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Biomedical subjects

G I Baroncelli

Publications and source records attributed to G I Baroncelli.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1998

Effect of central precocious puberty and gonadotropin-releasing hormone analogue treatment on peak bone mass and final height in females.

UNLABELLED: To evaluate the effect of central precocious puberty (CPP) and its treatment with gonadotropin-releasing hormone (GnRH) analogues on final height and peak bone mass (PBM), we measured lumbar bone mineral density (BMD) in 23 girls at final height. Patients were distributed in two groups. Group 1: 14 patients with progressive CPP were treated with GnRH analogues; seven patients received buserelin (1600 microg/daily), subsequently switched to depot triptorelin (60 microg/kg/26-28 days); seven patients were treated with depot triptorelin (60 microg/kg/26-28 days); mean age of treatment was 6.2 years (range 2.7-7.8 years); the treatment was discontinued at the mean age of 10.1 years (range 8.7-11.3 years); final height was reached at the mean age 13.4 years (range 12.0-14.9 years). Group 2: 9 patients (mean age 6.5 years, range 4.8-7.7 years) with a slowly progressing variant of CPP were followed without treatment; final height was reached at the mean age 13.6 years (range 12.5-14.8 years). Lumbar BMD (L2-L4 by dual energy X-ray absorptiometry) was measured in all patients at final height. In group 1, final height (158.9+/-5.4 cm) was significantly greater than the pre-treatment predicted height (153.5+/-7.2 cm, P < 0.001), but significantly lower than mid-parental height (163.2+/-6.2 cm, P < 0.005). Subdividing the girls of group 1 according to the bone age at discontinuation of therapy (i.e. < or =11.5 years, n=5, or > or =12.0 years, n=9), the former patients had a final height significantly higher than the latter (163.7+/-3.9 cm vs 156.5+/-4.6 cm, P < 0.02). In group 2, final height (161.8+/-4.6 cm) was similar to the pre-treatment predicted height (163.1+/-6.2 cm, P=NS) and was not significantly different from mid-parental height (161.0+/-5.9 cm). BMD values (group 1: 1.11+/-0.14 g/cm2, group 2: 1.22+/-0.08 g/cm2) were not significantly different from those of a control group (1.18+/-0.10 g/cm; n=20, age 16.3-20.5 years) and the patients' mothers (group 1: 1.16+/-0.07 g/cm2, n=11, age 32.9-45.1 years; group 2: 1.20+/-0.08 g/cm2, n=7, age 33.5-46.5 years). In group 1, the girls who stopped therapy at a bone age < or =11.5 years had significantly higher BMD (1.22+/-0.10 g/cm2) compared to those who discontinued therapy at a bone age > or =12.0 years (1.04+/-0.12 g/ cm2, P < 0.05). CONCLUSION: In girls with progressive CPP, long-term treatment with GnRH analogues improves final height. A subset of patients with CPP does not require treatment because good statural outcome (slowly progressing variant). In CPP, the abnormal onset of puberty and the long-term GnRH analogue treatment do not impair the achievement of PBM. In GnRH treated patients, the discontinuation of therapy at an appropriate bone age for pubertal onset may improve both final height and PBM.

Adolescent↗
PubMed1998

[Growth hormone treatment of familial hypophosphatemic rickets].

X-linked hypophosphatemic rickets (XLHR) is frequently associated with growth retardation and short adult stature, even with an appropriate conventional treatment associating phosphate and calcitriol or 1 alpha-hydroxyvitamin D. Its pathogenesis is unclear; growth hormone (GH) secretion is usually normal. Six children with XLHR and growth retardation were treated with GH during 6 years. In addition, they received the conventional treatment. At the beginning of the treatment mean age was 7.8 +/- 1.8 years, and height mean Z score was -3.4 +/- 0.5. A control group was composed of six children with XLHR (age: 7.9 +/- 2.5 years) receiving the conventional treatment only. Under GH treatment statural growth was improved, with significant increase in Z score and predicted adult height; the height gain was significantly higher in the GH treated group as compared with the group receiving the conventional treatment only. In addition, radial bone mineral density increased significantly under GH treatment. GH treatment thus appears to be a useful treatment to improve statural growth in children with XLHR.

