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Biomedical subjects

S Edelstein

Publications and source records attributed to S Edelstein.

At least 91 records · Page 5Linked to original sources
PubMed1983

Production of the hydroxylated metabolites of vitamin D in a neonate with a single hypoplastic-dysplastic kidney.

The ability to produce dihydroxylated metabolites of vitamin D was studied in a term neonate suffering from severe renal insufficiency. The infant died at age 26 days owing to end-stage renal failure and the necropsy examination showed a single dysplastic kidney weighing 1.5 g. At age 2 weeks the serum levels of the dihydroxylated metabolites of vitamin D were found to be normal and a pronounced increase was noted 24 hours after injection of 100 000 IU vitamin D2. The study suggests that during the neonatal period a small renal mass is sufficient to maintain optimal circulating levels of the dihydroxylated metabolites of vitamin D.

Dihydroxycholecalciferols↗
PubMed1983

The management of siblings with familial hypophosphatemic rickets.

Two siblings (boy and girl) born to a mother with familial hypophosphatemic rickets had abnormal values of serum phosphorus and serum alkaline phosphatase at the age of six weeks. At this age therapy with 1 alpha-hydroxycholecalciferol (1 alpha OHD3) and phosphate was started resulting in both siblings having normal growth of body length and radiological healing of the bone lesions but persistently low values of fasting serum phosphorus during the time of observation up to 60 and 26 months of age, respectively. Phosphate and 1 alpha OHD3 have a positive influence on serum phosphorus through their effect on the intestine. Neither of the patients developed hypercalcaemia during treatment. It seems, therefore, that the early administration of 1 alpha OHD3 with phosphate in infants with familial hypophosphatemic rickets prevents dwarfism and has a positive effect on intestinal absorption of phosphorus but not on fasting hypophosphatemia.

Female↗
PubMed1982

Effect of cholecalciferol derivatives on the mechanical properties of chick bones.

Chicks were depleted of vitamin D, divided into groups, and treated daily with (a) cholecalciferol, (b) 1 alpha-hydroxycholecalciferol [1 alpha (OH)-D3], (c) 24R, 25-dihydroxycholecalciferol [24R,25-(OH)2D3], or (d) 1 alpha (OH)D3 and 24R,25(OH)2D3. Two additional groups of chicks were studied, one that was continuously depleted of vitamin D, and another that was continuously supplemented with the vitamin, since day 1. After killing, the tibiae were removed and tested for their mechanical properties. Bending load was applied to the midshaft, and the intrinsic properties of this site, its quantity and geometry were analyzed. From a mechanical point of view, the weakest bones found were of birds depleted of vitamin D, whereas the strongest were of those treated with 1 alpha (OH)D3. Only the bones of the 24R,25(OH)2D3-treated or the 1 alpha (OH)D3 and 24R,25(OH)2D3-treated groups of birds showed mechanical properties comparable to those obtained with vitamin D-replete chicks.

24,25-Dihydroxyvitamin D 3↗
PubMed1982

The effect of toxic doses of 1,25-dihydroxycholecalciferol on dental tissues in the rat.

Vitamin D-depleted rats 4-weeks old were divided into three groups and given daily for 5 weeks cholecalciferol (0.25 microgram) or 1,25(OH)2D3 (0.075 microgram). The third group received no treatment with vitamin D sterols. A fourth control group was fed a diet containing vitamin D. The animals were killed after 5 weeks, plasma was prepared for calcium analysis, and incisors and molars were taken for histology. Growth was monitored throughout. Plasma calcium, body weight and the physical condition of the 1,25(OH)2D3-treated animals indicated that they were toxemic. The pulp-dentine complex of their incisors showed premature aging of fibroblasts and odontoblasts, disturbances in the dentinal matrix and osteodentine formation. That of molars was not affected. There was hypercementosis and bone-like tissue formation in the periodontal-ligament which in the incisors was considerably enlarged; some molars were ankylosed. The pulp-dentine complex of the incisors and molars of the rats in the remaining three groups appeared normal except for zones of hypomineralization in incisors of the third group. The supporting tissues of the teeth of the rats in the other three groups were within normal limits. Thus toxic doses of 1,25(OH)2D3 affected the dental tissues of both developing and mature teeth.

Animals↗
PubMed1982

Cholecalciferol requirements of young turkeys under normal conditions and during recovery from rickets.

