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Results for “Vitamin D Deficiency”

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At least 19 recordsLinked to original sources

PubMed1976

A morphometric investigation of the duodenal mucosa of normal, vitamin D-deficient, and vitamin D-replete rats.

Light and electron microscopy were utilized to determine differences in morphology and size in duodenal villi and microvilli from normal, vitamin D-deficient, and vitamin D-replete rats. An increase in villus diameter and surface area was observed in vitamin D-deficient rats. Administration of vitamin D reversed the increase in diameter but the height of villi increased resulting in longer, thinner villi without a significant change in surface area. A decrease in microvillus surface area seen in vitamin D-deficient animals was reversed by the administration of vitamin D.

Animals↗

PubMed1975

Intestinal CaBP: a new quantitive index of vitamin D deficiency in the rat.

Rats raised from weaning on regiments adequate in calcium and phosphorus but deficient in vitamin D will have no detectable intestinal calcium-binding proteins (CaBP), whether or not they show other signs of vitamin D deficiency, such as hypocalcemia. When hypocalcemic, vitamin D-deficient animals were treated with 25-hydroxycholecalciferol, a vitamin D metabolite, they showed a dose-dependent increase in plasma calcium and CaBP; both responses can be described by a single linear relationship, which appears to apply whether the metabolite is 25-hydroxycholecalciferol or dihydrotachysterol. Since vitamin D status is only one determinant of plasma calcium, whereas CaBP (or its expression) appears to depend on vitamin D quantitatively, CaBP may be used as an index of vitamin D status, provided calcium intake is controlled.

Animals↗

PubMed1977

A case of idiopathic hypoparathyroidism and dietary vitamin D deficiency: the requirement for calcium and vitamin D for bone, but not renal responsiveness to PTH.

A patient with concurrent idiopathic hypoparathyroidism and dietary vitamin D deficiency was studied. Acute renal responsiveness to PTH was demonstrated by immediate increases in urinary cyclic AMP and phosphorus excretion. An impaired bone response to sustained PTH administration was demonstrated by absence of significant increases in serum calcium or urine hydroxyproline during 3 days of PTH administration. Skeletal responsiveness was restored either by raising the initial serum calcium with constant calcium infusion or by raising serum 25-OH-D levels to normal by administration of 1,000 units vitamin D daily. These results extend to the human, animal observations which suggest that vitamin D is required for the skeletal but not for the renal actions of parathyroid hormone.

Bone Resorption↗

PubMed1976

Vitamin D deficiency and rickets.

Classical experimental rickets in the rat is a dual deficiency, resulting from both phosphate and vitamin D deficiency, with many of the features of rickets reproducible by simple phosphorus deficiency. Simple vitamin D deficiency differs markedly from experimental rickets, with only the absence of the vitamin D-dependent calcium-binding proteins common to both situations. The expression at the bone level of vitamin D deficiency differs in the two conditions, with rickets leading to profound structural and metabolic changes, whereas simple vitamin deficiency primarily compromises the regulatory function of bone, without obvious structural alterations. It is proposed that human nutritional rickets is the result of a nutritional vitamin D deficiency that aggravates the expression of a pre-existing metabolic defect in phosphate transport. Simple nutritional vitamin D deficiency, unaccompanied by rickets, may occur, but probably has always been rare.

Animals↗

PubMed1976

Vitamin-D deficiency rickets in Jamaican children.

Vitamin-D deficiency is not as rare in Jamaica as previously believed. 9 children with vitamin-D deficiency rickets have been seen at the University Hospital of the West Indies during the past 5 years. All were over 3 years of age at time of presentation. Both dietary deficiency of vitamin D and lack of exposure to sunlight seem to be important causes. Children living in rural Jamaica seem to be more susceptible to the disease than those living in a city, due perhaps to more prolonged breast feeding and lack of fortified milk feeds on weaning.

Black or African American↗

PubMed1978

An estimation of the parathyroid hormone secretion rate in vitamin D deficient rats.

In an attempt to define the rate of endogenous secretion of parathyroid hormone in vitamin D deficiency, graded amounts of hormone were infused constantly into vitamin D deficient and vitamin D fed acutely thyroparathyroidectomized rats in a perfusion balance study. The dose of hormone needed to compensate for acute thyroparathyroidectomy was estimated. Serum levels of calcium and phosphorus, renal clearances of phosphorus and urinary excretion of cyclic AMP, each determined 16 hr after the surgery, were employed as parameters of the hormone effect. It was concluded that, in the condition of the perfusion balance study, the secretion rate of parathyroid hormone was 5.1-8.6 USP u/hr in the vitamin D deficient animals compared with 0.81-0.84 USP u/hr in the control.

Animals↗

PubMed1978

[Vitamin D deficiency and osteomalacia in old people (author's transl)].