Adult↗
PubMed1998

Altered bone mineral density in patients with complete androgen insensitivity syndrome.

Androgens have major influences on the regulation of bone mineralization. Because of their unique peripheral metabolism androgens may act on bone via activation of the androgen and/or estrogen receptor. Patients with complete androgen insensitivity syndrome (cAIS) are natural models to assess androgen actions on bone. We studied bone mineral density (BMD) in 10 patients with cAIS (mean age 13.70, range 4.7-19.8 years); 3 patients were studied before gonadectomy; the others were castrated and 6 were on hormonal replacement therapy. The BMD area (aBMD) was measured by dual energy X-ray; lumbar 'apparent' volumetric density (vBMD) was calculated using the formula vBMD = aBMD x [4/(pi x width)]. In the patients, aBMD (0.72 +/- 0.16 g/cm2) and vBMD (0.23 +/- 0.04 g/cm3) were significantly (p < 0.001) reduced in comparison with those of a control group (n = 15, age 5.0-20.5 years: aBMD 1.028 +/- 0.20 g/cm2; vBMD 0.35 +/- 0.04 g/cm3). Both aBMD and vBMD were also reduced in comparison with normal values for males (aBMD -2.66 +/- 0. 99 SDS, p < 0.001; vBMD -3.08 +/- 1.53 SDS, p < 0.0005) and females (aBMD -2.88 +/- 1.05 SDS, p < 0.001; vBMD -2.84 +/- 1.18 SDS, p < 0. 0007). Real lumbar bone density, assessed by computed tomography in 1 patient, was also reduced (-6.2 SDS and -3.5 SDS for male and female normal values, respectively). Biochemical markers of bone metabolism were normal and not significantly different in patients and controls. Girls with cAIS did not have more fractures than controls. In conclusion, both aBMD and vBMD are reduced in cAIS patients, while bone turnover and the fracture risk seem not to be increased. Our data indicate that both androgens and estrogens may be required for acquisition of bone density during childhood.

Absorptiometry, Photon↗
PubMed1998

Normal volumetric bone mineral density and bone turnover in young men with histories of constitutional delay of puberty.

It has been suggested that an appropriate timing of puberty is necessary for normal bone mineral density (BMD) acquisition, which may not be achievable in children with constitutional delay of puberty (CDP). To assess the effect of pubertal delay on BMD, we measured areal BMD (aBMD) at lumbar spine, by dual-energy x-ray absorptiometry (DEXA), in a group of patients with CDP (n=21; mean age, 21.8+/-1.7 yr) at final height and in healthy controls (n=12; mean age, 19.3+/-1.3 yr). A subset of seven patients (group a) were untreated, whereas six subjects (group b) had received im testosterone depot (100 mg/month, for 6-12 months) and 8 boys (group c) oral oxandrolone (1.25-2.5 mg/daily, for 6-28 months) for their pubertal delay. Volumetric BMD (vBMD) was calculated from DEXA measurements. aBMD was reduced in patients with CDP (1.101+/-0.134 g/cm2), in comparison with controls (1.222+/-0.091 g/cm2; P < 0.009); no significant differences were found among the groups (group a, 1.089+/-0.133 g/cm2; group b, 1.111+/-0.118 g/cm2; group c, 1.103+/-0.160 g/cm2). vBMD was not significantly different in patients with CDP (0.327+/-0.021 g/cm3) and in controls (0.337+/-0.017 g/cm3; P= not significant); no significant differences were found among the groups (group a, 0.326+/-0.016 g/cm3; group b, 0.332+/-0.022 g/cm3; group c, 0.330+/-0.021 g/cm3). No differences were found in mineral metabolism and in bone markers between patients and controls; patients did not report an increased fracture rate, compared with controls. Our data indicate that: 1) men with CDP have normal vBMD; 2) the reduced aBMD may be the result of uncritical use of DEXA measurements in subjects with altered growth pattern; and 3) androgen administration during pubertal years did not improve BMD in young men with a history of CDP.

Absorptiometry, Photon↗
PubMed1998

Measurement of volumetric bone mineral density accurately determines degree of lumbar undermineralization in children with growth hormone deficiency.

