Biomedical subjects

G I Baroncelli

Publications and source records attributed to G I Baroncelli.

At least 55 records · Page 3Linked to original sources

PubMed1995

Short-term effect of testosterone treatment on reduced bone density in boys with constitutional delay of puberty.

We studied bone mineral content (BMC), bone mineral density (BMD), cortical thickness/total width (CT/TW) ratio and cortical area/total area (CA/TA) ratio in boys with constitutional delay of puberty and the effect of short-term testosterone treatment on bone mass. Seventeen boys (age 13.1-15.8 years) who met the family history and the clinical criteria of constitutional delay of puberty were selected and enrolled in the study. All subjects were eating a diet assuring an adequate intake of calories and calcium. A subset of 8 boys (group A) was treated with testosterone depot (100 mg/month x 6 months) while 9 boys (group B) were not. At inclusion, BMC and BMD were reduced in the patients according to their chronological age (BMC -4.04 +/- 1.34 standard deviation scores [SDS]; BMD -2.95 +/- 0.56 SDS), statural age (BMC -1.75 +/- 0.79 SDS; BMD -1.69 +/- 0.78 SDS), and bone age (BMC -1.80 +/- 0.65 SDS; BMD -1.86 +/- 0.68 SDS). No significant differences between the groups were found (group A: BMC 0.480 +/- 0.57 g/cm, BMD 0.488 +/- 0.037 g/cm2, CT/TW ratio 0.43 +/- 0.4, CA/TA ratio 0.68 +/- 0.04; group B: BMC 0.476 +/- 0.060, p = NS vs. group A; BMD 0.491 +/- 0.036 g/cm2, p = NS vs. group A). At 12 months of follow-up, BMC, BMD, CT/TW ratio, and CA/TA ratio significantly increased in group A (BMC 0.70 +/- 0.13 g/cm, delta +41.1 +/- 28.8%, p < 0.003 vs. 0 month; BMD 0.617 +/- 0.082 g/cm2, delta +26.2 +/- 13.6%, p < 0.005 vs. 0 month; CT/TW ratio 0.52 +/- 0.05, delta +20.59 +/- 10.65%, p < 0.001 vs. 0 month; CA/TA ratio 0.77 +/- 0.05 vs. 0 month; CT/TW ratio 13.60 +/- 6.65%, p < 0.004 vs 0 month), but not in group B (BMC: 0.48 +/- 0.05 g/cm; delta +5.1 7.8%, p = NS vs. 00 month; BMD: 0.492 +/- 0.037 g/cm2; delta +0.54 +/- 8.7%, p = NS vs. 0 month; CT/TW ratio 0.44 +/- 0.04, delta +4.04 +/- 6.75%, p = NS vs. 0 month; CA/TA ratio 0.68 +/- 0.05, delta +2.39 +/- 5.90%, p = NS vs. 0 month). We conclude that boys with constitutional delay of puberty have reduced BMC and BMD. The delay in statural and bone ages did not totally account for the decreased bone mass. Testosterone treatment for 6 months significantly increased BMC, BMD, CT/TW ratio, and CA/TA ratio in these patients, but definitive conclusions on the efficacy of the treatment in improving adult bone mass can be drawn only when our patients reach early childhood.

Adolescent↗

PubMed1995

Association between X-linked hypophosphatemic rickets and Klinefelter's syndrome: effects on growth and body proportion.

Growth failure with disproportionate short stature is the major clinical feature of patients with X-linked hypophosphatemic rickets (HYP). We studied the pattern of linear growth and body proportion in an untreated normally growing HYP child also affected by Klinefelter's syndrome. Auxologic data were compared with those of a HYP half-brother who showed growth failure despite long-term treatment either with vitamin D or with vitamin-D-analog plus phosphate salt supplementation. The degree of body disproportion changed from negative values to positive values in the proband, whereas it was reduced in the half-brother. We conclude that, in the proband, the normal pattern of growth and the lack of the typical body disproportion as seen in HYP patients are attributable to the concomitant presence of Klinefelter's syndrome.