The frequency and causes of vitamin D deficiency in old age were investigated in 53 hospital patients, 88 persons from old people's homes, 21 tenants of a hostel, and 29 members of a seniors meeting group, aged between 65 and 93 years. In all persons 25-hydroxyvitamin D, calcium, phosphate, alkaline phosphatase, leucine arylamidase and creatinine were determined. In 27 cases immunoreactive parathormone was measured. In hospital patients there was evidence of vitamin D deficiency significantly more frequently as compared with the other groups. The 25-hydroxyvitamin D concentration was on average lower in the cases from old people's homes and hostels than in the members of the seniors group. The results in the groups investigated showed a relation to the average exposure to the sun. The results in 10 further patients in this age group with florid osteomalacia indicate a multifactorial aetiology of vitamin D deficiency disease due to reduced exposure to sun, inadequate nutrition and reduced absorption of vitamin D.

Age Factors↗

PubMed2025

Treatment response variations to a single large bolus of enteral cholecalciferol in vitamin D deficient critically Ill children: Metabolomic insights for precision nutrition.

Vitamin D deficiency (VDD) is prevalent globally and in pediatric intensive care units, where it represents a modifiable risk factor that may impact patient recovery during hospitalization. Herein, we performed a retrospective analysis of serum samples from a phase-II randomized placebo-controlled trial involving a single large bolus of 10,000 IU/kg vitamin D3 ingested by critically ill children with VDD (25-OH-D < 50 nmol/L). Targeted and untargeted methods were used to comprehensively measure 6 vitamin D metabolites, 239 lipids, 68 polar metabolites, and 4 electrolytes using a multi-step data workflow for compound authentication. Complementary statistical methods classified circulating metabolites/lipids associated with vitamin D repletion following high-dose vitamin D3 intake (n = 20) versus placebo (n = 11) comprising an optional standard of care maintenance dose (< 1000 IU/day). There was a striking increase in median serum concentrations of 25-OH-D3 (4.7-fold), 3-epi-25-OH-D3 (24-fold) and their C3-epimer ratio (6.7-fold) in treated patients on day 3, whereas serum vitamin D3 peaked on day 1 (128-fold) unlike placebo. Treatment response differences were attributed to D3 bioavailability and C3-epimerase activity without evidence of hypercalcemia. For the first time, we report the detection of circulating 3-epi-D3 that was strongly correlated with vitamin D3 uptake (r = 0.898). Metabolomic studies revealed that vitamin D sufficiency (serum 25-OH-D >75 nmol/L) coincided with lower circulating levels of 3-methylhistidine, cystine, S-methylcysteine, uric acid, and two lysophosphatidylcholines 7 days after treatment. Rapid correction of VDD was associated with indicators of lower oxidative stress, inflammation, and muscle protein turn-over that may contribute clinical benefits in high-risk critically ill children.

Humans↗

PubMedDate not supplied

[Effect of protein and vitamin D deficiency on several indices of calcium metabolism].

The effect of the proteins and vitamin "D" deficiency in the diet on the formation of the calcium-binding protein (CaBP), absorption of calcium in the small intestine and on the Ca and P content in blood serum of rats was studied. The resulting data demonstrate that hypovitaminosis "D" leads to a significantly reduced formation of CaBP, diminished absorption of tagged C35 in the small intestine and Ca and P level in the blood serum. The decline of these values is observed in cases of protein deficiency and with rising protein shortage these changes become more marked. A further fall of the CaBP level, of the labelled calcium absorption and of the serumal Ca and P is observed with simultaneous action on the organism of the proteins and vitamin "D" deficiency.

Animals↗

PubMed1979

[Erythrocyte metabolism in vitamin D deficiency rickets].

In an attempt to explain the hemolysis observed in vitamin D deficiency rickets in the infant, we studied erythrocytic glycolysis, the level of ATP and some of the key enzymes of the glycolytic pathway. This study was performed in one group of vitamin D deficient infants and in one control group. The values obtained in these two groups did not differ significantly. In the absence of a defect in the glycolytic pathway, we suggest that an anomaly exists in the red cell membrane of these patients.

Adenosine Triphosphate↗

PubMed1976

Clinical and subclinical vitamin D deficiency in Bradford children.

A survey of the vitamin D status of Bradford schoolchildren was carried out in April 1973, employing conventional biochemistry, radiology, and measurement of 25-hydroxycholecalciferol levels. Biochemical evidence of rickets was present in 45% of the Asians. When re-examined in September, several children showed spontaneous biochemical resolution; nevertheless, radiological abnormalities were present in 12% of the original sample. No evidence of rickets was detected in the smaller White sample. Minor biochemical abnormalities were present in 9 of the 40 West Indian children. A study of admissions of Bradford hospitals in the 4 years 1969-1972 inclusive confirmed that clinical vitamin D deficiency was confined to Asians except for a few cases of infantile rickets in White children. The probability that one Asian child in 40 may require admission during the period from birth to adolescence emphasizes the urgent need for the introduction of prophylactic measures.

Adolescent↗

PubMed1978

The influence of 1,25-dihydroxycholecalciferol on the ultrastructural organization of skeletal muscle fibres. Morphometric analyses on vitamin D deficient or calcium deficient growing rats.