The effect of anthropometric variables and bone size on bone mineral density (BMD) was examined in 22 children with GH deficiency (GHD) aged 6.1-8.0 yr at diagnosis and in 40 sex- and chronological age-matched controls. In all patients and controls, bone mineral content (BMC), BMDarea and BMD corrected for the apparent bone volume (BMDvolume) were measured by dual-energy x-ray absorptiometry in the lumbar spine at L2-L4 level. In patients, BMDarea was corrected for body height (BMDheight), body mass index (BMDBMI), and bone age (BMDBA). Patients showed significantly reduced (P < 0.0001) BMC (males 11.55 +/- 0.71 g, females 10.13 +/- 1.48 g) and BMDarea (males 0.502 +/- 0.033 g/cm2, females 0.515 +/- 0.034 g/cm2) compared with controls (BMC: males 18.09 +/- 1.23 g, females 15.58 +/- 1.87 g; BMDarea: males 0.689 +/- 0.065 g/cm2, females 0.685 +/- 0.059 g/cm2). In patients, BMDheight (males 0.537 +/- 0.031 g/cm2, females 0.548 +/- 0.032 g/cm2) and BMDBMI (males 0.641 +/- 0.028 g/cm2, females 0.624 +/- 0.035 g/cm2) remained significantly lower (P < 0.02 to P < 0.0001) than BMDarea of controls. BMDBA of patients was significantly reduced (-1.49 +/- 0.51 Z score, P < 0.0001) in comparison with bone age-matched controls (n = 35). BMDvolume was significantly lower (P < 0.01 to P < 0.0005) in patients (males 0.268 +/- 0.006 g/cm3, females 0.276 +/- 0.010 g/cm3) compared with chronological age-matched controls (males 0.283 +/- 0.013 g/cm3, females 0.293 +/- 0.017 g/cm3). Mean bone volume of patients was affected to a greater extent than bone area (-2.36 +/- 0.49 Z score and -1.56 +/- 0.70 Z score, respectively). Bone area/bone volume ratio was significantly higher in patients than in chronological age-matched controls (0.53 +/- 0.02 and 0.42 +/- 0.08, P < 0.0001, respectively). Chronological age, body height, BMI, and bone age correlated significantly with BMDarea (r2 = 0.389-0.450, P < 0.002 to P < 0.001) but not with BMDvolume (P = not significant). The results show that anthropometric variables and bone size affect lumbar BMC and BMDarea in children with GHD. Reduced lumbar BMDvolume indicates that apparent true bone density is decreased in children with GHD, suggesting a role of GH in bone mineralization.

Absorptiometry, Photon↗
PubMed1997

Androgen-receptor blockade does not impair bone mineral density in adolescent females.

The effect of peripheral androgen hypersensitivity on bone mineral density (BMD) was investigated in a group of adolescent women with idiopathic hirsutism (n = 17; mean age 17.0 +/- 1.7 years). The effect of long-term androgen-receptor blockade with flutamide (500 mg daily in two divided doses for 12 months) on BMD was assessed too. BMD was measured at lumbar spine (L2-L4) by a dual energy X-ray densitometer. Before flutamide treatment, patient BMD (1.14 +/- 0.07 g/cm2) was not significantly different from that of the control group (1.16 +/- 0.12 g/cm2, n = 22), and was normal for age and sex (BMD 0.14 +/- 0.69 SDS, P = NS vs. 0). After 12 months of treatment, absolute BMD in patients increased (1.18 +/- 0.08 g/cm2, P < 0.002), but SDS BMD did not change (0.21 +/- 0.72, P = NS vs. baseline). Flutamide treatment determined a clinical, marked improvement of androgen hypersensitivity (Ferriman-Gallwey score: before 22.0 +/- 6.2; 6 months: 13.2 +/- 6.4, P < 0.003; 12 months; 7.6 +/- 4.1, P < 0. 001; acne score: before 3.8 +/- 0.8; 3 months 0.8 +/- 0.5, P < 0. 001; later disappeared). The serum levels of 3alpha-androstenediol-glucoronide decreased (before: 8.6 +/- 1.1 microg/liter; 12 months: 7.2 +/- 1.0 microg/liter, P < 0.02), whereas the other endocrinological parameters did not change. No relationship was found between BMD and clinical or biochemical parameters of hyperandrogenism. We concluded that in adolescent women, peripheral hyperandrogenism is not associated with abnormal BMD; long-term treatment with flutamide, which blocks the androgen receptor, does not alter their BMD.

