Osteoporosis and the role of vitamin D and calcium-vitamin D deficiency, vitamin D insufficiency and vitamin D sufficiency.
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Bone and Bones↗
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Serum levels of bone-specific alkaline phosphatase and procollagen type I carboxyterminal peptide in vitamin D deficiency.
Vitamin D deficiency in adults causes osteomalacia where there is a defect in bone mineralization resulting in an excess of unmineralised osteoid in the bone matrix. The aim of this study was to evaluate the markers of bone formation: total (TALP), bone-specific alkaline phosphatase (BSALP) and procollagen type I carboxyterminal peptide (PICP) in vitamin D deficiency. We studied 100 vitamin D deficient subjects and 82 gender-matched controls. Vitamin D deficiency was defined as serum 25-hydroxyvitamin D level of less than 7 ng/ml, and greater than 10 ng/ml for normal controls. Serum TALP assay was performed by a standard automated method, BSALP and PICP were measured by enzyme immunoassays (Metra Biosystems) and vitamin D by radioimmunoassay. There was significant difference in the TALP between female vitamin D deficient and control subjects (mean +/- sem = 99.8 +/- 8.2 vs 70.5 +/- 2.8 iu/l, p<0.001). Elevated serum TALP (>130 iu/l) was found in 20% (20/100) of the vitamin D deficient patients. There were no significant differences in BSALP or PICP between vitamin D deficient patients and gender-matched control subjects. There was no correlation between vitamin D and PICP in patients but in control subjects, a significant negative correlation (r= -0.431, p<0.0001) was found. In conclusion, although elevated TALP was observed in a minority of vitamin D deficient patients, it is a better marker than PICP. The lack of PICP response in vitamin D deficient subjects suggests the possibility of vitamin D deficiency leading to a block in osteoblast differentiation.
Adult↗
Routine biochemistry in suspected vitamin D deficiency.
Vitamin D deficiency, which continues to be widespread amongst persons of Asian descent in the UK, is often detected from abnormal results on routine biochemistry. The aim of this study was to assess the frequency of abnormal results from routine baseline tests of serum calcium, phosphate, and alkaline phosphatase in patients who subsequently proved to have vitamin D deficiency and secondary hyperparathyroidism. A retrospective examination was undertaken to assess these baseline indices in a cohort of 84 such patients seen in Bradford-5 male; 80 of Asian descent; median age 46 years (range 16-82); serum 25-hydroxyvitamin D<10 microg/L; parathyroid hormone >54 ng/L. Calcium was normal in 55 patients (66%), phosphate in 68 (81%) and alkaline phosphatase in 24 (29%). In only 5 patients were all three indices outside the normal range. The median parathyroid hormone concentration was significantly greater in patients with abnormal routine biochemistry (145 [range 55-1662] ng/L) than in patients with normal routine biochemistry (88 [59-322] ng/L) but the median 25-hydroxyvitamin D levels did not differ (3.1 [1.3-9.9] and 3.0 [1.5-7.3] microg/L). Routine biochemistry was normal in 20% of cases. If routine biochemistry is relied upon to detect vitamin D deficiency and osteomalacia, a substantial minority of cases will be missed.
Adolescent↗
Identification of rat osteoclasts in bone smears with quantification of acid phosphatase activity in vitamin D deficiency.
Vitamin D deficiency may depress bone formation but its effect on bone resorption is not well defined. As an index of bone resorption, the activity of acid phosphatase, a lysosomal enzyme found in osteoclasts, was quantitated in situ from a bone tissue smear preparation. Activity of the enzyme, measured by integrative microdensitometry increased linearly from 25 to 60 min. The distribution of activity in osteoclasts quantitated appeared to follow a normal distribution with a median value of 0.19 integrated optical density units. Animals treated with vitamin D or 1,25 dihydroxycholecalciferol had significantly increased activity of acid phosphatase in osteoclasts compared to animals which were vitamin D deficient. The increase of acid phosphatase activity averaged 63%. Vitamin D or its metabolites may have a permissive effect on the action of parathyroid hormone or act directly to increase bone resorption.
Acid Phosphatase↗
Parathyroid function in human vitamin D deficiency and vitamin D deficiency in primary hyperparathyroidism.
