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Biomedical subjects

L Miravet

Publications and source records attributed to L Miravet.

At least 91 records · Page 5Linked to original sources
PubMed1977

[Effect of cortisone on calcium metabolism. Attempt at correction by 5,6 trans 25-hydroxycholecalciferol, 25-hydroxycholecalciferol and vitamin D2].

14 patients receiving small doses of predisolone and 7 high doses were divided at random into three groups. Each group received for four weeks, 100 microgram of vitamin D2 or 25 hydroxyvitamin D3 or 5,6 trans-25 hydroxyvitamin D3. The 25 hydroxy and 5,6 trans-25 hydroxyvitamine D3 were able to increase intestinal calcium absorption. 25 Hydroxyvitamin D3 had an osteolytic action, increasing urine calcium and hydroxyproline and, once, in a patient slight hypercalcemia was observed. By constrast, 5,6 trans-25 hydroxyvitamin D3 decreased PTH and caused a significant decrease in urine hydroxyproline.

Calcium↗
PubMed1976

The biological activity of synthetic 25,26-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol in vitamin D-deficient rats.

The biological activity of synthetic 24,25 and 25,26 diOHD3 was studied in vitamin D-deficient rats. The purpose of this study was to investigate the influence of small doses of both metabolites (0.125-0.250 mug) upon intestinal calcium transport and bone calcium mobilization. Both metabolites were able to increase calcium absorption in rats maintained on a calcium-deficient diet, but failed to do it in rats on a normal calcium diet. Bilateral nephrectomy suppressed this effect. The "bone calcium mobilization" of both derivatives was measured in vitamin D and calcium- or phosphorus-deprived rats after one intravenous dose. When serum calcium was initially low, 24,25 and 25,26 diOHD3 increased serum calcium moderately, but the increment was only significant with 24,25 diOHD3. When serum calcium was normal before the injection, both metabolites decreased serum calcium significantly, and the decrease was greater with 24,25 diOHD3. Intraperitoneal administration of the metabolites for 5 consecutive days produced a significant increase of calcium in serum and bone ash.

Animals↗
PubMed1976

1,25-Dihydroxycholecalciferol effect on serum phosphorus homeostasis in rats.

It has recently been shown that 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) increases the serum phosphorus concentration of rats on a low-phosphorus diet. While studying the biological activity of 1,25(OH)2D3, we observed that under certain circumstances 1,25-(OH)2D3 would decrease the serum phosphorus concentration. The analysis of all data obtained in rat experiments during the past 3 years revealed highly significant linear correlations (P less than 0.001) between changes of serum phosphorus concentrations after the administration of 1,25-(OH)2-D3 (130 pmol/d for 1 or 5 days) and serum phosphorus or calcium levels in the animals before injection. Similar correlations could only be found with the higher dose of 25-hydroxycholecalciferol (130 pmol/d for 5 days). Another vitamin D3 metabolite, 24,25-dihydroxycholecalciferol, had no effect on serum phosphorus concentrations under our experimental conditions. The 1,25-(OH)2D3 effect on serum phosphorus concentration does not require the presence of circulating parathormone and/or calcitonin. We suggest that 1,25-(OH)2D3 might be an important factor in serum phosphorus homeostasis.

Animals↗
PubMed1976

[Effects of different metabolites of vitamin D3 and of calcium concentration on the intestinal absorption of strontium].

The effect of calcium concentration and vitamin B3 25 OHD3 and 1.25 diOHD3 upon intestinal strontium transport was studied in vitamin D deficient rats with duodenal perfusion in situ. When the calcium concentration was increased, the strontium passive absorption was decreased. The vitamin D3 and its derivatives increased intestinal strontium transport significantly and this increment was not modified by calcium. In our experiment, calcium is competitive with strontium only in passive absorption.

Animals↗
PubMed1975

[4 cases of osteomalacia during anticonvulsant or sedative treatment].