Adolescent↗

PubMed1995

Long-term growth hormone treatment in children with renal hypophosphatemic rickets: effects on growth, mineral metabolism, and bone density.

OBJECTIVE: To evaluate the effects of treatment with recombinant human growth hormone (rhGH) on growth, mineral metabolism, and bone density in children with renal hypophosphatemic rickets (RHR). DESIGN: Long-term rhGH treatment combined with conventional therapy with 1,25-dihydroxyvitamin D3 plus inorganic phosphate salts. SETTING: Endocrine unit, department of pediatrics, university hospital. SUBJECTS: Twelve patients (5 boys; age range 4.6 to 12.5 years, median 7.0 years) were subdivided into two groups of six patients on the basis of the median of height z score (-2.41) and the median bone age/statural age (BA/SA) ratio (1.23). Group A included patients with a severe degree of short stature (height z score -3.4 +/- 0.5) (mean +/- SD) and altered BA/SA ratio (1.26 +/- 0.08); group B included patients with a lesser degree of short stature (height z score -2.1 +/- 0.6, p < 0.001 vs group A) and more normal BA/SA ratio (1.04 +/- 0.15, p < 0.01 vs group A). INTERVENTION: Group A received rhGH treatment (0.6 IU/kg per week subcutaneously) combined with conventional therapy; group B received conventional therapy alone. MEASUREMENTS: Height, growth velocity, predicted adult height, serum values of calcium, phosphate, bone alkaline phosphatase isoenzyme, osteocalcin, propeptides of type I and type III procollagen, intact parathyroid hormone, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and urinary calcium/urinary creatinine ratio and tubular maximum for phosphate reabsorption normalized to the glomerular filtration rate (TmP/GFR), as well as radial bone density, were measured at baseline and for 3 years. RESULTS: Height z score, growth velocity z score, predicted adult height, serum values of phosphate, bone alkaline phosphatase isoenzyme, osteocalcin, propeptides of type I and type III procollagen, intact parathyroid hormone 1,25-dihydroxyvitamin D, and TmP/GFR, as well as radial bone density, improved significantly only in group A. Serum calcium and 25-hydroxyvitamin D, and urinary calcium/urinary creatinine ratio did not change in either group. CONCLUSIONS: Long-term rhGH administration may benefit growth, phosphate retention, and bone density in patients with RHR, without evidence of side effects.

Bone Density↗

PubMed1995

Effect of combined treatment with gonadotropin releasing hormone analogue and growth hormone in patients with central precocious puberty who had subnormal growth velocity and impaired height prognosis.

Growth hormone-insulin-like growth factor-I status and response to growth hormone therapy (0.6 IU/kg/week sc, six times a week for 12 months) were evaluated in 12 girls (chronological age 9.4 +/- 1.6 years) suffering from central precocious puberty with growth velocity less than 4 cm/year and no substantial increase or decrease in predicted adult height during gonadotropin releasing hormone Bn-RH) analogue treatment (D-Trp6-LH-RH, 60 micrograms/kg im/28 days). At baseline, large variations were observed in nocturnal growth hormone (GH) means (pathological values stimulated levodopa GH peaks (pathological values (< 10.0 micrograms/l) 28.6%) and serum insulin-like growth factor-I (IGF-I) levels. Neither GH-nor IGF-I levels were correlated with growth velocity. During recombinant GH therapy, growth velocity increased significantly (baseline 3.0 +/- 0.9 cm/year; 6 months 6.4 +/- 1.9 cm/year, p < 0.001 versus baseline; 12 months 6.0 +/- 1.3 cm/year, p < 0.0001 versus baseline). There was a significant increase in height SDS for bone age (baseline -1.6 +/- 0.5 SDS; 12 months -1.04 +/- 0.6 SDS; p < 0.002) and in predicted adult height (baseline 152.0 +/- 3.6 cm; 12 months 155.9 +/- 3.4 cm; p < 0.002). Our results suggest that combined therapy with Gn-RH analogues and recombinant GH can improve growth velocity and predicted adult height in girls with central precocious puberty and impaired height prognosis during Gn-RH analogue treatment.

