BACKGROUND: Admission to Pediatric Departments for 0/18- year-old patients is an important issue for the best organization of pediatric hospital assistance. Aim of the study. To locate adolescent health care and identify the percentage of adolescent admissions to Pediatric Departments in an Italian region (Tuscany). METHODS: Adolescent health care in pediatric departments and pediatric admissions (0-18 years old) in 1999 into the reference hospital of Pisa and into 5 other regional hospitals in Tuscany are reported. The percentages of patients, subdivided by age, hospitalyzed in Pediatric Departments have been determined. RESULTS: In 1999 the admissions for subjects aged 0 to 18 years were 12573 of which 4966 adolescents (39.6 %). The percentage of adolescent admissions is not smaller than children's admissions (aged 0 to 1 year: 16.2%; aged 2 to 5 years: 26.2%; aged 6 to 9 years: 17.8%; aged 10 to 14 years: 20.4%; aged 15 to 18 years: 19.2%). Analysis by age demonstrated a continuous decrease of patient percentages admitted to Pediatric Departments with the increased age. A minority of 15/18- year-old subjects has been admitted to Pediatric Departments. CONCLUSIONS: The percentage of adolescent admissions is similar to there of children. Most adolescents are admitted to structures unsuitable for assistance to subjects aged 0 to 18 years. These data underline the necessity for a strong recovery of adolescent admissions to pediatric structures also equipping suitable nursing rooms.

Adolescent↗

PubMed2000

Final height, gonadal function and bone mineral density of adolescent males with central precocious puberty after therapy with gonadotropin-releasing hormone analogues.

UNLABELLED: Few data are available on the outcome of boys with central precocious puberty (CPP) treated with gonadotropin-releasing hormone (GnRH) analogues. We report on final height, endocrine and exocrine testicular function, and bone mineral density (BMD) in nine males (age 16.7 +/- 1.5 years) treated with GnRH analogues from the age 6.0 +/- 1.8 years for a mean period of 5.6 +/- 2.4 years. The following parameters were evaluated: final height, serum gonadotropin and gonadal steroid levels, spermarche, semen analysis, area and volumetric BMD. Final height (-0.4 +/- 1.1 SDS) was significantly higher than pre-treatment predicted adult height (-2.0 +/- 1.2 SDS) and not significantly different than midparental height (-0.1 +/- 0.8 SDS). Pubertal response of gonadotropins to GnRH test occurred within 1.5 years (mean 0.7 +/- 0.4 years) and spermarche (n = 7) from 0.7 to 3 years (1.8 +/- 0.9 years) after the discontinuation of GnRH analogue therapy. No alteration in semen analysis was found (n = 6, sperm count, 10(6)/ml: 52.0 +/- 18.7; normal motility (%): 49.5 +/- 18.7; atypical morphology (%): 44.5 +/- 11.4). Area and volumetric BMD were not reduced (0.2 +/- 1.0 SDS and -0.1 +/- 0.9 SDS, respectively). CONCLUSION: Long-term treatment with gonadotropin-releasing hormone analogues improves final height in boys with central precocious puberty. Post-therapy data demonstrating normal endocrine and exocrine testicular function support the safety of gonadotropin-releasing hormone analogues on reproductive function. Long-term pharmacological suppression of testicular function in childhood does not impair bone mineral density in late adolescence.

Adolescent↗

PubMed2000

Bone turnover in children with vitamin D deficiency rickets before and during treatment.

