[Vitamin-D-resistant rickets: results of 12 months combined vitamin D and phosphate therapy].
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Child↗
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Vitamin D physiology and some clinical aspects of the vitamin D endocrine system.
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Adolescent↗
[Differential diagnostic problems resulting from massive doses of vitamin D and suspected pituitary dwarfism in the father of a child with vitamin-D-resistant rachitis (author's transl)].
A 1.8-year-old female child with retarded statomotor development and growth was reported. Radiologically and chemically, a rachitis was found which clearly improved following administration of 600,000 U. vitamin D3. Examination of the father who was thought to be suffering from pituitary dwarfism revealed hypophosphatemia and radiologic signs of osteomalacia. The diagnosis of a hypophosphatemic vitamin-D-resistant rachitis in this child could only be established with certainty during the course of the following months.
Adult↗
Recent advances in our understanding of the vitamin D endocrine system.
Vitamin D3 gives rise to at least one hormone in which the kidney is utilized as an endocrine system. This hormone arises from 25-OH-D3 which in turn is synthesized in the liver from vitamin D3. The production of this calcium and phosphorus mobilizing hormone, namely 1,25-(OH)2D3, is strongly regulated by the need for calcium and phosphorus. The regulation of its production can occur only after initial 1,25-(OH)2D3 is made and brings about the appearance of 25-OH-D3-24hydroxylase. The need for calcium brings about a stimulation of parathyroid hormone secretion. The parathyroid hormone suppresses the 24-hydroxylase and stimulates the 1-hydroxylase. Alternatively, the need for phosphorus directly stimulates the 1-hydroxylase and suppresses the 24-hydroxylase. The 24-hydroxylation appears to be the initial reaction leading to the inactivation and excretion of vitamin D whereas the 1-hydroxylation is the reaction bringing about the activation of the molecule to 1,25-(OH)2D3. The 1,25-(OH)2D3, the 25-OH-D3 and an analog of 1,25-(OH)2D3, namely 1alpha-OH-D3, are potentially extremely useful in the treatment of metabolic bone diseases such as renal osteodystrophy, hepatically related disorders of calcium and bone metabolism, hypoparathyroidism, and vitamin D dependency disease. The 1alpha-OH-D3 is effective by virtue of its conversion to 1,25-(OH)2D3. The 25-hydroxylation of both 1alpha-OH-D3 and vitamin D3 itself occurs predominantly in the liver. Finally, it is not entirely settled whether 1,25-(OH)2D3 is active directly in all of the functions of viramin D or whether it must be further converted metabolically. A new metabolic pathway for vitamin D has been discovered in which 1,25-(OH)2D3 loses its 26 and 27 carbons to carbon dioxide, producing an unknown metabolite. It is not certain whether this pathway represents degradation of the 1,25-(OH)2D3 or its further activation.
25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
[Effect of vitamin D metabolites on mineralization of bone tissue and phosphocalcium metabolism disorders in the course of vitamin D deficiency osteomalacia].
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Adult↗
Determination of vitamin D in foods: a review.
Determining vitamin D content in foods is difficult because in natural foods of highest vitamin D activity, and even in vitamin D-fortified foods, only small quantities are present, and many other compounds are extracted along with vitamin D that cause difficulties in purifying the extract or in the spectrophotometry or colorimetry that follows. Several physicochemical methods--such as spectrophotometric, colorimetric, thin-layer chromatographic, adsorption, partition, gas-liquid, and high-performance column chromatographic--have been tried for assay foods for vitamin D, but none of them have been accepted for official or routine use; they are time consuming and expensive, or lack the required sensitivity, precision, or accuracy. Curative biological assays, based on degree of healing of a leg bone of rats previously made rachitic, is the generally accepted method to determine vitamin D content of foods. However, that method also requires too much time and is expensive. The recently developed high-performance liquid chromatographic method may offer the most for establishing a satisfactory physicochemical method for determining vitamin D in foods. Many of the difficulties and problems in assaying foods for vitamin D are discussed.