Absorptiometry, Photon↗
PubMed1997

Long-term outcome of male-limited gonadotropin-independent precocious puberty.

Long-term outcome of five new cases of male-limited precocious puberty (MPP) is reported. Three patients had positive family history. One patient was untreated; 2 boys received cyproterone acetate (2.0-3.6 mg/kg/daily) without clinical effects. Two patients were treated with ketoconazole (600 mg/daily); in 1, GnRH analogue therapy (Buserelin, 1,600 microg/day) was added after 6 months of effective ketoconazole treatment for development of central precocious puberty. The other patient did not develop central puberty under ketoconazole treatment and improved his predicted adult height from 172.4 to 181.1 cm. Four patients reached final height [B.A. (therapy cyproterone acetate): age 22.0 years, -2.0 SDS; B.G. (untreated): age 15.5 years, -1.7 SDS; M.M. (therapy cyproterone acetate): age 19.5 years, -1.6 SDS; M.F. (therapy ketoconazole plus GnRH analogue): age 21.3 years, -2.2 SDS]; three had reduced testicular volume (B.A.: -1.6/-1.6 SDS; B.G.: -2.1/-2.1 SDS; M.F.: -2.4/-1.9 SDS); one (M.F.) showed oligospermia. We concluded that in MPP cyproterone acetate treatment did not improve final height; ketoconazole was effective in reducing testosterone secretion, but its real effect on final height cannot be determined; the timing of central puberty may be precocious, suggesting that an adjunctive GnRH analogue treatment may be needed. In some patients, testicular impairment may be present in young adulthood.

Androgen Antagonists↗
PubMed1997

Sex steroids and the acquisition of bone mass.

Bone mineralization increases with age, height and weight through childhood, with a significant gain during pubertal development. Approximately 37% of bone mass is accumulated between pubertal stages 2-5. The factors driving the pubertal increase of bone mass is not fully known, but a crucial role is played by the sex steroids. Patients with central precocious puberty show an increased bone mineral density (BMD) for their chronological age, but appropriate for their bone age and pubertal stage. In girls and boys with hypogonadism, as well as in constitutional delay of puberty, the 'tempo' of puberty seems to be another important determinant of peak bone mass. Hypogonadal patients increase their BMD when treated in adulthood with sex steroid substitutive therapy, but normal adult BMD values are not reached. If these patients start sex steroid therapy at the appropriate age for the onset of pubertal development, however, a greater increase in BMD occurs. Both oestrogen and androgen receptors have been demonstrated in bone cells. Patients with oestrogen resistance or aromatase deficiency had a severely undermineralized skeleton. Reduced area and volume BMD are also present in patients with complete androgen resistant syndrome compared to normal. The pubertal increase of BMD may be the result of the coordinated activation of oestrogen and androgen receptors at the bone level in both sexes. In conclusion, the gonadal secretion of sex steroids, the tempo of puberty, and the normal function of both oestrogen and androgen receptors seem to be important factors in the acquisition of bone mass.

Adult↗
PubMed1997

Biochemical selection of prepubertal patients with androgen insensitivity syndrome by sex hormone-binding globulin response to the human chorionic gonadotropin test.

