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Biomedical subjects

G I Baroncelli

Publications and source records attributed to G I Baroncelli.

At least 73 records · Page 4Linked to original sources

Mineral metabolism and calcitriol therapy in idiopathic juvenile osteoporosis.

Idiopathic juvenile osteoporosis is a rare cause of osteoporosis during childhood. We examined four children (three boys and one girl, ranging in age from 2.3 to 12.6 years) with idiopathic juvenile osteoporosis. All of these patients had normal serum calcium, ionized calcium, phosphate, magnesium, 25-hydroxyvitamin D, intact parathyroid hormone, and total and extractable calcitonin levels. 1,25-Dihydroxyvitamin D values were low in three patients and slightly decreased in one. Three children were treated with calcitriol (1,25-dihydroxycholecalciferol) (0.50 micrograms/d in two and 0.25 microgram/d in the other). The fourth patient was not treated because of parental refusal. Therapy reduced the fracture rate. Follow-up at 6 and 12 months showed a significant increase in bone mineralization, which reached normal values in two children after 12 months of treatment. No side effects of calcitriol therapy were observed. The untreated patient did not show an improvement of bone mineralization in the same time.

Bone Density↗

Calcitonin secretion in children with insulin-dependent diabetes mellitus.

To test the hypothesis that calcitonin (CT) deficiency may contribute to bone mineral loss in insulin-dependent diabetes mellitus (IDDM), we studied basal and calcium stimulated (2 mg/kg body wt. in 5 min) CT levels in 15 children with IDDM and osteopenia. Ten age-sex matched healthy children were studied as controls. Since extractable CT (exCT) allows more sensitive and specific measurement of CT monomer, we measured both total serum CT (tCT) and exCT. Diabetic children had slightly but significantly (P less than 0.05) higher basal levels of both tCT (24.5 +/- 7.1 ng/l) and exCT (5.6 +/- 1.6 ng/l) than controls (tCT: 18.7 +/- 5.4 ng/l; exCT: 4.3 +/- 1.2 ng/l). Calcium stimulation test pointed out significant increase (P less than 0.001) of tCT and exCT in both groups with peak values not significantly different in IDDM in respect to controls. However, diabetic children showed a reduced CT reserve evidenced by a lower peak/basal ratio (diabetics: tCT 1.68, exCT 1.84; controls: tCT 2.49, exCT 2.88) and by a more rapid decrease in CT levels. We conclude that CT deficiency is not a causative factor of diabetic osteopenia. The slightly higher basal CT values suggest that an increased bone reabsorption may be operative in IDDM and it stimulates CT secretion. This chronic "C" cell stimulation may induce the reduction in CT reserve observed employing the calcium infusion test.

Adolescent↗

Bone loss during gonadotropin-releasing hormone agonist treatment in girls with true precocious puberty is not due to an impairment of calcitonin secretion.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty, while estrogen deprivation in postmenopausal women results in bone mass reduction. We looked for bone mineralization in girls with true precocious puberty (TPP) before and after six months of LH-RH analogs treatment. Calcitonin secretion in these girls were studied too. Bone mineral content (BMC) and BMC/BW ratio (single photon absorptiometry) were measured in seven girls (aged 4.3 to 8.7 years) with TPP before LH-RH agonist therapy (long acting D-Trp6-LH-RH 60 micrograms/kg im every 28 days) was started; the patients were reevaluated after six months of therapy. Before therapy, BMC and BMC/BW were increased for chronological age but appropriate for bone age according to our mineralization normative data. After six months of LH-RH analog administration, 17 beta-estradiol and LH levels were suppressed and BMC and BMC/BW showed a small but significant decrease (respectively -5.4%, p less than 0.02 and -6.3%, p less than 0.02). Basal and calcium stimulated calcitonin levels (total and extractable) did not significantly change during the study period. We conclude that in girls with TPP bone mineralization was increased for chronological age but normal for bone age. The estrogen withdrawal secondary to LH-RH analog therapy caused a reduction in bone mass. Such a bone loss is not due to an impairment of calcitonin secretion.

Age Determination by Skeleton↗

Hypomagnesemia and the parathyroid hormone-vitamin D endocrine system in children with insulin-dependent diabetes mellitus: effects of magnesium administration.

Because insulin-dependent diabetes mellitus is associated with altered electrolyte metabolism and a derangement of the parathyroid hormone (PTH)-vitamin D endocrine system, we studied 23 children with diabetes (age 9.4 +/- 2.5 years) and found lower serum values for total and ionized calcium, magnesium, intact PTH, calcitriol, and osteocalcin than in age- and sex-matched control subjects. All patients were given magnesium orally (6 mg/kg daily of elemental magnesium) for up to 60 days. During treatment, serum magnesium, total and ionized calcium, intact PTH, calcitriol, and osteocalcin concentrations significantly increased, reaching control values. After a 3-day low-calcium diet, the patients had a significantly reduced delta-increment of PTH and calcitriol in comparison with values obtained during hypomagnesemia. After magnesium repletion, the delta-increments of both PTH and calcitriol, in response to the low-calcium diet, were not significantly different from control values. These data suggest that magnesium deficiency plays a pivotal role in altering mineral homeostasis in insulin-dependent diabetes mellitus.