Age Determination by Skeleton↗

PubMed1995

Effects of growth hormone on phosphocalcium homeostasis and bone metabolism.

In this review the effects of growth hormone (GH) on phosphocalcium homeostasis and bone metabolism are reported. Some in vitro effects of GH on chondrocytes and osteoblasts are discussed too. The main GH effects on phosphocalcium homeostasis are the permissive action on renal 1 alpha-hydroxylase activity by the hypophosphatemic stimulus and the antiphosphaturic effect by the stimulation of the maximum rate of renal tubular reabsorption of phosphate. On bone, GH is able to stimulate bone turnover and to increase bone mass. In addition, GH stimulates type I and type III collagen metabolism. In vitro, GH increases the proliferation of chondrocytes from the human growing cartilage together with the levels of interleukin-6 in the supernatant. The hormone increases also the proliferation of the human osteosarcoma-derived osteoblast-like cells and augments the osteocalcin levels in the supernatant. Thus, GH markedly influences phosphocalcium homeostasis and bone metabolism in childhood and adolescence. In addition, it is possible that GH continues to play a role in bone physiology during adulthood when final height is reached.

Animals↗

PubMed1994

Parathyroid hormone-related protein in healthy pregnant women.

The object of this study was to determine whether increased circulating levels of parathyroid hormone-related protein (PTH-rp) may explain the increased parathyroid hormone (PTH) bioactivity in pregnancy. In 41 healthy pregnant women (age 19-41 years), PTH-rp and corrected calcium levels were measured and compared with those of nonpregnant control women (n = 18, age 20-39 years). PTH-rp and corrected calcium levels were significantly higher in pregnant women (PTH-rp 21.9 +/- 7.9 pg/ml, P < 0.001; corrected calcium 2.38 +/- 0.07 mmol/liter, P = 0.001) than in nonpregnant women (PTH-rp 10.3 +/- 7.8 pg/ml; corrected calcium 2.30 +/- 0.10 mmol/liter). Our data indicate that circulating PTH-rp levels may significantly increase in pregnancy, suggesting a possible role of this peptide in the modification of calcium homeostasis in pregnant women.

Adult↗

PubMed1994

Growth hormone secretion in poorly growing children with renal hypophosphataemic rickets.

We evaluated growth hormone (GH) secretion and baseline serum free insulin-like growth factor-I (IGF-I) levels in 12 poorly growing patients (5 males and 7 females; age 1.6-12.5 years, median 6.4) with renal hypophosphataemic rickets treated with 1,25-dihydroxy-vitamin D3 plus inorganic oral phosphate salts. Eleven healthy normally growing children (6 males and 5 females; age 3.1-10.8 years, median 6.6) were studied as control group. All patients had a normal GH response (GH peak > or = 10 micrograms/l) to at least one provocative pharmacological stimulus (levodopa or insulin tolerance test), as well as all the controls. Mean growth hormone concentrations (MGHC), mean pulse amplitude, number of GH peaks above 5 micrograms/l, and IGF-I values overlapped between patients and controls, even though four patients had MGHC below the lower limit of MGHC of controls. In these patients, however, height-SDS, serum calcium, phosphate, alkaline phosphatase, intact parathyroid hormone, 1,25-dihydroxyvitamin D concentrations and maximum tubular phosphate reabsorption/glomerular filtration rate ratio did not differ in respect to the patients who showed MGHC in the range of controls (n = 6). MGHC IGF-I and biochemical parameters of phospho-calcium metabolism did not differ when the patients were subdivided in two groups on the basis of the median (-2.4) of height-SDS. No relationship was found between MGHC or IGF-I and height-SDS or growth velocity-SDS. Height-SDS and years of treatment or age at which therapy was started were not related.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗

PubMed1994

Twenty-four-hour osteocalcin, carboxyterminal propeptide of type I procollagen, and aminoterminal propeptide of type III procollagen rhythms in normal and growth-retarded children.