Ultrastructural evidence was obtained from vitamin D deficient and calcium deficient rats that the sarcoplasmic reticulum (SR) is involved in the intracellular calcium transport of the muscle cell. In the absence of vitamin D there was a relative decrease in SR volume and a compensatory increase in mitochondrial volume. Administration of exogenous doses of 1,25-dihydroxycholecalciferol significantly increased SR volume, while mitochondrial volume correspondingly decreased. This supports the hypothesis that the production of calcium binding proteins within the SR is influenced by active metabolites of vitamin D.

Animals↗

PubMed1979

[Effects of 1,25(OH)2D3 on bone mineralization in vitamin D deficiency (author's transl)].

Two cases with vitamin D-deficient osteomalacia of digestive origin (coeliac disease) have been treated orally with 1,25(OH)2D3 in dosages of respectively 8 and 3 microgram/24 h. Serial transiliac bone biopsies have been performed. Mineralization fronts were normalized after respectively 4 and 1.5 months, whereas mineralization rates, as demonstrated by double tetracycline labeling, were normalized respectively after 2 and 1.5 months. In both cases osteomalacia healed completely despite persistently low 25(OH)D levels in the serum. It is obvious from these studies that 1,25(OH)2D3 per se is able to cure vitamin D-deficient osteomalacia, a finding that has been disputed. Whether 25(OH)D acts more rapidly on bone, as suggested by the studies performed in one case with anticonvulsant osteomalacia, remains to be proven.

Bone and Bones↗

PubMed1979

[Renal acidification disturbance in vitamin D deficiency (author's transl)].

Extensive studies of renal acidification process have been performed in states of vitamin D deficiency. Results show that the process of hydrogen ion excretion is strongly impaired on the entire length of the nephron. Vitamin D and parathyroid hormone probably interfere within tubular cells regulating the concentration of calcium and cyclic AMP; the modification of such an equilibrium carried out by vitamin D deficiency would explain the renal dysfunction.

Bicarbonates↗

PubMed1975

The comparative effects of vitamin d deficiency and ethane-1-hydroxy-1,1-diphosphonate administration on the histology and glycolysis of chick epiphyseal and articular cartilage.

A comparison has been made between the effect of a vitamin D--deficient diet and treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) on the morphology of chick epiphyseal cartilage and on the production of lactate in vitro by epiphyseal and articular cartilage. The cell populations in the growth plate were different following the two treatments. Vitamin D deficiency was characterized by an increase in proliferating cells, with a relative paucity of hypertrophic cells; EHDP treatment was characterized by an increase in hypertrophic cells. When similar cell types were compared, neither treatment changed lactate production from the control value. This stresses the need to correlate the morphology of cell types with their metabolic function. The present results indicate that the major effect of vitamin D deficiency in the chick is to block the differentiation of proliferating to hypertrophic cells. In contrast, EHDP may act by inhibiting calcification directly. Even though EHDP at the doses used is known to interfere with the production of 1,25-dihydroxycholecalciferol there is no block to cell differentiation under EHDP similar to that seen in dietary deficiency of vitamin D.

Animals↗

PubMed1975

Proximal renal tubular acidosis in vitamin D deficiency rickets.

A proximal renal tubular acidosis (RTA) is the mechanism underlying the systemic acidosis found in vitamin D deficiency rickets. Acidotic subjects have high levels of PTH. In non-acidotic subjects proximal bicarbonate wasting can be induced by exogenous PTH injection. Carbonic anhydrase activity is not involved in this process. Calcium infusion is able to suppress both the spontaneous and the PTH-induced bicarbonate leak. The development of RTA in vitamin D deficiency is related to a particular equilibrium between two antagonizing factors at tubular level, parathyroid hormone and calcium.

Acetazolamide↗

PubMed1978

Plasma vitamin D-binding globulin in vitamin D deficiency, pregnancy and chronic liver disease.

Plasma concentrations of vitamin D-binding globulin were measured by radial immunodiffusion in healthy subjects, pregnancy, and during oestrogen therapy. Subjects with disorders of vitamin D metabolism (dietary deficiency, malabsorption, anticonvulsant therapy, chronic liver disease) were also studied. Neither sex nor age influenced the plasma vitamin D-binding globulin concentration in healthy subjects, but there was a significant increase in concentration during pregnancy and oestrogen therapy. Elevated levels were found in vitamin D deficient elderly but not younger subjects, while levels in subjects with chronic liver disease were significantly reduced. Normal levels of vitamin D-binding globulin were present in hypervitaminosis D and no vitamin D-binding globulin was detected in human milk. No correlation was observed between plasma 25-hydroxycholecalciferol levels and plasma vitamin D-binding globulin concentrations.

Adult↗

PubMed1975

Vitamin D deficiency rickets. Two cases with faulty infant feeding practices.

Two cases of vitamin D deficiency rickets verify the occurrence of deficiency rickets in the United States in 1973. The two cases demonstrate the need for periodic reviews of feeding practices, especically when the possibility of so-called milk allergy is postulated. This may lead to avoidance of milk products. Fortification of various kinds of food with vitamin D does not ensure the protection from nutritional rickets of all children with peculiar feeding habits.

Alkaline Phosphatase↗