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Adolescent↗
Maternal vitamin D deficiency and vitamin D supplementation in healthy infants.
The objective of this study was to evaluate the common effects of maternal vitamin D deficiency, various doses of vitamin D given to newborns and the effects of these on vitamin D status in early childhood. Seventy-eight pregnant women and 65 infants who were followed up in various health centers were included in the sudy. 25-hydroxyvitamin-D (25-OHvitD), calcium (Ca), phosphorus (P) and alkaline phosphatase levels were measured in blood samples drawn from pregnant women in the last trimester. Infants born to these mothers were given 400 or 800 IU of vitamin D subsequently at the start of the second week. 25-OHvitD, Ca, P and alkaline phosphatase levels of the 65 infants who were brought in for controls (May-September 2000) were measured and hand-wrist X-rays were evaluated. We analyzed the relationship between vitamin D status of the mothers and infants and socio-economic status; mothers' dressing habits (covered vs uncovered), educational level, and number of pregnancies; and sunlight exposure of the house. Covered as a dressing habit meant covering the hair and sometimes part of the face and wearing dresses that completely cover the arms and legs. In 40 infants who were breast-fed and received the recommended doses of vitamin D on a regular basis, the relationship between serum vitamin D levels and supplementation doses given was analyzed. Serum 25-OHvitD level of the mothers was 17.50 +/- 10.30 and 94.8% of the mothers had a 25-OHvitD level below 40 nmol/L (below 25 nmol/L in 79.5%). The risk factors associated with low maternal 25-OHvitD were low educational level (p = 0.042), insufficient intake of vitamin D within diet (p = 0.020) and "covered" dressing habits (p = 0.012). 25-OHvitD level of the infants was 83.70 +/- 53.70 nmol/L, and 24.6% of the infants had 25-OHvitD levels lower than 40 nmol/L. Risk factors for low 25-OHvitD levels in infants were a) not receiving recommended doses of vitamin D regularly (p = 0.002) and b) insufficient sunlight exposure of the house (p = 0.033). There was a pour but significant correlation between maternal vitamin D levels and infants' 25-OHvitD levels at four months (r = 0.365, p < 0.05). No significant correlation was found between 25-OHvitD levels and supplementation doses of vitamin D (19 infants were supplemented with 400 IU/day and 21 with 800 IU/day of vitamin D) (p = 0.873). Severe maternal vitamin D deficiency remains a commonly seen problem in Turkey. However, vitamin D deficiency can be prevented by supplementation of vitamin D to newborns (at least 400 IU). Supplementation of 800 IU vitamin D in the areas of maternal vitamin D deficiency has no greater benefits for the infants.
Adult↗
The status of biochemical parameters in varying degrees of vitamin D deficiency.
Vitamin D (Vit D) is an essential element for the regulation of serum calcium, phosphate, and alkaline phosphatase (Alk Ph). Because the Vit D serum level is not usually measured directly, Vit D deficiency is diagnosed indirectly by changes in serum calcium, phosphate, and Alk Ph leves. The current study assessed the status of these biochemical parameters in subjects with different degrees of Vit D deficiency. We selected 1,210 subjects, between 20 and 69 years old, randomly from the Tehran population. Subjects with diseases or medications that modified bone metabolism were excluded from the study. Serum 25(OH) D, calcium, phosphate, Alk Ph, and parathyroid hormone (PTH) levels were measured and the status of these biochemical parameters was compared in subjects with different degrees of Vit D deficiency. Vit D deficiency was diagnosed in 79.6% of the subjects. Different degrees of Vit D deficiency were classified as follows: group 1, severe; group 2, moderate; and group 3, mild. Serum PTH levels in the Vit D-deficient groups were significantly higher than that in group 4 (normal Vit D). Serum calcium and phosphate levels in groups 1 and 2 were significantly lower than those in groups 3 and 4. No significant difference was seen in serum Alk Ph in the groups with different degrees of Vit D deficiency. The sensivity for at least one biochemical variable (calcium, phosphorus, or Alk Ph) for the detection of severe, moderate, and mild Vit D deficiency was 24.2%, 13.8%, and 6%, respectively. When the serum 25(OH) D level was reduced to less than 25 nmol/l (groups 1 and 2), the effects of Vit D deficiency on calcium and phosphate levels were obvious. Therefore, the usual biochemical parameters (calcium, phosphate, Alk Ph) alone do not have sufficient sensitivity to detect mild deficiency of Vit D.