UNLABELLED: Biochemical markers of bone formation [alkaline phosphatase, osteocalcin, and carboxyterminal propeptide of type I procollagen (PICP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and cross-linked N-telopeptides of type I collagen (NTX)] were measured in 14 children aged 8.5-10.5 mo with vitamin D deficiency rickets before and longitudinally during vitamin D treatment (3000-4000 IU/daily). Forty-four healthy children aged 8-10.5 mo were enrolled as sex- and age-matched controls. Before treatment, serum levels of alkaline phosphatase, PICP, and ICTP, and urinary excretion values of NTX were significantly higher, and serum osteocalcin levels significantly lower than controls (31.4 +/- 3.5 microkat/L and 9.8 +/- 2.9 microkat/L, p < 0.001; 1025 +/- 89 microg/L and 952 +/- 97.4 microg/L, p < 0.02; 15.6 +/- 2.6 microg/L and 14.2 +/- 1.3 microg/L, p < 0.01; 370.7 +/- 109.4 nmol BCE and 201.8 +/- 69.2 nmol BCE, p < 0.001: 17.6 +/- 9.1 microg/L and 22.5 +/- 7.6 microg/L, p < 0.05, respectively). During treatment, serum alkaline phosphatase levels progressively declined in association with the radiographic healing of the skeletal lesions. Serum levels of osteocalcin, PICP, and ICTP, and urinary excretion values of NTX showed a transient but significant (p < 0.05 to p < 0.001) increase in comparison with baseline values during the first 2-4 wk of treatment, and decreased slowly thereafter. They were within the mean +/- 2 SD of controls before the recovery of the skeletal lesions. CONCLUSIONS: These findings suggest that children with vitamin D deficiency rickets have increased bone turnover before and during the first weeks of treatment. Alkaline phosphatase is a more reliable marker than osteocalcin, PICP, ICTP and NTX for diagnosing and monitoring these patients.

Alkaline Phosphatase↗

PubMed2000

Volumetric bone mineral density in young women with Turner's syndrome treated with estrogens or estrogens plus growth hormone.

To explore the effects of estrogen replacement therapy (ERT) and recombinant growth hormone (GH) treatment on bone mineral density (BMD) in Turner's syndrome, we assessed volumetric BMD (vBMD), which is less dependent on body and bone sizes, in these patients at final height. The areal BMD (aBMD) was measured in 26 young women with Turner's syndrome (age range 17.5-25.0 years) by dual-energy X-ray absorptiometry, and vBMD was calculated. Patients were subdivided as group 1 (n = 12; ERT alone) and group 2 (n = 14; GH + ERT). Years of estrogen exposure were not different between the groups (group 1: 6. 4 +/- 1.5 years; group 2: 5.3 +/- 1.7 years); in group 2, GH therapy was 5.3 +/- 1.4 years. Final heights were significantly higher in group 2 than in group 1 (148.1 +/- 3.0 vs. 142.0 +/- 2.8 cm; p < 0. 0001) as well as aBMD (1.073 +/- 0.118 vs. 0.968 +/- 0.122 g/cm(2); p < 0.04). vBMD was higher in group 2 but not significantly different from group 1 (0.374 +/- 0.030 vs. 0.358 +/- 0.027 g/cm(3); p = 0.169). aBMD was reduced with respect to the normative values in both groups (group 1: -1.97 +/- 1.04 SDS, p < 0.0001 vs. 0; group 2: -0.93 +/- 1.01 SDS, p < 0.005 vs. 0), whereas vBMD was not (group 1: -0.07 +/- 0.79 SDS; group 2: 0.42 +/- 0.82 SDS). Our data suggest that: in Turner's syndrome GH administration improves final height and aBMD, but it does not significantly increase vBMD; aBMD reduction in Turner's syndrome is likely due to the impaired growth and reduced bone size; Turner's patients on ERT from adolescence show vBMD values in the normal range in young adulthood.

Adolescent↗

PubMed2000

Hypophosphataemic rickets.

X-Linked hypophosphataemic rickets (XLH) is frequently associated with short stature even when conventional treatment (1, 25-dihydroxyvitamin D(3) or 1alpha-hydroxyvitamin D(3) plus inorganic phosphate salts) is administered for a long time. The pathogenesis of growth retardation is probably multifactorial. Affected patients usually show normal growth hormone (GH) secretion. In some poorly growing XLH patients, long-term GH treatment associated with conventional therapy improves linear growth. GH treatment also increases phosphate retention but this effect is transient.

