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Biomedical subjects

M Garabedian

Publications and source records attributed to M Garabedian.

At least 127 records · Page 7Linked to original sources
PubMed1972

Control of 25-hydroxycholecalciferol metabolism by parathyroid glands.

Thyroparathyroidectomy of rats on a diet low in calcium reduces production of 1,25-dihydroxycholecalciferol from 25-hydroxycholecalciferol to negligible levels within 40 hr, and increases production of another metabolite, called Va. Parathyroid extract, at a dose of 20 units per day, prevents these changes. When 40 units per day of parathyroid extract is given 48 hr after thyroparathyroidectomy, 1,25-dihydroxycholecalciferol production is restored almost to control levels within 36 hr. The change brought about by parathyroid extract cannot be attributed to resulting changes in serum calcium or phosphorus concentration. It appears that the parathyroid hormone serves as a tropin for production of 1,25-dihydroxycholecalciferol, the hormonal form of vitamin D responsible for calcium mobilization from intestinal contents and bone.

Animals↗
PubMed1972

25-Hydroxycholecalciferol. A comparative study in deficiency rickets and different types of resistant rickets.

The effects of 25-hydroxycholecalciferol were studied in 4 children with deficiency rickets and 22 children with D-resistant rickets, including patients with hereditary hypophosphatemic D-resistant rickets, "pseudo-deficiency" rickets, and rickets secondary to cystinosis or to tyrosinosis. Three protocols were used. (a) 8 days after a single oral dose of 16,000 IU of 25-hydroxycholecalciferol, normalization of all biological parameters was observed in all cases of deficiency rickets. A complete lack of response was observed in the different types of resistant rickets. (b) Under prolonged administration of 2,640 IU/day for 2 months, clinical-biological symptoms and X-ray lesions disappeared, and a catch-up growth pattern was observed in deficiency rickets; no relapse of rickets occurred up to 5 months after therapy was stopped. The same dose had no significant effect in 10 patients with hereditary hypophosphatemic D-resistant rickets. A bone biopsy performed in one case showed the persistence of characteristic lesions. (c) With increasing doses of 25-hydroxycholecalciferol varying from 6,000 to 30,000 IU/day and a follow-up of 6 months up to 2 yr duration, clinical-biological-radiologic recovery and catch-up growht was obtained in all cases of "pseudo-deficiency" rickets. In hypophosphatemic hereditary D-resistant rickets, 5 out of 13 patients' serum concentration of phosphorus reached at least 30 mg/liter, but a catch-up growth pattern was not observed. These results indicate that (a) 25-hydroxycholecalciferol is highly active in deficiency rickets; (b) a defect in the conversion of vitamin D(3) to its active 25-hydroxy metabolite is probably not the metabolic defect in any of the different types of vitamin D-resistant rickets studied.

Administration, Oral↗
PubMed1971

Gastroscopy.

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Abdomen, Acute↗
PubMed1971

Duodenoscopy.

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Abdomen, Acute↗
PubMed1971

Colonoscopy.

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Abdomen, Acute↗
PubMedDate not supplied

[Dysregulation of plasma 1,25(OH)2D in calcium restriction in hypercalciuric children].

BACKGROUND: The effect of calcium restriction on the plasma concentration of 1,25(OH)2D in normo- and hypercalciuric children remains unknown. METHODS: We studied phosphate and calcium metabolism of 8 normocalciuric and 8 hypercalciuric children aged 4 to 16 years, under 3 conditions: on a normal dietary calcium intake after a 5-day calcium-restricted diet, and after oral calcium loading. The healthy, normocalciuric children had histories that included no renal failure of abnormalities of phosphate and calcium metabolism. Four of the 8 hypercalciuric children had urolithiasis, 1 had hematuria and the 3 others had idiopathic hypercalciuria. Blood samples were analyzed for calcium, creatinine, immunoreactive parathyroid hormone, cAMP, 25(OH)D and 1,25(OH)2D concentrations. Urine samples were analyzed for calcium, phosphorus, creatinine and cAMP. RESULTS: On the normal dietary calcium intake, the hypercalciuric children had higher urinary calcium excretion and plasma 1,25(OH)2D levels and lower TmP that did the controls. The 1,25(OH)2D levels of the normocalciuric children were significantly increased after 5 days of dietary calcium deprivation, but those of the hypercalciuric children were not. The other parameters (essentially PTH, cAMP and TmP) varied similarly in the two groups. CONCLUSION: The results suggest that: a) calcium restriction influences 1,25(OH)2D levels in normocalciuric subjects via a PTH- and phosphor-independent mechanism; b) dietary control of renal vitamin D metabolism is impaired in hypercalciuric patients.

Adolescent↗
PubMedDate not supplied

[Biological and bone histomorphometric studies in hypophosphatemic vitamin-resistant rickets treated with 1,25-(OH)2D and phosphorus].

Five children aged 6 to 15 years were studied. They presented all the biological signs of hypophosphatemic vitamin resistant rickets: normal calcemia, hypophosphatemia, decrease in phosphorus Tm and normal PTH plasma level. Two children had never been given vitamin D treatment previously. The 1.25 (OH)2D has been given in 4 doses a day, to a total of 1 microgram/day, for one year. Phosphate was administered for the same time, doses varying from 40 to 150 mg/kg/day. Bone biopsies were performed at the onset and the end of treatment. Normal growth concerning bone age was observed in 3 cases. In the two others, growth remained disturbed. Radiological recovery was observed in all cases. Treatment induced and increase in serum phosphate. Tm PO4/FG remained lower than normal and even decreased during treatment. After one year of treatment, the osteoid volumes and surfaces decreased in all cases but did not always return to normal. The thickness index of osteoid and the speed of calcification were improved in 4 cases and worsened in the 5th. In two previously untreated patients an increase in plasma PTH and in the osteoclastic surface of resorption were observed on the bone biopsy during treatment.