Calcitriol↗

Intact parathyroid hormone levels during pregnancy, in healthy term neonates and in hypocalcemic preterm infants.

We measured parathyroid hormone levels in pregnant and nonpregnant women and at 1, 2 and 5 days of life in healthy term neonates and in hypocalcemic preterm infants using a new immunoradiometric assay which measures only biologically active intact parathyroid hormone and by a mid-molecule parathyroid hormone radioimmunoassay. During pregnancy intact and mid-molecule parathyroid hormone levels did not show any modification and were not different from parathyroid hormone levels of nonpregnant age-matched controls. Serum calcium and phosphorus levels did not vary during each trimester of pregnancy. In cord serum intact and mid-molecule parathyroid hormone values were low in both term and preterm infants. In term neonates intact and mid-molecule parathyroid hormone levels peaked on day 1; in preterm infants intact parathyroid hormone levels peaked on day 1 while mid-molecule parathyroid hormone values peaked on day 2. Intact parathyroid hormone levels showed a more marked increase in preterm (19-fold) than in term neonates (7.5-fold) on day 1. Our data do not confirm the previously reported "physiologic" hyperparathyroidism in pregnancy. Moreover we found a normal parathyroid gland responsiveness to decreasing serum calcium levels in the first days of life in term and preterm infants. Our results suggest that measurement of intact parathyroid hormone 1-84 by immunoradiometric assay in the first days of life is a more sensitive index of parathyroid gland secretory function than the measurement of middle or carboxyl-terminal parathyroid hormone fragments allowing the detection of the dynamic changes of parathyroid hormone which occur in hypocalcemic preterm infants.

Adult↗

Determination of intact parathyrin by immunoradiometric assay evaluated in normal children and in patients with various disorders of calcium metabolism.

We report the reference values for intact parathyrin (PTH) measured by a two-site immunoradiometric assay (IRMA) during childhood. The study has been carried out in 215 healthy children and adolescents, ages 2.0 to 18.7 years. Some patients with altered mineral homeostasis were also studied to assess the sensitivity of the method in a clinical setting. Mean intact PTH concentrations were 30.8 (SD 9.6) ng/L; the median was 28.5 ng/L. Normal reference values were 16.0-59.0 ng/L (95% confidence interval). The distribution of intact PTH values was nongaussian. We found no significant variations between males and females and no age-related variations. The IRMA used was sufficiently sensitive to detect differences in PTH concentrations between healthy children and patients with hypocalcemia or hypercalcemia.

Adolescent↗

Evaluation of a peptide family encoded by the calcitonin gene in selected healthy pregnant women. A longitudinal study.

We conducted a longitudinal study on serum levels of peptides encoded by the calcitonin gene before conception, every month during pregnancy, and 24 h and 5 days after delivery in 26 healthy women. Only subjects fulfilling optimality criteria according to the literature were included. Blood samples for ionized calcium, total (tCT) and extractable (exCT) calcitonin, katacalcin, and calcitonin gene-related peptide (CGRP) were collected. We found no significant changes of ionized calcium, tCT, exCT, and katacalcin levels, while CGRP serum levels showed a significant increase during pregnancy and a fall to preconceptional values after delivery. Since variations of calcitonin levels did not occur in our selected pregnant women, we conclude that thyroidal C cell secretion is not increased during pregnancy. Our data suggest that calcitonin is not involved in the modifications of mineral homeostasis occurring in pregnancy. In addition, the variations of CGRP serum levels we found suggest that such a hormone participates in circulation modifications of pregnant women.

Adult↗

[Chronic granulomatous disease and McLeod phenotype. Description of a case].

Chronic granulomatous disease (CGD) is a genetic syndrome, mostly inherited as an X-linked recessive trait, characterized by severe and recurrent infections due to defective neutrophil leukocytes and monocytes respiratory burst and microbicidal activity. Consequently, the affected patients are prone to infections by catalase-positive bacteria and fungi. The Authors describe a case of X-linked CGD with red cells of the rare McLeod phenotype. These red cells show acanthocytosis and are not reacting with anti-Kx antibody. Moreover, the Authors discussed the diagnosis and chemotherapy of CGD in addition to biochemical and clinical characterization of McLeod phenotype.

Erythrocytes, Abnormal↗

[Katacalcin levels in healthy children and children with spasmophilia].