Adult↗
Skin calcium-binding protein: effect of vitamin D deficiency and vitamin D treatment.
The amount of skin calcium-binding protein, evaluated using a sensitive radioimmunoassay and indirect immunofluorescence, was decreased in vitamin-D deficient rats and increased after one week vitamin D3 or 1 alpha-hydroxyvitamin D3 treatment. In vitamin D replete and in vitamin D-deficient animals, skin calcium-binding protein was not sensitive to changes in dietary and/or serum calcium concentrations. These results indicate that this protein is different from other calcium-binding proteins such as parvalbumin and calmodulin which are not vitamin D-dependent, and also different from intestinal calcium-binding protein which, in D replete animals, is sensitive to changes in dietary and serum calcium concentrations. Skin calcium-binding protein may, therefore, represent a new class of vitamin D-dependent protein.
Animals↗
Influence of vitamin D deficiency and vitamin D receptor polymorphisms on tuberculosis among Gujarati Asians in west London: a case-control study.
BACKGROUND: Susceptibility to disease after infection by Mycobacterium tuberculosis is influenced by environmental and host genetic factors. Vitamin D metabolism leads to activation of macrophages and restricts the intracellular growth of M. tuberculosis. This effect may be influenced by polymorphisms at three sites in the vitamin D receptor (VDR) gene. We investigated the interaction between serum vitamin D (25-hydroxycholecalciferol) concentrations and VDR genotype on susceptibility to tuberculosis. METHODS: This study was a hospital-based case-control analysis of Asians of Gujarati origin, a mainly vegetarian immigrant population with a high rate of tuberculosis. We typed three VDR polymorphisms (defined by the presence of restriction endonuclease sites for Taq1, Bsm1, and Fok1) in 91 of 126 untreated patients with tuberculosis and 116 healthy contacts who had been sensitised to tuberculosis. Serum 25-hydroxycholecalciferol was recorded in 42 contacts and 103 patients. FINDINGS: 25-hydroxycholecalciferol deficiency was associated with active tuberculosis (odds ratio 2.9 [95% CI 1.3-6.5], p=0.008), and undetectable serum 25-hydroxycholecalciferol (<7 nmol/L) carried a higher risk of tuberculosis (9.9 [1.3-76.2], p=0.009). Although there was no significant independent association between VDR genotype and tuberculosis, the combination of genotype TT/Tt and 25-hydroxycholecalciferol deficiency was associated with disease (2.8 [1.2-6.5]) and the presence of genotype ff or undetectable serum 25-hydroxycholecalciferol was strongly associated with disease (5.1 [1.4-18.4]). INTERPRETATION: 25-hydroxycholecalciferol deficiency may contribute to the high occurrence of tuberculosis in this population. Polymorphisms in the VDR gene also contribute to susceptibility when considered in combination with 25-hydroxycholecalciferol deficiency.
Calcifediol↗
Acute plasma calcium regulation in rats: effect of vitamin D deficiency.
Vitamin D-replete (+D) and vitamin D-deficient (-D) rats received large doses of calcium (2-18 mg) by intraperitoneal injection and their responses to the calcium load was analysed in terms of the instantaneous and time-dependent responses of the plasma calcium concentration, [Cas]. Following an initial expansion, [Cas] returned to the preinjection value in a strictly exponential manner, with t1/2 = 22.5 +/- 2.0 (SE) min in +D and 51 +/- 5.2 min in -D animals. In both groups of animals, these rates were independent of the calcium load. Extraprolation of [Cas] to t = 0, i.e., the time just after administration of the calcium, revealed that the amount of calcium circulating at that moment was only about one-fifth of the amount that would have been found if all of the injected calcium had remained in the plasma. Calculations suggest that in all animals about four-fifths of the injected calcium load became distributed virtually instantaneously in the extracellular water. In both +D and -D groups the fraction of the injected load that left the plasma instantaneously was independent of the calcium load, of [Cas] at t = 0 or of the animals' plasma volume. The ability of rats to disperse some 80% of the load to outside the plasma would seem to constitute a major mechanism of acute plasma calcium regulation. Dilution was insufficient, however, totally to reduce [Cas] to the preinjection level. That occurred exponentially, with most of the calcium presumed to enter the skeleton. This exponential rate was markedly and significantly slower in the vitamin D-deficient animals than in their controls.