Animals↗
A family with massive acute vitamin D intoxication.
Acute massive vitamin D overdosage occurred in a family after eating food cooked in a nut oil containing 5 million units of vitamin D3/ml. The plasma vitamin D was 55 and 60 i.u./ml in the father and mother respectively, and 9.6 i.u./ml in their 11-month-old infant (normal range, 0--1.6 i.u/ml). All the family presented with symptoms of hypercalcaemia and the infant responded quickly to prednisone. After steroids had failed to control the hypercalcaemia in the parents, neutral phosphate was successful, although necessary for 9 months. Before phosphate therapy it was shown that both parents were in strongly negative calcium balance, indicating that the vitamin D was mobilizing calcium from bone. Eleven years later all 3 patients are well but a renal biopsy in one of them shows persistent nephrocalcinosis.
Acute Disease↗
[Possible role of free radicals in the transformations and mechanism of physiological action of vitamin D].
Deficiency of vitamine D is accompanied with a decrease of ESR signal intensity from g = 2.003, as well as of the signals with g = 1.94 and gav. = 2.25 in the liver and kidneys of young rats. Injection of 2.5 g ergocalciferole (vitamine D2) to these animals results in a complete or partial normalization of the intensity of these signals during 6--16 hrs and an increase of the ESR signal intensity from g = 2.003 in small intestine mucosa.
Animals↗
Vitamin-D in human milk.
The vitamin-D concentration in human milk is reported to be very low, yet breast-fed infants do not develop rickets. All the earlier assays of vitamin D were made on the lipid fraction of milk, and the aqueous phase was discarded. It is now clear that most of the vitamin D in human milk is present as a water-soluble conjugate of vitamin D with sulphate. The concentration of vitamin-D sulphate in the aqueous fraction of human milk collected at different stages of lactation has been chemically measured. Milk was collected from twenty-two women 3-8 days post partum and fourteen women 4-6 weeks post partum. The vitamin-D sulphate concentration in milk collected between the 3rd and 5th days was 1-78 mug/dl, significantly higher that the 1-00 mug/dl for milk collected between the 6th and 8th days. After the 8th day there was no significant change.
Breast Feeding↗
Relative contributions of diet and sunlight to vitamin D state in the elderly.
In winter the vitamin D state of elderly people may reach levels associated with osteomalacia, although the disease may not be clinically apparent. A statistical correlation was observed in a group of elderly subjects during the winter between dietary vitamin D intake and vitamin D state, but the intake was generally too low to make a biologically important contribution to maintaining vitamin D concentrations. Ultraviolet light (UVL) is the primary determinant of vitamin D state in summer and winter, in winter owing to the pools of vitamin D built up during the previous summer. Plasma concentrations of 25-hydroxy vitamin D (25-OHD) in winter of 15.0-22.5 nmol/l (6-9 ng/ml) require that the concentration in the previous summer was over 40 nmol/l (16 ng/ml). To maintain plasma concentrations in the elderly above those associated with osteomalacia a mean dietary vitamin D intake of over 5 microgram/day is required. A more physiological approach, however, would be to increase exposure to UVL.
Aged↗
The calcium and vitamin D status in an elderly female population and their response to administered supplemental vitamin D3.
Recent reports have implicated the importance of impaired calcium absorption, inadequate dietary vitamin D, and low serum vitamin D levels in the genesis of metabolic bone diseases in the elderly. This study evaluated the dietary intakes of calcium and Vitamin D, calcium absorption, and serum 25 hydroxycholecalciferol (25 OH D) levels in a population of women (mean age 83 yrs) compared to healthy volunteers (mean age 35 yrs). Dietary intakes of both calcium and vitamin D and serum 25 OH D levels were found to be comparable in both groups. Calcium absorption was normal in the subjects studied and did not change significantly after two 2-week periods of oral supplementation with vitamin D3 in doses of 500 I.U./day and 10,000 I.U./day, although the serum 25 OH D levels rose significantly and comparably in both groups. Thus other etiological factors may play relevant roles in the causation of bone diseases in the elderly and unless deficient dietary or serum vitamin D levels are demonstrated, empirical supplementation with vitamin D should not be undertaken. The differences of the above findings from previously published data are discussed.