The authors report osteomalacia in 3 cases of epilepsy and one case of coronary heart disease treated with phenobarbitone, either alone or associated with other anticonvulsants. There were clinical signs in all cases and typical radiological signs in 3 cases, a characteristic laboratory syndrome in 4 cases. In the 3 cases where it was estimated, serum levels of parathormone were high. Finally, in 3 cases where it was measured, daily urinary excretion of glucaric D acid was increased. The bony histological signs studied in 3 cases, were similar to those in deficiency osteomalacia. A study of Ca45 metabolism in one case, showed the characteristic changes found in osteomalacia. Finally, a study of the metabolism of tritiated vitamin D, or tritiated 25 OH CC, carried out in 3 cases, gave 3 different patterns; only one of them was characteristic of enzyme induction under the dependency of anticonvulsant. Started in 2 cases, treatment with 125 OH2CC, brought about a rapid fall in blood PTH levels which then rose again before falling progressively in one case, under treatment with 25 OH CC. The bony histological signs of hyperparathyroidism then regressed whilst serum PTH levels remained high. Phosphorous and calcium balance improved in only one case. Treatment with 25 OH CC in high dosage brought about clinical, radiological and laboratory cure of osteomalacia in both cases, reducing the frequency of fits in the epileptic patient.

Adult↗
PubMed1975

[Osteomalacy induced by anticonvulsants. One case with a study of vitamin D metabolism].

A case of osteomalacia, with no cause apart from the ingestion of anti-convulsants, is reported. As was shown by a study with tritium labelled vitamin D, the metabolism of the latter was accelerated in this case in comparison with deficiency type osteomalacia. This lends support to the hypothesis that anti-convulsant medications, acting via a hepatic enzyme induction process, cause increased transformation of vitamin D into inactive metabolites, thus explaining a certain deficiency in vitamin D in treated epileptics, a deficiency state which requires treatment.

Adult↗
PubMed1975

[Osteomalcaia and chronic pancreatis. 5 cases].

The authors report five cases of an association between osteomalacia and chronic calcifying pancreatitis. The pancreatic involvement, which was pain-free in four patients, resulted in all cases in enzyme insufficiency with steatorrhoea. The deficiency-type osteopathy was highly vitamin sensitive. Aetiological study of these cases of osteomalacia revealed the constant presence of factors aggravating the vitamin deficiency, playing a role by increasing deficient intake or malabsorption, or by increasing Vitamin D requirements. It thus appears that hypovitaminosis D alone, of particular severity, was sufficient to result in the appearance of clinically evident osteomalacia. Such a vitamin deficiency, necessary when the intestinal mucosa is intact, is only rarely encountered, which accounts for the extreme rarity of osteomalacia in association with chronic pancreatic disorders.

Adult↗
PubMed1974

The effect of Prednisolone upon the metabolism and action of 25-hydroxy-and 1,25-dihydroxyvitamin D3.

Treatment of vitamin D-deficient rats with Prednisolone(R) does not alter the rate of conversion of [(3)H]25-hydroxyvitamin D(3) to [(3)H]1,25-dihydroxyvitamin D(3), but the further conversion of [(3)H]1,25-dihydroxyvitamin D(3) to a more polar metabolite is more rapid in the Prednisolone(R)-treated animals. This more polar metabolite is biologically inactive, periodate-insensitive, and persists in the intestine as long as 1,25-dihydroxyvitamin D(3). Also, the time course of action of 1,25-dihydroxyvitamin D(3) upon intestinal calcium transport is altered by Prednisolone(R) treatment. Treatment with Prednisolone(R) did not change the magnitude of the initial response to 1,25-dihydroxyvitamin D(3) at 7 hr, but did decrease the response at 24 and 48 hr after a single dose of 1,25-dihydroxyvitamin D(3). The present results show that one of the means by which large doses of adrenal corticoids alter intestinal calcium transport is by stimulating the further metabolism of 1,25-dihydroxyvitamin D(3) to a more polar, biologically inactive intestinal metabolite.

Animals↗