The relationships between spontaneous variations in serum 24-h osteocalcin (OC), carboxyterminal propeptide of type I procollagen (PICP), and aminoterminal propeptide of type III procollagen (PIIINP) concentrations and GH secretion, measured as GH response to provocative pharmacologic stimuli and spontaneous GH secretion during 24 h, were evaluated in prepubertal normal children and in GH-deficient and GH-secreting short normal children (SNC). All the subjects showed a circadian rhythm in smoothed 24-h OC and PICP mean data with higher nocturnal values in comparison with diurnal values. Conversely, serum PIINP concentrations did not vary throughout the day. In children with classic GH deficiency and nonclassic GH deficiency, mean 24-h serum levels and smoothed 24-h mean data for OC, PICP, and PIIINP were significantly reduced (p < 0.001) with respect to age-matched controls. SNC showed mean 24-h OC concentrations similar (p = NS) to those we found in age-matched controls, but they had significantly lower (p < 0.001) diurnal 12-h mean data in comparison with controls. SNC also showed both 24-h PICP and PIIINP mean data and smoothed 24-h PICP and PIIINP mean data significantly lower (from p < 0.02 to p < 0.001) at all the time points of measurement in comparison with controls. Twenty-four-hour PICP and PIIINP mean data were positively related to spontaneous 24-h GH concentrations (r = 0.77, p < 0.005 and r = 0.69, p < 0.005, respectively) and growth velocity (r = 0.85, p < 0.005, and r = 0.70, p < 0.005, respectively), whereas 24-h OC mean data were not.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Determination by Skeleton↗

PubMed1993

Ketoconazole decreases the serum ionized calcium and 1,25-dihydroxyvitamin D levels in tuberculosis-associated hypercalcemia.

OBJECTIVE: To evaluate whether tuberculosis-associated hypercalcemia is related to abnormal synthesis of 1,25-dihydroxyvitamin D (1,25[OH]2D) and whether ketoconazole administration may be useful in treating tuberculosis-associated hypercalcemia. DESIGN: Case study. SETTING: Endocrine Unit, Pediatric Clinic, University of Pisa (Italy). PARTICIPANTS: Two boys (aged 10.5 years and 14.7 years) with active tuberculosis and hypercalcemia. MEASUREMENTS/MAIN RESULTS: At admission, serum 1,25-dihydroxyvitamin D levels were elevated. Oral ketoconazole administration (3.0 mg/kg every 8 hours) decreased 1,25-dihydroxyvitamin D levels within the first week of therapy (from 208.8 to 57.6 pmol/L [-72.4%] in one boy and from 321.6 to 115.2 pmol/L [-64.2%] in the other). We also found a coincident normalization of serum ionized calcium concentration (from 1.45 to 1.24 mmol/L [-13.0%] in one boy and from 1.55 to 1.26 mmol/L [-17.0%] in the other). CONCLUSIONS: Abnormal elevated levels of 1,25-dihydroxyvitamin D caused hypercalcemia in our patients; ketoconazole administration may be effective in the treatment of hypercalcemia in patients with tuberculosis, which decreases 1,25-dihydroxyvitamin D synthesis.