The calcitonin (CT) gene encodes at least 3 peptides: CT, the 21-aminoacid carboxyl-terminal flanking peptide (katalcin or PDN-21) and CT-gene related peptide. Normal thyroid C-cells as well as malignant ones co-secrete CT and PDN-21 in response to hypercalcemia, so assay of PDN-21 may be an usefull method to assess C-cells secretion. Because of our knowledge no data are available on PDN-21 values in children, we measured this peptide in healthy children and in spasmophilia (Sp), a disease that has been related to CT deficiency. We studied 16 healthy children (9 males, 7 females; aging from 3.0 to 11.6 years) and in 21 patients with diagnosed Sp (8 males, 13 females, aging from 4.6 to 13.0 years). PDN-21 were assayed in whole serum by RIA using synthetic human PDN-21 for standards, 125I-PDN-21 for tracer and specific antiserum. CT was measured the serum of the same subjects by RIA using an ultrasensitive methods. In healthy children PDN-21 serum values were 12.3 +/- 2.0 pg/ml and no significant differences were found between males and females. Children with Sp showed slow higher PDN-21 concentrations (14.0 +/- 1.4 pg/ml) than normals, but the difference was not statistically significant. Also CT values were not significantly different between normal children (21.4 +/- 3.7 pg/ml) and patients with spasmophilia (22.5 +/- 1.8 pg/ml). A high significant positive relation was found between katalcacin and CT levels in normals as well as in spasmophilics. The physiological effects of PDN-21 are actually unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

[Calciotropic hormones in osteoporosis caused by anorexia nervosa].

The authors evaluated bone mineralization by single photon absorptiometry and mineral homeostasis in 7 patients with anorexia nervosa. The patients with anorexia nervosa showed a reduction of bone mineralization in respect to age-sex matched normal values. Serum levels of calcium, ionized calcium, phosphate, magnesium, alkaline phosphatase, calcitonin and 25-hydroxyvitamin D were normal as well as phosphate and hydroxyproline urinary excretion. Osteocalcin levels were significantly low as compared to normal values (5.0 +/- 3.0 ng/ml vs 14.3 +/- 5.2 ng/ml, p less than 0.01) as well as urinary calcium excretion (0.02 +/- 1.01 vs 0.08 +/- 0.06, p less than 0.05); 1,25-dihydroxyvitamin D values were low only in 4 patients. Parathyroid hormone means levels were increased in respect to normal values (74.1 +/- 12.7 pg/ml vs 38.0 +/- 12.0, p less than 0.02). We confirm that adolescents with anorexia nervosa showed a reduced bone mineral content and alterations of mineral homeostasis that may contribute to the development of bone mineral loss.

1-Carboxyglutamic Acid↗

Bone demineralization and impaired mineral metabolism in insulin-dependent diabetes mellitus. A possible role of magnesium deficiency.

Osteoporosis, a recognized complication of insulin-dependent diabetes mellitus (IDDM), may be related to this complex metabolic disorder; moreover, some data emphasize an altered vitamin D metabolism or parathyroid hormone secretion. Mineral homeostasis was studied in 29 children with IDDM (18 males, 11 females; 2.6-18.0 years). In 17 patients a stimulatory test (low-calcium diet) was performed for PTH and 1.25(OH)2D. Bone mineral content (BMC) and BMC/BW were lower in respect to our normal values; bone mineral loss was directly related to HbA1c levels and insulin requirements. A significant decrease of ionized calcium (p less than 0.001) and magnesium (p less than 0.001) was found; intact PTH values were in the low normal range but decreased for the ionized calcium values. 1.25(OH)2D levels were not significantly different from normal levels. 1.25(OH)2D and intact PTH did not rise during stimulatory test. The lack of 1.25(OH)2D and intact PTH increase after the stimulatory test may be due to the parathyroid gland's hyporesponsiveness related to hypomagnesemia which impaired PTH release and/or PTH action. Our data confirm an involvement of 1.25(OH)2D and PTH regulation in diabetic osteoporosis.

Adolescent↗

[Dynamic tests for calcium-regulating hormones in childhood. Evaluation of the incremental response in normal subjects].

Some tests to study the dynamic secretion of calcium-regulating hormones in childhood are presented. A low-calcium diet (less than or equal to 2 mg/kg/daily) for 1,25-dihydroxyvitamin D [1.25-(OH)-2D], ASU-eel-CT i.m. injection (80 U MRC/1.73 mq) for parathyroid hormone (PTH), and calcium infusion (2 mg/kg in 5') for calcitonin (CT) are employed. A significant increase in 1,25-(OH)-2D level (1 degree day: 47.0 +/- 6.7 pg/ml; 3 degree day: 73.2 +/- 6.9 pg/ml; p less than 0.001; n = 19), intact PTH values (basal: 29.7 +/- 7.5 pg/ml; +120': 68.2 +/- 7.8 pg/ml; p less than 0.001; n = 10) and monomeric CT concentrations (basal: 5.2 +/- 2.3 pg/ml; +10': 26.2 +/- 4.4 pg/ml; p less than 0.001; n = 18) have been observed. The employed tests are able to show a significant increase in calcium-regulating hormones in healthy children. These tests are a simple and reliable method without side-effects that may provide further information on the pathogenesis of some pediatric diseases with altered mineral homeostasis.

Adolescent↗

[Idiopathic juvenile osteoporosis].

Four cases (3 males and 1 female) of idiopathic juvenile osteoporosis, a rare form of bone demineralization, are described. The pathogenesis is unknown. The males showed osteoporosis at X-ray while in the female osteoporosis was only identified by computerized bone densitometry. The age of onset of the disease is perpuberal, but in one case it appeared in a small child. Biochemical data were in the normal range, only 1.25 (OH) 2D was reduced in two patients.

Age Factors↗