Animals↗
Family screening is effective in picking up undiagnosed Asian vitamin D deficient subjects.
Vitamin D deficiency has been described in the Asian migrants to the UK from the early 1960s. In spite of some suggestions that this problem is declining, we continue to see clinical cases of vitamin D deficiency with osteomalacia presenting to hospital. As the aetiology of this condition is associated with social, cultural and dietary factors, we screened associated family members of 18 index cases (three males 15 females, age range 12-73 years) who presented with clinical vitamin D deficiency to hospital. Of the 36 (21 females, 15 males) screened, 67% of these had evidence of vitamin D deficiency as judged by a 25(OH)VitD of < 5 microg L-1 (5-40). Some subjects also had hypocalcaemia (n=2), low PO4 (n=7), raised PTH (n=8) and raised alkaline phosphatase (n=11), indicating severe symptomatic, but unrecognized, vitamin D deficiency. Family screening seems an effective way of identifying Asian subjects with vitamin D deficiency who otherwise remain undiagnosed. A preventative policy with implementation is long overdue for this easily treatable condition.
Adolescent↗
Vitamin D-binding protein prevents vitamin D deficiency and presents vitamin D for its renal activation.
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Animals↗
Direct measurement of bone resorption and calcium conservation during vitamin D deficiency or hypervitaminosis D.
When bone is remodeled during the growth of a given size bone to a larger size, some bone is resorbed and some is deposited. Much of the resorbed bone mineral, calcium, can be reutilized during bone formation. The net and absolute effects of normal growth, vitamin D deficiency, or vitamin D excess were compared on bone resorption, bone formation, and calcium reutilization. Growing chicks were prelabeled extensively with three isotopes: (45)Ca, [(3)H]tetracycline, and [(3)H]proline. Data were obtained weekly during 3 weeks of control growth, vitamin D deficiency, or vitamin D overdosage while on a nonradioactive diet. Bone resorption as measured by increases in the marrow (inner) diameter of the midshaft of the femur and humerus and by the weekly losses of total [(3)H]tetracycline and [(3)H]collagen per whole bone was not significantly different among any of the groups studied. The data indicated that the high rate of cortical bone resorption in experimental chicks was not increased above that observed in experimental chicks was not increased above that observed in control chicks. Vitamin D deficiency had little effect on the total (45)Ca in whole bones, whereas vitamin D-treated chicks lost 40% of their (45)Ca. Thus, vitamin D overdosage resulted in a decrease of (45)Ca reutilization, whereas vitamin D deficiency resulted in an apparent increase of (45)Ca reutilization. Both vitamin D-deficient and vitamin D-treated chicks had a decreased accumulation of dietary calcium per whole bone. The insufficient mineral mass in vitamin D-deficient chicks resulted from the indirect inhibition of bone mineralization due to the low intestinal absorption of calcium rather than from a change in bone resorption. In vitamin D-treated chicks the apparent bone atrophy and net loss of (45)Ca from bone resulted from inhibiting bone matrix formation and mineralization instead of increasing bone resorption. The constancy of bone resorption under these experimental conditions suggests that bone mineralization is the major regulator of bone mass.
Animals↗
Vitamin D deficiency and osteoporosis: the role of vitamin D deficiency and treatment with vitamin D and analogues in the prevention of osteoporosis-related fractures.
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Adult↗
A case of dilated cardiomyopathy due to nutritional vitamin D deficiency rickets.
Vitamin D deficiency rickets was detected as the cause in a nine-month-old girl with dilated cardiomyopathy and signs of congestive heart failure. The patient responded to calcium and vitamin D supplementation promptly and left ventricular systolic functions normalized at the 3rd month of treatment. Nutritional rickets must be remembered in etiological assessment of dilated cardiomyopathy among infants living in regions in which nutritional rickets is still common.