Adolescent↗
PubMedDate not supplied

[Vitamin D metabolism in rat calvarium in vitro (author's transl)].

The in vitro formation of 24, 25-(OH) 2D3 during incubation of rat calvarium with 25-(OH) D3 could be demonstrated. The in vitro synthesis of 24, 25-(OH) 2D3 has been localized in the mitochondrial fraction of the calvarium tissue. It could be detected also in calvarium cells in culture, but results indicate that the ability to synthetize 24, 25-(OH) 2D3 may be specific of some cell types only. The in vitro formation of 24, 25-(OH) 2D3 was observed with calvarium from rat neonates as well as from younger fetal rats, yet, in this latter period the in vitro formation of 24, 25-(OH) 2D3 was not found at all days of pregnancy tested in our experimental conditions (17th to 21st day).

Animals↗
PubMedDate not supplied

[Synthesis of dihydroxycholecalciferols in maternal and fetal rat organs in the last days of gestation].

The in vitro synthesis of 3H1,25(OH)2D3 and 3H24,25-(OH)2D3 in different maternal (kidney and spleen), placental (maternal and fetal sides) and fetal (kidney, intestine, liver and skeleton) tissues and the relative contribution of each of these organs to total production was studied in the last six days of gestation in rats. On day 16, synthesis of both metabolites was higher in fetal tissues than in maternal kidney, and decreased as gestation advanced. On day 16, placental contribution represented more than 50% of the total production of 3H1,25(OH)2D3, while the maternal kidneys and the fetal tissues contributed only 16% and 26%, respectively. On day 18, the synthesis of 3H1,25(OH)2D3 by maternal placenta and fetal tissues was significantly reduced in comparison with that observed on day 16. Between days 16 and 19, the plasma concentrations of 1,25(OH)2D in mothers and fetuses were associated with the magnitude of its in vitro production. Starting on day 19, however, the in vitro production remained at the same level while the plasma concentration increased, suggesting lower utilization or lower catabolism of this metabolite. Similarly, the total synthesis of 3H24,25(OH)2D3 decreased on day 19. Between days 16 and 18, a higher synthesis of 3H24,25(OH)2D3 corresponded with lower plasma concentration of this metabolite suggesting greater utilization. In contrast, between days 19 and 21, the in vitro synthesis and plasma concentration of 24,25(OH)2D increased in parallel fashion. In summary we report the following findings: a) inhibition of the in vitro synthesis of 3H1,25(OH)2D3 and 3H24,25(OH)2D3 on day 19 of gestation in the rat; b) the contribution of each of the different maternal, placental and fetal tissues to the total synthesis of these metabolites in the last six days of gestation; and c) a parallelism between in vitro production and plasma concentration of both metabolites.

Animals↗
PubMedDate not supplied

Lower circulating insulin-like growth factor I and 1,25-dihydroxyvitamin D levels in preeclampsia.

OBJECTIVE: To assess whether the circulating levels of insulin-like growth factor I (IGF-I) are lower in preeclamptic than in normotensive pregnant women and whether serum concentrations of IGF-I are associated with those of 1,25 dihydroxyvitamin D (1,25-(OH)2D). STUDY DESIGN: The study was cross-sectional and was done at 26.7 to 39.7 weeks of pregnancy. The results obtained from preeclamptic women were compared with those obtained from normotensive pregnant women with the same gestational age (control group). SETTING: All the volunteers were patients attending the General Hospital of Mexico City and all laboratory measurements were done at the National Institute of Nutrition Salvador Zubiran, Mexico City. SUBJECTS: The study included 26 preeclamptic women and 26 normotensive pregnant women. All participated voluntarily and signed an informed consent. PROCEDURE: The following measurements were done: serum concentrations of IGF-I, 1,25-(OH)2D, intact parathyroid hormone (PTH), inorganic phosphorus, creatinine, and total and ionic calcium and magnesium. Also urinary calcium and creatinine clearance were measured and dietary and anthropometric data were obtained. All determinations were done blindly. Comparisons between groups were done using the Mann-Whitney U-test. Associations between variables were tested using the Spearman rank correlation and stepwise regression. RESULTS: Serum IGF-I levels were 26.1 +/- 10.2 nmol/L (mean +/- SD) in the preeclamptic group and 40.9 +/- 14.3 in the normotensive group (p = 0.0003); serum 1,25-(OH)2D levels were 43.6 +/- 8.2 pg/mL in the preeclamptic group and 52.1 +/- 10.2 in the normotensive group (p = 0.005). Serum intact PTH was similar in both groups. Serum levels of IGF-I, 1,25-(OH)2D, and intact PTH correlated significantly in the control group. In the preeclamptic group correlation was found only between IGF-I and 1,25-(OH)2D. CONCLUSIONS: Our study brings out two interesting observations. First, that serum IGF-I levels were significantly lower in preeclamptic than in control pregnant women; and second, the existence of a significant correlation between serum IGF-I and 1,25-(OH)2D concentrations in both preeclamptic and normotensive pregnant women.

Adult↗