majority of patients cortical area to total area ratio by metacarpal radiogrammetry (n = 120) and lumbar bone mineral density (BMD) by dual-energy x-ray absorptiometry (n = 99) were also assessed. In patients with X-linked hypophosphatemic rickets radial BMD by single-photon absorptiometry instead of lumbar BMD was measured. Mean values of amplitude-dependent speed of sound, cortical area to total area ratio, lumbar BMDarea, or lumbar BMD corrected for bone sizes estimated by a mathematical model (BMDvolume), as well as mean values of radial BMD in patients with X-linked hypophosphatemic rickets, expressed as z score, were significantly reduced (p < 0.0001) in comparison with their reference values (-1.7 +/- 1.0, -2.0 +/- 0.9, -3.0 +/- 1.3, -1.9 +/- 1.0, -2.7 +/- 0.7, respectively). A positive relationship was found between amplitude-dependent speed of sound and cortical area to total area ratio (r = 0.90, p < 0.0001), lumbar BMDarea (r = 0.62, p < 0.0001), or lumbar BMDvolume (r = 0.66, p < 0.0001). Fifty-two patients (38.5%) had suffered fractures in the 6 mo preceding the bone measurements, the radial distal metaphysis being the most frequent fracture site (28.8%). Mean values of amplitude-dependent speed of sound, cortical area to total area ratio, lumbar BMDarea, or lumbar BMDvolume, expressed as z score, of fractured patients were significantly lower (p < 0.0001) than those of fracture-free patients (-2.2 +/- 1.0 and -1.4 +/- 0.8, -2.6 +/- 0.9 and -1.7 +/- 0.7, -3.5 +/- 1.2 and -2.5 +/- 1.0, -2.5 +/- 1.0 and -1.3 +/- 0.7, respectively). Phalangeal quantitative ultrasound may be a useful method to assess bone quality and fracture risk in children and adolescents with bone and mineral disorders.

Adolescent↗
PubMed2003

Pubertal changes in biochemical markers of growth.

Puberty is a crucial period of life during which dramatic hormonal changes induce notable modifications in linear growth, bone mass and body composition. These changes are associated with variations in some biochemical parameters such as markers of bone turnover and leptin, which may reflect changes in bone growth and fat mass, respectively. Children with growth hormone (GH) deficiency have reduced concentrations of bone markers, which increase during GH administration, while the levels of leptin decrease. There have been few studies analysing the behaviour of bone markers during puberty in GH-treated GH-deficient patients and no studies analysing the behaviour of leptin. Results from a longitudinal study showed that there was no change in serum osteocalcin, carboxy-terminal propeptide of type I procollagen, and cross-linked carboxy-terminal telopeptide of type I collagen levels during puberty in GH-treated GH-deficient children. Some studies have shown that changes in markers of bone turnover and leptin after short-term GH treatment may predict the growth response (at 6-12 months) to GH administration in GH-deficient children. At present, insufficient data are available for the clinical use of these parameters as markers of growth response during pubertal development and as predictors of long-term growth response to GH treatment in children with GH deficiency. Nevertheless, the use of more and possibly new markers might improve the accuracy of growth prediction models in the future.

Adolescent↗
PubMed2003

Growth and puberty in Turner's syndrome.

Turner's syndrome is the commonest sex chromosome abnormality in females, resulting from the absence of an X chromosome or the presence of a structurally abnormal X chromosome. Short stature and ovarian failure are the most consistent clinical features and require specific and co-ordinated medical approaches in order to improve final height and well-being in adulthood. High doses of growth hormone (GH) are able to improve adult height in comparison with untreated patients. GH therapy should be started during childhood as soon as the growth curve declines below the 5th percentile and doses adjusted according to clinical response. Some studies reported that combined therapy with GH and an anabolic steroid--oxandrolone--is also beneficial at lower GH doses. Ovarian failure should be treated by appropriate substitutive estrogen therapy. Since estrogen administration may impair growth of patients with Turner's syndrome, the age at beginning of therapy should be individualized taking into consideration potential growth, the need for feminization, bone mineral density and the psychological well-being of each patient. Well co-ordinated endocrine interventions can permit better long-term outcome in adulthood.