Absorption↗
Abnormal vitamin D metabolism in cirrhosis.
Vitamin D metabolism was investigated in 10 patients with cirrhosis. Mean plasma 25 hydroxycholecalciferol (25 OHD) centration in alcoholic cirrhosis was lower than in controls but the difference was not significant. In three patients restudied after the summer, plasma 25 OHD had risen. In contrast to the finding in normal subjects, the half-life of intravenously administered 3H cholecalciferol was short in cirrhotics and showed no correlation with plasma 25 OHD. Furthermore, the appearance of 3H 25 OHD from 3H cholecalciferol was reduced compared to the control group four hours after injection. Increased rate of metabolism of cholecalciferol and deficient production of 25 ohd contribute to vitamin D deficiency in liver disease.
Adult↗
Measurement of 25-hydroxyvitamin D in serum and its relation to sunshine, age and vitamin D intake in the Danish population.
A competitive protein-binding assay for 25-hydroxyvitamin D (25-OHD) based upon a specific binding protein in the cytosol from rachitic rat kidneys is described. A diethyl ether extraction followed by separation by freezing was used. The extracts were chromatographed on short silicic acid columns, which separated 25-hydroxycholecalciferol from cholecalciferol, 24,25-dihydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. A small aliquot of the 25-OHD fraction was used in the assay and free and bound vitamin were separated by dextran coated charcoal. The lower detection limit was 0.8 ng/ml (2.0 nmol/l). The levels of 25-OHD were measured in 596 healthy subjects and a seasonal variation was demonstrated. This variation, however, was only found in those without regular vitamin D intake, whereas the level of 25-OHD remained constant throughout the year in subjects with regular vitamin D supplement. The levels of 25-OHD were lower in the elderly subjects compared to younger ones, but seasonal variation was observed in both groups. In the summer months there was a significant correlation between age and the 25-OHD level. The mean levels of 25-OHD in Denmark are within the range of means found in the United States and Sweden but are higher than those reported from England, Belgium and France. This indicates a relatively high vitamin D intake in the Danish population and a low risk of nutritional vitamin D deficiency.
Adolescent↗
25-Hydroxyvitamin D3 26,23-lactone: a new in vivo metabolite of vitamin D.
A major vitamin D metabolite was isolated in pure form from the blood plasma of chicks either maintenance levels or large doses of vitamin D3. The isolation involved methanol-chloroform extraction and five column chromatographic procedures. The metabolite purification and elution position on these columns were followed by a competitive protein binding assay. The metabolite was identified, using high- and low-resolution mass spectrometry, 270-MHz proton nuclear magnetic resonance spectrometry, ultraviolet absorption spectrophotometry, Fourier transform infrared spectrophotometry, and specific chemical reactions, as 3 beta,-25-dihydroxy-9,10-seco-5,7,10(19)-cholestatrieno-26,23-lactone. The trivial names 25-hydroxyvitamin D3 26,23-lactone or calcidiol 26,23-lactone are suggested for this compound.
Animals↗
Antiepileptic drugs and vitamin D supplementation.
The incidence of biochemical signs of vitamin D deficiency and the effects of vitamin D supplementation were investigated in 83 children and 95 adults on chronic antiepileptic therapy and 40 mentally retarded controls living under comparable conditions. Low 25-hydroxyvitamin D and serum calcium, and elevated immunoreactive parathyroid hormone and alkaline phosphatase was a common finding in all groups, but in patients on antiepileptic drugs, signs of vitamin D deficiency were recorded more frequently. Supplementation of 125 microgram or 250 microgram vitamin D3 per week for 9 months normalized the laboratory findings in most patients; the effect of 37.5 microgram/week only slightly exceeded the influences of season observed in the controls and in epileptic patients without vitamin D. It is suggested that a dose between 37.5 and 125 microgram vitamin D3/week might be most suitable to avoid biochemical signs of vitamin D deficiency in children and adults on antiepileptic drugs.