25-Hydroxyvitamin D 2↗

PubMed1993

Reduction of bone density: an effect of gonadotropin releasing hormone analogue treatment in central precocious puberty.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty. Oestrogen deprivation in women results in bone loss. We investigated bone mineralization by single photon absorptiometry in girls with central precocious puberty (n = 13, age 3.8-8.5 years) before and during 1 year of treatment with gonadotropin releasing hormone analogue (GnRH-a = long-acting D-Trp6-GnRH, 60 micrograms i.m. every 28 days). Before GnRH-a therapy, bone mineral density (BMD) was significantly higher in patients than in ten control girls matched for chronological age (patients 0.575 +/- 0.097 g/cm2, controls 0.433 +/- 0.049 g/cm2, P < 0.001). Patient BMD was not significantly different from that of ten control girls matched according to patient bone, age (0.550 +/- 0.046 g/cm2, P = NS). During GnRH-a treatment, pituitary-gonadal axis was suppressed and patient BMD significantly decreased (6 months: -6.0%, P < 0.002 vs baseline; 12 months: -8.0%, P < 0.001 vs baseline). We conclude that in girls with precocious puberty the activation of gonadal steroid secretion induces an increase in bone mineralization and that oestrogen deprivation by GnRH-a treatment caused a significant decrease in BMD.

Absorptiometry, Photon↗

PubMed1993

Effects of long-term treatment with growth hormone on bone and mineral metabolism in children with growth hormone deficiency.

The effects of growth hormone (GH) deficiency and recombinant human GH replacement (0.6 IU/kg per week) on bone and mineral metabolism in 26 GH-deficient children were studied for 12 months. Before therapy, all children had significantly reduced serum levels of osteocalcin, carboxyl-terminal propeptide of procollagen type I, and 1,25-dihydroxyvitamin D, whereas serum ionized calcium, phosphate, intact parathyroid hormone, calcitonin, and 25-hydroxyvitamin D concentrations were in the normal range. All children had significant reduction of bone density for their chronologic, statural, and bone ages. During therapy with recombinant human GH, a decrease of serum ionized calcium levels and increases of phosphate, osteocalcin, carboxyl-terminal propeptide of procollagen type I, and intact serum levels of parathyroid hormone were found. A significant increase of serum levels of 1,25-dihydroxyvitamin D was found at 12 months. The urinary phosphate/urinary creatinine ratio decreased, whereas values for nephrogenous cyclic adenosine monophosphate and the ratio of the maximum rate of renal tubular reabsorption of phosphate to the glomerular filtration rate increased. Bone density significantly improved at 12 months, with a complete recovery in 12 children (46.2%). Significant relationships were found among growth velocity, bone density, maximum tubular reabsorption/glomerular filtration rate ratio, and serum levels of carboxyl-terminal propeptide of type I procollagen. The changes in serum levels of this propeptide during the first week of recombinant human GH treatment were positively related to growth velocity at 6 and 12 months and to bone density at 12 months of treatment, whereas the changes in osteocalcin levels were not. We conclude that recombinant human GH treatment caused significant modifications of mineral metabolism and significantly increased bone density, and that measurement of serum levels of the propeptide during the first week of recombinant human GH administration may be a useful tool in predicting improved growth velocity and bone density during long-term recombinant human GH replacement.

Bone Density↗

PubMed1993

Growth velocity and serum aminoterminal propeptide of type III procollagen in precocious puberty during gonadotropin-releasing hormone analogue treatment.

Growth velocity and serum aminoterminal propeptide of type III procollagen (P-III-NP) were evaluated in 11 girls (age 3.8-8.5 years) with central precocious puberty during luteinizing hormone releasing hormone (LH-RH) analogue treatment (D-Trp6-LH-RH, 60 micrograms/kg im for 28 days, n = 7; D-ser(TBU)6-LH-RH, 1600 micrograms/day intranasally, n = 4). Before treatment, growth velocity (10.2 +/- 1.9 cm/year) and P-III-NP concentrations (12.8 +/- 4.3 micrograms/l) were in the pubertal range. During therapy, growth velocity significantly decreased to the prepubertal levels. P-III-NP concentrations decreased significantly after six months of therapy (7.9 +/- 3.7 micrograms/l, p < 0.001). Three girls with low growth velocity ( < 4 cm/year), stimulated growth hormone peak < 10 micrograms/l, and altered 12-h nocturnal growth hormone secretion at 12 and/or 18 months of treatment, had a more marked decrease in P-III-NP concentrations (patient 3: -65.9%; patient 5: -58.7%; patient 10: -61.0%) after 6 months of therapy. Our results suggest that LH-RH analogue treatment in central precocious puberty may impair growth. In these cases, measurement of serum P-III-NP levels may be an additional marker to monitor growth.