Child↗

PubMed2000

Critical ages and stages of puberty in the accumulation of spinal and femoral bone mass: the validity of bone mass measurements.

In growing children, lumbar and femoral areal bone mineral density (aBMD), as measured by dual-energy X-ray absorptiometry (DXA), is influenced by skeletal growth and bone size. Correction of lumbar bone mineral density (BMD) for bone volume (volumetric BMD [vBMD]), by the use of mathematical extrapolations, reduces the confounding effect of bone size, but vBMD remains dependent on age and bone size during growth. Femoral (neck and mid-shaft) vBMD, assessed by DXA, is independent of age prior to puberty, but a slight increase occurs in late puberty and after menarche. Femoral (mid-shaft) cortical bone density and radial cortical and trabecular bone densities, assessed by quantitative computed tomography (QCT), show no peak during childhood or adolescence. Bone strength index, calculated by peripheral QCT, increases with age and correlates with handgrip strength, bone cross-sectional area and cortical area. Puberty is one of the main factors that influences lumbar bone mineral content and aBMD accumulation, but a high incidence of fractures occurs during this period of life, which may be associated with a reduced aBMD.

Absorptiometry, Photon↗

PubMed2000

Is there a place for combined therapy with GnRH agonist plus growth hormone in improving final height in short statured children?

The availability of recombinant human growth hormone (GH) and the optimization of substitutive therapy have improved final growth in children with GH deficiency, but despite this some of them fail to grow to their genetic potential. In particular, this may occur in patients who started the substitutive therapy too late and/or in whom bone age progressed too fast during GH administration. In these patients, with unfavorable auxological characteristics, the administration of a GnRH agonist in combination with GH may slow down bone maturation and prolong prepubertal growth, mimicking, to some extent, the growth pattern of patients with GH + Gn deficiency who grow better than children with isolated GHD. A different condition in which such a combined therapy might be used is the short normal child. As they are short but normally-growing children, the onset of puberty is in general appropriate for their chronological age but precocious for their height age. Thus, slowing down pubertal maturation may increase the time available for growth. GH would sustain growth during both GnRHa administration and after its withdrawal, when puberty starts again. Our preliminary results suggest that the administration of GH + GnRHa in combination may have a positive effect on final height in selected children with isolated GHD and in short normal children.

Body Height↗

PubMed2000

Dynamics of bone turnover in children with GH deficiency treated with GH until final height.

OBJECTIVE: To examine the dynamics of bone turnover in children with growth hormone deficiency (GHD) during long-term treatment. DESIGN: We longitudinally measured growth velocity and serum concentrations of osteocalcin (OC), carboxyterminal propeptide of type I procollagen (PICP), and cross-linked carboxyterminal telopeptide of type I collagen (ICTP) in 24 patients with GHD during long-term GH treatment until final height (age: 7.7+/-0.7 and 16.9+/-0.5 years at baseline and at final height respectively). RESULTS: At baseline, OC, PICP, and ICTP levels were significantly (P<0.0001) reduced in comparison with prepubertal bone age-matched controls (10.2+/-2.3 microgram/l and 22.5+/-7.6 microgram/l; 187.8+/-26.2 microgram/l and 328. 4+/-74.3 microgram/l; 7.7+/-2.0 microgram/l and 14.2+/-1.3 microgram/l respectively). During the first year of treatment mean levels of the bone markers increased significantly (P<0.0001) with a peak at 12 months. After the first year of treatment, OC and PICP levels progressively declined, whereas ICTP levels remained stable until the final height; in any case, bone marker levels remained significantly higher (P<0.03-P<0.0001) than baseline. The change in bone marker levels at 6 and 12 months of treatment with respect to the baseline values was not related to growth rate during long-term treatment or final height. CONCLUSIONS: The results show that children with GHD have reduced bone turnover at baseline, and that long-term GH treatment is associated with a stimulation of bone turnover. OC, PICP, and ICTP do not predict growth rate during long-term treatment or final height in children with GHD.