Before puberty, the diagnosis of androgen insensitivity syndrome (AIS) can be difficult. We studied whether the decrease of sex hormone-binding globulin (SHBG) during the human chorionic gonadotropin (hCG) test may represent a biochemical test to select prepubertal patients with AIS. We examined prepubertal patients with AIS (n = 9, age 0.9-8.2 y), male pseudohermaphroditism not due to AIS (other-MPH) (n = 8, age 0.6-10.7 y), and control boys (n = 12, age 0.8-12.5 y). Testosterone and SHBG levels (mean +/- SD) were measured before (d 0) and after (d 5) a hCG test (1500 IU X 3 d). Testosterone levels (nmol/L) increased in all groups [AIS: from 1.5 +/- 1.2 to 22.1 +/- 11.8 (p < 0.001); other-MPH: from 0.6 +/- 0.6 to 9.2 +/- 7.4 (p < 0.02); controls: from 1.8 +/- 1.4 to 22.8 +/- 14.4 (p < 0.001)]. SHBG concentrations (nmol/L) did not change in AIS [from 66.2 +/- 15.1 to 67.5 +/- 18.6 (p = NS), delta-variation 1.7 +/- 12.7%], whereas they were significantly decreased in other-MPH [from 59.9 +/- 14.2 to 46.5 +/- 18.6 (p < 0.005), delta-variation -23.7 +/- 19.6%] and controls [from 63.0 +/- 16.9 to 33.7 +/- 14.6 (p < 0.003), delta-variation -46.9 +/- 15.2%]. Our data suggest that the SHBG changes during the hCG test can be used to assess in vivo the biologic response to androgens in prepubertal patients with ambiguous genitalia, selecting those patients in whom it is worth performing second level investigations to confirm the AIS diagnosis.

Androgens↗
PubMed1997

Bone demineralization in cystic fibrosis: evidence of imbalance between bone formation and degradation.

Bone turnover, collagen metabolism, and bone mineral status were investigated in 59 patients with cystic fibrosis and in 72 sex and age-matched control subjects. In all patients and control subjects serum concentrations of osteocalcin (OC), carboxy-terminal propeptide of type I procollagen (PICP), amino-terminal propeptide of type III procollagen (PIIINP), and cross-linked carboxy-terminal telopeptide of type I collagen (ICTP), and urinary values of cross-linked N-telopeptides of type I collagen (NTX), as well as total body bone mineral content (TBBM) were measured. Higher ICTP (microgram/L) and NTX (bone collagen equivalent/urinary creatinine (nmol/mmol) values were found in pre-pubertal, pubertal, and young adult patients than in control subjects (ICTP: 15.4 +/- 2.1 and 13.2 +/- 1.8, p < 0.001; 23.3 +/- 5.3 and 20.1 +/- 4.1, p < 0.02; 4.8 +/- 1.1 and 4.0 +/- 1.0, p < 0.05. respectively; NTX: 1047.5 +/- 528.6 and 227.8 +/- 71.8, p < 0.01; 997.8 +/- 391.7 and 376.3 +/- 91.0, p < 0.01; 993.2 +/- 398.0 and 73.9 +/- 28.5, p < 0.01, respectively). Lower OC and PICP levels (microgram/L) were showed in pubertal patients in comparison with control subjects (OC: 20.2 +/- 12.3 and 39.0 +/- 15.1, p < 0.01; PICP: 305.8 +/- 130.4 and 436.2 +/- 110.1, p < 0.02, respectively). Lower OC and higher PIIINP levels (microgram/L) were found in young adult patients than in control subjects (OC: 4.4 +/- 3.0 and 7.0 +/- 3.1, p < 0.05; PIIINP: 4.8 +/- 1.1 and 3.1 +/- 1.0, p < 0.001, respectively). TBBM (z score) was reduced in prepubertal, pubertal, and young adult patients (-0.8 +/- 0.4, -1.0 +/- 0.4, -1.1 +/- 0.5, respectively). Patients with cystic fibrosis have bone demineralization and imbalance between bone formation and degradation.

Adolescent↗
PubMed1996

Central precocious puberty in Klinefelter syndrome: a case report with longitudinal follow-up of growth pattern.

We report idiopathic central precocious puberty in a boy with Klinefelter syndrome and describe the pattern of linear growth and body proportion from the onset of precocious puberty to final height. The patient was not treated for precocious puberty. He reached adequate adult height, for both general population and normative values of Klinefelter syndrome and normal body proportions. We conclude that precocious puberty in Klinefelter syndrome may result in normal body proportion by inducing a major growth spurt of the trunk rather than in the limbs, and that adult height prognosis is not altered by precocious puberty. Given the possible occurrence of precocious puberty in Klinefelter syndrome, we advise a karyotype analysis in boys with sexual precocity, mainly in those who show small rather than enlarged testes.

Body Constitution↗
PubMed1996

Bone mineral density in adolescent females treated with L-thyroxine: a longitudinal study.