Adolescent↗
Metabolic and cellular activity of vitamin D.
Most of the effects of vitamin D on calcium and phosphorus homeostasis result from an increase in intestinal absorption of calcium and phosphorus and from bone mobilization. These effects are due to 1,25(OH)2D3, one of the renal vitamin D metabolites. Besides ionic mobilization, vitamin D may exert additional effects on bone which depend on metabolites other than 1,25(OH)2D3. Kidneys, parathyroid glands and muscle are probably target organs for vitamin D. The metabolite(s) responsible for these actions remain unknown.
Animals↗
Serum concentrations of 25-hydroxy vitamin D in Europeans and Asians after oral vitamin D3.
Serum concentrations of 25-hydroxy vitamin D (25-OHD3) were measured in seven Asians of Indian extraction and eight Europeans before and at intervals after taking 1 mg vitamin D3 by mouth. In all subjects the concentrations rose in the 24 hours after ingestion. There was little change over the next nine days in the concentrations in the Europeans but those in the Asians continued to rise until about day 10. Subsequent rates of fall in 25-OHD3 were similar in the two groups. Our observations suggest that the low serum concentrations of 25-OHD3 found in Asians are not caused by either impaired intestinal absorption of vitamin D or rapid clearance of 25-ODH3 from the plasma.
Administration, Oral↗
Prevalence and determinants of profound vitamin D deficiency (25-hydroxyvitamin D <10 nmol/L) in the UK Biobank and potential implications for disease association studies.
BACKGROUND: 25-hydroxyvitamin D (25OHD) is the principal biomarker of vitamin D status. Values below the assay detection limit (<10 nmol/L) are often reported as missing. Thus the most severely deficient participants are excluded from research which can lead to inaccurate findings such as underestimated prevalence of deficiency, overlooked risk factors, and biased evaluation of disease associations. METHODS: In total 369,626 individuals from the UK Biobank cohort were included in this study. Data on 25OHD concentration and relevant demographic and lifestyle factors such as age, supplement intake, diet, and time spent outdoors were used in the analyses. Ambient UVB radiation was approximated for each participant. 25OHD was evaluated as a categorical outcome and we reintroduced participants with 25OHD values < 10 nmol/L (conventionally reported as missing values) back to the dataset. Adjusted regression models were used to investigate the determinants of profound (25OHD <10 nmol/L) and severe (10-25 nmol/L) vitamin D deficiency and to assess disease associations (with 25-50 nmol/L as the reference category). RESULTS: 1,784 (0.48 %) individuals were profoundly deficient and a further 47,226 (12.78 %) individuals were severely vitamin D deficient. The proportions of profoundly and severely deficient were highest among Asians, 9 % and 47 %, respectively. Ambient UVB radiation was the second strongest predictor: comparing the lowest vs. highest quartile, the risk of profound deficiency was 17-fold increased and that of severe deficiency 7.5-fold increased. Use of vitamin D supplements substantially reduced risk of profound (4.4-fold) and severe (2.5-fold) deficiency, as did fish intake (5- and 1.9-fold, respectively). Profound deficiency was more strongly associated with chronic illness, diabetes, and emphysema compared to severe deficiency. CONCLUSION: The prevalence of profound and severe vitamin D deficiency among Asian and Black ethnicities in the UK is high and requires targeted action. Solar radiation is potent in protecting against profound and severe vitamin D deficiency. Studies evaluating the relationship between vitamin D status and other health outcomes may be biased if profoundly deficient participants are excluded.
Humans↗