Day-old turkeys fed vitamin D-deficient diets became rachitic within 17-24 days. The symptoms included reductions in body weight, plasma calcium and inorganic phosphorus, plasma and intestinal calcium-binding protein (CaBP), plasma 25-hydroxycholecalciferol [25(OH)D3], bone ash, and kidney 25(OH)D3-24-hydroxylase and a rise in kidney 25(OH)D3-1-hydroxylase activity. Supplementation of the diet with 12.5 micrograms cholecalciferol per kilogram was sufficient to promote maximal body weight and normal plasma calcium, Plasma calcium, plasma phosphorus and bone ash. Feeding diets containing 250 or 1250 micrograms cholecalciferol per kilogram resulted in a reduced body weight. An increased in the concentration of plasma 25(OH)D3 with increasing dietary cholecalciferol concentration was observed. Feeding vitamin D-deficient rachitic birds for 4 days a diet containing 50 micrograms cholecalciferol per kilogram restored plasma calcium and phosphorus and bone ash. Body weight remained lower than that of the control for an additional 6-day period. Additional cholecalciferol, 25(OH)D3 or 1 alpha-hydroxycholecalciferol in the diet, intramuscular injection of the vitamin D derivatives, or a high-calcium, high-phosphorus diet did not accelerate the recovery from the rachitic state.

Animals↗
PubMed1982

Metabolism of cholecalciferol in vitamin D intoxicated chicks.

Vitamin D intoxication was induced in chicks by treatment with large amounts of radioactive cholecalciferol (vitamin D3) either by s.c. injections or by stomach tube. Hypercalcemia and nephrocalcinosis were present, confirming toxicity. The distribution of cholecalciferol and its metabolites in the tissues of the intoxicated birds was compared with that in birds that were treated with physiological amounts of radioactive cholecalciferol. Treatment with pharmacological doses resulted in marked elevation of cholecalciferol and its metabolites in all tissues examined, including elevation of 1 alpha,25-dihydroxycholecalciferol in the intestine. The predominant form of cholecalciferol in these birds was found to be the unchanged vitamin, whereas in birds treated with physiological doses 25-hydroxycholecalciferol was the predominant metabolite. The route of vitamin administration was found to be of importance only when pharmacological doses were given: generally, higher levels were noted when administered via s.c. injections than via stomach tube, except in the arteries. It is suggested that in vitamin D intoxication, the factor responsible for the pathological changes in soft tissues is cholecalciferol itself. High levels of 1 alpha,25-dihydroxycholecalciferol may be responsible for the hypercalcemia.

Animals↗
PubMed1982

Intestinal loss of vitamin D3 metabolites in rats with cirrhosis of the liver.

The metabolism of cholecalciferol (vitamin D3) was studied in cirrhotic and in control rats that were either depleted of or supplemented with vitamin D3. The vitamin was supplemented by s.c. injections of radiolabeled cholecalciferol at doses which meat the daily nutritional requirements of rats. Excretion of vitamin D3 metabolites in the feces of the cirrhotic rats was greater than that in the control rats. Fecal excretion consisted mainly of vitamin D3 ester the unchanged vitamin D3 and 25-hydroxyvitamin D3. It is suggested that one of the causes for vitamin D3 depletion in cirrhosis of the liver is fecal loss.

Animals↗
PubMed1981

Decreased 1,25-dihydroxycholecalciferol and increased 25-hydroxy- and 24,25-dihydroxycholecalciferol in tissues of rats treated with thyroxine.

The effect of thyroxine on the metabolism of vitamin D was investigated in rats. Vitamin D depleted rats were repleted by injections of radiolabelled cholecalciferol or 25-hydroxycholecalciferol (25OHD3). After 3 weeks, a state of hyperthyroidism was induced by daily injections of L-thyroxine for 21 days. The lipid extracts of the Plasma and tissues were analyzed by successive Sephadex LH-20 and high pressure liquid chromatography. The concentrations of 25OHD3 and of 24,25-dihydroxycholecalciferol (24,25 (OH)2D3) were significantly higher and those of cholecalciferol and of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were significantly lower in the plasma and tissues of animals treated with thyroxine than in controls. The present study suggests that alterations in the metabolism of vitamin D may be involved in the disturbances of calcium metabolism observed in hyperthyroidism.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

1,25-dihydroxyvitamin D3 and the regulation of macrophage function.

Vitamin D3 deficient (D-) mice show a depressed inflammatory response and both inflammatory peritoneal macrophages and bone marrow polymorphonuclear leukocytes of D- mice exhibit a decreased spontaneous migration under agarose. The impaired phagocytic response of peritoneal macrophages from D- mice can be corrected by incubation with 1,25-dihydroxyvitamin D3 and is not affected by interaction with other vitamin D3 metabolites. Transfer of mice from the D- to the D+ state results in correction of both the inflammatory and the phagocytic response. Intactness of phagocyte function is thus directly dependent on vitamin D3 metabolism.

Animals↗
PubMed1981

Methemoglobinemia from isobutyl nitrite preparations.