UNLABELLED: It has been suggested that chronic treatment with L-thyroxine (L-T4) could be implicated in reducing bone mineral density (BMD). The purpose of this longitudinal study was to determine whether appendicular and axial BMD is decreased by L-T4 treatment in adolescent girls. Thirteen adolescent girls with subclinical hypothyroidism caused by chronic lymphocytic thyroiditis were enrolled in the study at the median age of 13.4 years (range 9.2-18.1 years). L-T4 was administered in a single dose of 1-5 micrograms/kg daily. BMD was evaluated at the distal one-third of the non-dominant radius by single photon absorptiometry (SPA) and at the lumbar spine (L2-4) by dual energy X-ray densitometry (DEXA). Osteocalcin levels were measured to assess bone turnover before and during L-T4 treatment. Before the start of therapy, mean BMD at both the radial and lumbar level was not significantly different from that of a control group (median age 13.0 years; range 9.0-18.5 years). during L-T4 therapy for 2-5 years, BMD did not change at any site. Before treatment, osteocalcin levels were not significantly different from those of controls and did not change during follow up. CONCLUSION: Long-term L-T4 therapy in adolescent girls has no adverse effect on BMD and bone turnover. Our data indicate that attainment of peak bone mass is not impaired by L-T4 administration.

Absorptiometry, Photon↗
PubMed1996

Bone mineral density and biochemical parameters of bone turnover in children with growth hormone deficiency.

Growth hormone (GH) is a crucial factor in the build-up and in the maintenance of peak bone mass. Children with GH deficiency have osteopenia and a concomitant reduction in bone turnover. On the other hand, GH therapy improves bone mineral density and stimulates bone turnover. These data suggest that GH treatment may have a beneficial effect on peak bone mass. In children with GH deficiency, the values of some biochemical markers of bone turnover may be closely related to growth response during GH therapy. However, further studies are needed to define the usefulness of bone markers in order to optimize the treatment and to predict the growth outcome in GH-treated children.

Biomarkers↗
PubMed1996

The effect of long-term growth hormone (GH) treatment on bone mineral density in children with GH deficiency. Role of GH in the attainment of peak bone mass.

The effect of long-term GH treatment on bone mass was examined in 32 children with GH deficiency (GHD) aged 7.2-16.3 yr by measuring radial (distal third, single-photon absorptiometry) and lumbar (L2-L4, dual energy x-ray absorptiometry) bone mineral density (BMD) (group A). All patients were longitudinally followed and received recombinant hGH therapy for a mean period of 48.2 +/- 13.2 months. BMD values were corrected for bone age and expressed as Z-score in comparison with normative data. In addition, lumbar BMD and lumbar BMD corrected for the estimated vertebral volumes were assessed in 11 patients with GHD aged 16.0 - 18.7 yr at the time they reached their final height (group B) and, in 17 subjects with familial short stature aged 16.4 - 19.8 yr, as controls (group C) for patients of group B. Patients of group B had received discontinuous treatment with pituitary-derived hGH and subsequently recombinant hGH (total duration of treatment 151.5 +/- 9.7 months). The off-treatment period was 4.7 +/- 2.6 months. Before treatment, patients of group A showed significantly reduced (P < 0.001) radial and lumbar BMD (-1.7 +/- 0.4 Z-score and -1.5 +/- 0.5 Z-score, respectively) compared with normative data. During treatment, radial and lumbar BMD Z-scores improved significantly (P < 0.001); in the patients treated for the longest time, the BMD was within 0.5 SD of age-matched mean levels. In patients of group B, lumbar BMD and lumbar BMD corrected for the estimated vertebral volumes were significantly reduced in comparison with subjects of group C (-1.2 +/- 0.4 Z-score and -1.0 +/- 0.4 Z-score, P < 0.01 and P < 0.03, respectively). The results show that children with GHD have reduced BMD. Optimal GH treatment improves BMD, whereas inappropriate treatment is a main cause of reduced BMD at time of final height. These findings suggest an important role of GH therapy in the attainment of peak bone mass in children with GHD. GH treatment should be continued until the attainment of peak bone mass irrespective of the height achieved.

Adolescent↗