Adolescent↗

PubMed2000

[How many adolescents are admitted in pediatrics?].

Explore the source record for details and available documents.

Adolescent↗

PubMed2000

[When and how to induce pubertal development?].

Explore the source record for details and available documents.

Adolescent↗

PubMed1999

Mucus of the human olfactory epithelium contains the insulin-like growth factor-I system which is altered in some neurodegenerative diseases.

Growth factors are believed to be involved in the mitotic regulation of the animal olfactory epithelium (OE). We investigated mucus covering the human OE area to see if it contained the insulin-like growth factor-I (IGF-I) and its binding proteins (IGFBPs) and to examine their behaviour in neurodegenerative diseases. Thirty patients with idiopathic late onset cerebellar ataxia (ILOCA), Parkinson's disease, and amyotrophic lateral sclerosis (ALS) and 30 age- and sex-matched healthy subjects were studied. In 10 controls, we also analyzed the mucus of the respiratory mucosa of the nose and tears. We detected IGF-I in the mucus covering the OE and Western ligand blot analysis (WLB) showed IGFBPs with an apparent Mr of 41, 500/38,500, 34,000 and 24,000, which were immunoprecipitated by specific antisera to IGFBP-3, -2 and -4, respectively. Their levels were higher than those observed in the respiratory mucosa of the nose or in tears. Mucus of the OE of the patients contained significantly reduced levels of IGF-I in comparison with those of controls. The intensity of all the IGFBPs-related bands were reduced in the ILOCA, while the remaining patients had a loss in the amounts of IGFBP-3. Plasma IGF-I and IGFBPs levels were similar in patients and controls. In conclusion, our data show that mucus covering the human OE contains IGF-I and IGFBPs, suggesting that these factors have a role in the activity of the OE. The amounts are reduced in the patients' mucus, possibly reflecting a dysfunction of the OE itself.

Amyotrophic Lateral Sclerosis↗

PubMed1999

Can growth hormone treatment in boys without growth hormone deficiency impair testicular function?

Four young male subjects (age range, 17 4/12 to 25 5/12 years), previously treated with human growth hormone for non-growth hormone-dependent short stature, showed reduced testicular volume and hypergonadotropic hypogonadism. They also showed impaired spermatogenesis and altered testicular texture as determined by ultrasonography. No clinical or laboratory finding showed disease associated with testicular dysfunction. An unfavorable gonadal outcome could occur in boys without growth hormone deficiency treated with human growth hormone.

Adolescent↗

PubMed1999

Vitamin-D receptor genotype does not predict bone mineral density, bone turnover, and growth in prepubertal children.

We examined whether the polymorphism for BsmI restriction enzyme in the vitamin-D receptor (VDR) gene influenced radial (distal third) and lumbar (L2-L4) bone mineral density (BMD), phospho-calcium metabolism (calcium, phosphate, intact parathyroid hormone, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D), biochemical markers of bone formation (osteocalcin and carboxy-terminal propeptide of type-I procollagen) and bone resorption (carboxy-terminal telopeptide of type-I collagen and urinary cross-linked N-telopeptides of type I collagen), insulin-like growth factor I and insulin-like growth factor-binding protein 3, and growth in 209 healthy prepubertal children (112 males and 97 females) aged 7.1-10.0 years. Genotype frequencies were BB 19%, Bb 46%, and bb 35% in the pooled group of children. Clinical findings, dietary calcium intake, calcium density, and physical activity rate were not different (p NS) among the VDR genotypes. Radial BMD, lumbar BMDarea and lumbar BMD adjusted for the apparent bone volume (BMDvolume), and all the biochemical parameters did not differ (p NS) in relation to the VDR genotype. In conclusion, our data show that polymorphism for BsmI restriction enzyme in the VDR gene is not associated with radial and lumbar BMD, parameters of phospho-calcium metabolism and bone turnover, growth hormone-dependent growth factors, and growth in prepubertal children.

Alleles↗