Cardiomyopathy, Dilated↗
Effects of long-term vitamin D deficiency and response to vitamin D repletion in the mature and aging male and female rat.
This study investigated the sex- and age-related alterations in calcium homeostasis in 39- to 82-week-old rats raised from weaning on a vitamin D deficient (-D) diet. It was found that vitamin D deprivation decreased the life span of male, but not female, rats. Female -D animals exhibited a steady increase in serum calcium with age from 39 to 82 weeks, although circulating calcium of -D animals never reached normocalcemic levels. There was no attenuation of the secondary hyperparathyroidism. Serum calcium of -D males was significantly lower than that of age-matched females at all ages when sufficient males were alive to make the comparison. Serum parathyroid hormone levels were decreased in -D females when serum calcium was elevated to hypercalcemic levels by calcium injection. Similarly, administration of vitamin D3 or 1,25-dihydroxyvitamin D3 elevated serum calcium and depressed parathyroid hormone in 14- and 22-month-old -D females. These animals also exhibited increased intestinal calcium binding protein content. Administration of vitamin D3 or dihydroxyvitamin D3 repaired renal adenylate cyclase refractoriness to parathyroid hormone. The sex- and diet-related alterations in serum phosphorus that were found at earlier ages disappeared by 67 weeks of age. Serum calcitonin was elevated in mature and aging +D males and females and -D females relative to younger animals. In -D males, calcitonin levels were less markedly elevated. The results of this study indicate that there are several important sex differences related to the regulation of calcium homeostasis in mature and aging rats. In addition, it was found that mature (14 month) and old (22 month) chronically -D female rats were able to respond to repletion with dihydroxyvitamin D3 or vitamin D within 10 days.
Aging↗
Improvement in glucose tolerance and beta-cell function in a patient with vitamin D deficiency during treatment with vitamin D.
Glucose metabolism was studied in a patient with vitamin D deficiency during its treatment with small doses of vitamin D. A continuous infusion of glucose test was performed to assess glucose tolerance and insulin sensitivity and beta-cell function were derived by mathematical modelling. Fasting glucose was 5.6 mmol/l and achieved glucose after the infusion was 10.4 mmol/l confirming diabetes. The test was repeated 0.5, 1, 3 and 5 months after starting treatment. Serum calcium increased glucose intolerance from 1.76 to 2.0, 2.08, 1.96 and 2.0 mmol/l, respectively; vitamin D reached supraphysiological levels initially and returned to normal levels, and parathyroid hormone levels were normalized. Her weight did not change during treatment. Glucose tolerance improved during treatment and achieved glucose was 9.4, 8.6, 9.2 and 9.0 mmol/l at 0.5, 1, 3 and 5 months, respectively; insulin sensitivity did not change. Beta-cell function improved from 101% at diagnosis to 126%, 147%, 173% and 198% at 0.5, 1, 3 and 5 months, respectively. Improvement in beta-cell function and consequently in glucose tolerance is likely to have been due to correction of hypocalcaemia, vitamin D deficiency and secondary hyperparathyroidism.
Aged↗
Treatment of malabsorption vitamin D deficiency myopathy with intramuscular vitamin D.
A nearly 5 year-old boy presented with proximal muscle weakness, reduced muscle bulk, a positive Gower sign and Trendelenburg gait. He was known to have cholestatic liver disease. Investigations revealed markedly low serum total calcium, elevated alkaline phosphatase, very low serum 25-hydroxyvitamin D, and radiographs consistent with active rickets despite the ongoing administration of a water-soluble preparation of vitamin D. Only i.v. calcitriol acutely corrected the hypocalcemia, despite trying several oral preparations, suggesting that malabsorption secondary to chronic liver disease was the cause of his rickets. Intramuscular calciferol quickly corrected his muscle weakness and X-ray findings. Myopathy secondary to vitamin D deficiency is an uncommon diagnosis in children. Intermittent calciferol is an inexpensive and practical treatment for vitamin D deficiency, especially if associated with malabsorption.
Child, Preschool↗