Anabolic Agents↗
PubMed2003

Acquisition of bone mass in normal individuals and in patients with growth hormone deficiency.

Children and adolescents with growth hormone (GH) deficiency (GHD) have reduced bone turnover and bone mass in comparison with normal individuals. GH replacement therapy stimulates bone turnover and improves bone mass during childhood and adolescence. At final height, patients with GHD treated with GH have normal mean values of bone mass, but some patients have reduced lumbar BMD (Z score <1) with an increased susceptibility to fractures. Children and adolescents with GHD have approximately a fourfold decreased fracture frequency during treatment in comparison with controls. The changes of bone mass during the transition to adulthood in patients with GHD who discontinued GH treatment after final height are not defined. An increase of lumbar BMD after final height has been reported until 2 years after discontinuation of GH treatment; this could be the result of a spontaneous progression towards peak bone mass or of a persisting effect of GH treatment on bone mass accumulation. GH has an important role in the accrual of bone mass during childhood and adolescence, but the impact of GHD on bone mass during the transiton to adulthood is unknown.

Aging↗
PubMed2002

Puberty and bone development.

Puberty has a key role for bone development. Skeletal mass approximately doubles at the end of adolescence. The main determinants of pubertal gain of bone mass are the sex steroids, growth hormone and insulin-like growth factors (by their effects on bone and muscle mass), 1,25-dihydroxyvitamin D (by stimulating calcium absorption and retention) and muscle mass (by regulating modelling/remodelling thresholds). Calcium intake is an additional factor influencing bone formation. The interactions among these factors are undefined. The accrual of bone mass during puberty is a major determinant of peak bone mass and, thereby, of the risk of osteoporotic fractures during advanced age.

Adolescent↗
PubMed2002

Lumbar bone mineral density at final height and prevalence of fractures in treated children with GH deficiency.

Lumbar bone mineral density (BMD) by dual energy x-ray absorptiometry was assessed in 46 (29 boys, 17 girls) treated patients with growth hormone deficiency (GHD) at final height, comparing the BMD results with normative data. Prevalence of fractures in patients during treatment and healthy controls (n = 100) during the corresponding time period was assessed. Lumbar BMD values at final height of fractured and fracture-free patients were compared between them. Lumbar BMD corrected for bone area was significantly (P < 0.01) reduced (boys, -0.4 +/- 0.8 Z score; girls, -0.5 +/- 0.7 Z score), but lumbar BMD corrected for bone size (BMDvolume) did not differ [P = not significant (NS); boys -0.2 +/- 1.0 Z score; girls, -0.3 +/- 1.0 Z score] from normal mean. Approximately 22% of patients had reduced lumbar BMD (Z score, -1 to -2). The fact that patients had a complete or partial GHD did not influence lumbar BMD. The prevalence of fractured patients did not differ (P = NS) from that of controls [n = 7 (15.2%) and n = 24 (24.0%), respectively; odds ratio, 1.837]. Lumbar BMDvolume of fractured patients was significantly (P < 0.02) lower than that of fracture-free (n = 39) patients (boys, 0.310 +/- 0.005 and 0.351 +/- 0.032 g/cm(3), respectively; girls, 0.326 +/- 0.027 and 0.382 +/- 0.036 g/cm(3), respectively). The percentage of the fractured patients with lumbar BMDvolume less than 1 SD of normal mean was significantly (P < 0.0001) higher than that of fracture-free patients [n = 6 (85.7%) and n = 4 (10.3%), respectively; odds ratio, 26.092). The fractured patients also showed reduced lumbar BMD corrected for bone area and BMDvolume at the time of fractures (-1.6 +/- 0.4 and -1.5 +/- 0.2 Z score, respectively). The results show that treated patients with GHD have normal mean values of lumbar BMDvolume at final height, but some patients have reduced lumbar BMD (Z score <1) with an increased susceptibility to fractures.

Adolescent↗