Child↗

PubMed1993

Commercial kits for 1,25-dihydroxyvitamin D compared with a liquid-chromatographic assay.

Three commercially available kits for 1,25-dihydroxyvitamin D [1,25(OH)2D] determination were compared with a liquid-chromatographic method. Serum samples were analyzed for 1,25(OH)2D from 70 healthy subjects (age 2.2-17.5 years; 35 males, 35 females), some (n = 5) given orally high vitamin D3 doses. In addition, 1,25(OH)2D was measured in 28 patients with untreated diseases associated with low (n = 16) or high (n = 12) serum concentrations of the hormone. The results showed that the commercial kits were sufficiently accurate with respect to the comparison method and suitable for routine clinical work.

Adolescent↗

PubMed1992

Idiopathic juvenile osteoporosis: evidence of normal osteoblast function by 1,25-dihydroxyvitamin D3 stimulation test.

Idiopathic juvenile osteoporosis (IJO) is a rare form of bone demineralization that occurs during childhood. The mechanism of bone loss is unclear. Some bone hystomorphometric studies have found osteoblast failure and decreased bone formation in the affected patients whereas others have reported increased bone resorption. To elucidate this issue, we studied osteoblast function in six patients with IJO (five males, one female; aged 2.3-14.6 years) and five healthy sex- and age-matched subjects (four males, one female; aged 2.0-15.1 years) measuring serum values of osteocalcin under basal condition and during an osteoblast stimulation test performed by oral 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] administration (1.8 micrograms/1.73 m2/daily). After a baseline day (day 0), all the subjects (patients and controls) received 1,25(OH)2D3 in four divided doses for 6 days (days 1-6). Fasting blood samples were obtained every morning (0800 h) for the determination of serum osteocalcin. Baseline osteocalcin levels were not significantly different between IJO and controls (13.58 +/- 6.05 ng/ml versus 16.04 +/- 5.09 ng/ml, respectively) even if two patients had low osteocalcin values. During 1,25(OH)2D3 administration, serum osteocalcin values significantly increased (P less than 0.001) from baseline in both children with IJO and controls, reaching peak values not significantly different in the two groups. Our results do not support the hypothesis that defective osteoblast function is the primary factor of bone demineralization in IJO.

Adolescent↗

PubMed1992

Serum levels of carboxyterminal propeptide of type I procollagen in healthy children from 1st year of life to adulthood and in metabolic bone diseases.

Type I collagen is the major component of bone matrix; circulating carboxyterminal propeptide of type I procollagen (P-I-CP) levels reflect type I collagen synthesis in tissues and may be an useful index to investigate bone metabolism. We measured P-I-CP by a new radioimmunoassay in 300 healthy children and adolescents and in 40 healthy adults to provide reference data for P-I-CP values. In addition, 79 patients with diagnosed disorders of phospho-calcium metabolism (rickets, vitamin D deficient and vitamin D resistant, hyperparathyroidism, hypo- and pseudo-hypoparathyroidism, osteopenia) were evaluated. In the healthy subjects, serum P-I-CP values were higher in children than in adults; variations of P-I-CP levels were observed according to age and sexual maturation: higher values were found in the first years of life and during pubertal development; pubertal increase reflects the different timing of pubertal development in the two sexes. P-I-CP levels were increased in primary hyperparathyroidism and reduced in diseases related to impaired secretion or action of parathyroid hormone. Higher P-I-CP levels were found in vitamin D deficient and vitamin D resistant rickets. P-I-CP was reduced in anorexia nervosa and during chronic glucocorticoid treatment while it was increased in thyrotoxic osteoporosis. In idiopathic juvenile osteoporosis, P-I-CP values ranged from reduced to increased values. We conclude that P-I-CP may represent an additional biochemical marker of bone metabolism. Since age-related variations are present, reference data for the various ages are need for clinical application of this assay.