Ingestion of preparations containing isobutyl nitrite can lead to rapidly fatal methemoglobinemia. We report the cases of three patients presenting with methemoglobinemia secondary to ingestion or inhaling the contents of an over-the-counter room odorizer preparation containing isobutyl nitrite. The condition was treated successfully with administration of intravenous methylene blue.

Adolescent↗
PubMed1981

Transplacental effects of 1,25-dihydroxycholecalciferol and of 24,25-dihydroxycholecalciferol on the limb skeleton of fetuses and offspring rats.

The transplacental effects of 1,25(OH)2D3 and of 24,25(OH)2D3 on bone formation in rat fetuses and pups have been investigated. Pregnant rats treated with 1,25(OH)2D3 or with 1,25(OH)2D3 and 24,25(OH)2D3 showed hypercalcemia, while those treated with 24,25(OH)2D3 did not. Fetal weight was markedly reduced by treatment with 1,25(OH)2D3 and not with 24,25(OH)2D3 or with a combination of both metabolites. Microscopical examination of fetal long bones showed after treatment with 1,25(OH)2D3 a marked reduction in diaphysial length. Diaphyseal trabeculae were thin and disorganized. The epiphysis had a thinner layer of hypertrophic and calcified cartilage. The numbers of osteoclasts in the diaphysis and metaphysis were the same as in controls. Treatment with 24,25(OH)2D3 did not affect fetal bone length; many bone trabeculae were found in the diaphyseal cavity leaving small bone marrow spaces; the number of osteoclasts in the metaphysis and in the diaphysis was increased. All changes in the skeleton disappeared during the first week after birth. It can be suggested that high doses of 1,25(OH)2D3 inhibit bone formation and maturation of cartilage. The addition of 24,25(OH)2D3 to 1,25(OH)2D3 seemed to reduce the toxic effects of the latter on the fetal skeleton. These results point to a definite difference between the action of high doses of 1,25(OH)2D3 and 24,25(OH)2D3 on fetal bone.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Inadequate status and impaired metabolism of vitamin D in the elderly.

The mean serum concentrations of 25-hydroxyvitamin D and of 24,25-dihydroxyvitamin D were significantly lower (P less than 0.01) in 82 elderly people than in 30 young control subjects. The levels in 30 elderly people confined to their rooms were 8.0 +/- 0.7 (SE) and 0.54 +/- 0.04 ng/ml, respectively; in 31 active old-age-home residents who spent part of their time outdoors, they were 11.4 +/- 0.8 and 0.82 +/- 0.08 ng/ml, respectively; and in 21 elderly farm workers, 14.6 +/- 1.4 and 0.98 +/- 0.10 ng/ml, respectively. In the young control subjects, the levels were 21.5 +/- 1.4 and 1.91 +/- 0.12 ng/ml, respectively. In addition, an intestinal absorption test with a standard oral dose of 25-hydroxyvitamin D3 showed that the serum 25-hydroxyvitamin D3 responses at 4 and 6 h were considerably depressed in 10 of the 20 elderly subjects in whom the test was performed.

Aged↗
PubMed1980

End-organ resistance to 1,25-dihydroxycholecalciferol.

A 13-year-old girl with total alopecia who in infancy had rickets unresponsive to large doses of vitamin D2 is described. She had profound hypocalcaemia which was resistant to treatment with high doses of dihydrotachysterol, 1 alpha-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. Serum concentrations of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxycholecalciferol were markedly raised (674 and 745 pg/ml). In addition, 24,25-dihydroxyvitamin D was undetectable in serum. Administration of synthetic 24,25-dihydroxycholecalciferol was followed by normocalcaemia which persisted long after treatment was stopped. Her sister, who died at the age of 10 months, also had had total alopecia, rickets, and hypocalcaemia resistant to vitamin-D2 therapy. In this familial syndrome there seems to be end-organ resistance to the action of 1,25-dihydroxycholecalciferol, possibly as a result of changes at the receptor sites.

Adolescent↗
PubMed1980

Absorption and excretion of cholecalciferol and of 25-hydroxycholecalciferol and metabolites in birds.

The absorption and excretion in vivo of cholecalciferol or 25-hydroxycholecalciferol (25-HCC) were determined in chicks (Gallus domesticus) and turkeys (Meleagris gallopavo). The overall net cholecalciferol or 25-HCC absorption in chicks and cholecalciferol in turkey poults was 66.5 +/- 3.3, 74.9 +/- 3.7 and 83.6 +/- 7.1% of the intake, respectively. The absorption of cholecalciferol or 25-HCC in chicks and turkeys occurred at the upper part of the intestine. 25-HCC, esters and non-polar metabolites of cholecalciferol or 25-HCC, and their polar metabolites, were secreted in the duodenum of chicks and turkeys but were partially reabsorbed at the upper part of the jejunum.

Animals↗