Adolescent↗

PubMed1992

Elevated calcitonin gene-related peptide in polycythemic newborn infants.

In this study, calcitonin gene-related peptide levels were measured in cord and at 16-36 h of extrauterine life in 43 polycythemic newborns; 20 healthy term infants were also studied as controls. Calcitonin gene-related peptide values were significantly higher in polycythemic neonates in comparison with controls both at delivery and at 16-36 h after birth. Five polycythemic (11.6%) infants who develop hypocalcemia had greater elevated calcitonin gene-related peptide concentrations. Our data suggest that calcitonin gene-related peptide may be implicated in the circulatory adaptation to extrauterine life. In polycythemic neonates, calcitonin gene-related peptide is probably increased to compensate for blood hyperviscosity; in some cases, high calcitonin gene-related peptide concentrations may induce hypocalcemia.

Adaptation, Physiological↗

PubMed1992

Mineral metabolism in Turner's syndrome: evidence for impaired renal vitamin D metabolism and normal osteoblast function.

We examined intact PTH and 1,25-dihydroxyvitamin D [1,25-(OH)2D] in both baseline and dynamic conditions (low calcium diet) in 14 patients with Turner's syndrome (mean age, 12.6 +/- 5.9 yr; range, 4.2-21.0 yr) and bone demineralization as well as in a control group of 15 healthy girls (mean age, 12.8 +/- 5.6 yr; range, 3.8-22.7 yr). In both groups we also measured osteocalcin serum levels in response to oral 1,25-(OH)2D3 administration (1.8 micrograms/m2/daily for 6 days) to assess osteoblast function. The low calcium diet decreased ionized calcium (Ca2+) levels and elevated PTH values to the same extent in both patients (Ca2+, -8.40 +/- 3.78%; intact PTH, +47.88 +/- 13.24%) and controls (Ca2+, -9.09 +/- 3.25%; intact PTH, +52.77 +/- 10.52%; P = NS vs. patients). While controls showed an increment in their serum 1,25-(OH)2D levels (+52.15 +/- 8.95%), patients did not (+10.93 +/- 4.71%; P = NS vs. baseline; P < 0.001 vs. controls). 1,25-(OH)2D3 administration caused a rise in the serum osteocalcin levels in a similar fashion in both groups (peak values: patients, +35.38 +/- 7.20%; controls, +34.09 +/- 7.98%; P = NS). We conclude that in patients with Turner's syndrome there is an altered renal vitamin D metabolism in response to physiological stimulus, while osteoblast function in response to 1,25-(OH)2D3 administration is not affected.

Adolescent↗

PubMed1992

[Vitamin D prophylaxis in childhood].

The past 10 years have seen a return of rickets. Clinical and/or biochemical signs of vitamin D deficiency are still found in some children and adolescents, mainly during the winter. Sunlight exposure is able to prevent vitamin D deficiency and rickets but the dramatic influence of changes in solar ultraviolet-B radiation on cutaneous vitamin D3 synthesis, related to latitude and season effects, suggest that a vitamin D supplementation may be advisable. Moreover, human milk and common foods contain low quantities of vitamin D. So, we recommend routinely 400 IU of supplementary vitamin D per day in all infants. The vitamin D requirements in low-birth-weight infants are higher than at term infants; it is recommended the use of 1000-1600 IU per day in the first months of life. Intermittent high-dose of vitamin D and vitamin D metabolites are not advisable for prophylaxis of rickets.

Animals↗