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PubMed1991

On the mechanisms for the selective action of vitamin D analogs.

A variety of analogs of 1,25-(OH)2D3 with less calcemic activity and lower receptor binding affinity than 1,25-(OH)2D3 have been developed. However, these compounds have equal or greater ability to differentiate leukemia cells and psoriatic fibroblasts and to suppress PTH synthesis and secretion. The mechanism for this selectivity has not been elucidated. Because the lower potency of ergocalciferol compared to cholecalciferol in preventing or curing rickets in chicks was associated with a lower affinity of the avian vitamin D binding protein (DBP) for vitamin D2, we tested five analogs with low calcemic activity including 22-oxa-1,25-(OH)2D3 (OCT), MC903, 1,25-(OH)2-16 ene-23-yne D3, 1,25-(OH)2-26,27 dihomo-22-ene-D3, and 1,25-(OH)2-24-trihomo-22-ene-D3 for their affinity for rat serum DBP. All analogs had a low affinity for DBP, ranging from 50-3000 times less than that of 1,25-(OH)2D3. OCT also bound with low affinity to dog and human serum DBP. We tested with OCT the possible consequences of its low affinity for serum DBP. One of the functions of DBP is to prolong the lifetime of 1,25-(OH)2D3 in circulation. Quantification of the metabolic clearance rate (MCR) of OCT in 8 normal dogs using a single bolus injection technique showed that OCT was cleared at a rate of 48.2 +/- 7.5 ml/min, approximately 6-7 times more rapidly than 1,25-(OH)2D3 (6.8 +/- 0.4 ml/min). The estimated half-life of OCT in the circulation was 2.5 +/- 0.3 h compared to 7.0 +/- 0.6; n = 7 for 1,25-(OH)2D3. As our primary interest is the potential of OCT in treating the secondary hyperparathyroidism of CRF, we also measured the MCR of OCT in 5/6 nephrectomized dogs. Uremia does not affect the rate of clearance of OCT from the circulation (MCR: 56.8 +/- 4.5; t1/2 = 2.1 +/- 0.2 n = 4). Despite its shorter half-life, OCT suppressed PTH secretion in vivo in uremic dogs. The effects of low binding to DBP on the percentage uremic dogs. The effects of low binding to DBP on the percentage of free sterol were determined using an ultrafiltration procedure. We compared the proportion of free (unbound) OCT and 1,25-(OH)2D3 in 0.1% BSA-PBS with concentrations of human serum ranging from 0-25%. The proportion of OCT in the free form was significantly higher than that of 1,25-(OH)2D3 for every serum concentration tested. The physiological relevance of a higher percentage of free OCT was tested in normal human macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1981

X-linked hypophosphatemia: effect of calcitriol on renal handling of phosphate, serum phosphate, and bone mineralization.

Eleven patients with the Mendelian phenotype of x-linked hypophosphatemia (XLH) were treated with calcitriol [1,25-(OH)2D3] and phosphate. Ten patients had received prior treatment with ergocalciferol and phosphate. Five subjects were prepubertal and six were postpubertal. Response to calcitriol was measured under nonfasting and overnight fasting protocols. Bone biopsies were obtained before and after treatment. Calcitriol (mean dose, 30 ng/kg. day) 1) raised serum phosphorus uniformly in prepubertal patients but in only two of six postpubertal subjects; 2) did not change the theoretical renal phosphate threshold in the total patient group and thus had no effect on the primary transport defect in XLH; 3) improved trabecular bone mineralization in the total patient group, as determined by bone histomorphometry. The beneficial effect on extracellular phosphorus homeostasis was attributed to improved intestinal absorption of phosphorus; improvement in bone mineralization may reflect an additional effect of 1,25-(OH)2D3 on bone itself in XLH. Mild transient hypercalcemia occurred during 0.6% of 3545 treatment days and was readily controlled by adjusting the dosage of 1,25-(OH)2D3.

Adolescent↗
PubMed2002

Stimulative effects of (22E,24R)-ergosta-7,22-diene-3beta,5alpha,6beta-triol from fruiting bodies of Tricholoma auratum, on a mouse osteoblastic cell line, MC3T3-E1.

We screened the differentiation-inducing activities of 39 mushroom extracts from Akita prefecture, Japan, on the mouse osteoblastic cell line, MC3T3-E1. Sixteen phosphate buffered saline (PBS), 8 boiled PBS, 14 ethanol and 12 methanol extracts induced alkaline phosphatase (ALP) activities, an indicator of MC3T3-E1 cell differentiation. The enzyme activities were markedly induced by extracts of Tricholoma auratum, and we isolated the active compound from methanol extracts of this mushroom. Physical data for the isolated active compound were identical to those for (22E,24R)-ergosta-7,22-diene-3beta,5alpha,6beta-triol (1). 1 induced ALP activities of MC3T3-E1 cells and promoted cell proliferation. To investigate the relationships between the chemical structure and differentiation-inducing activity of the compound, ALP-inducing activities of MC3T3-E1 cells by 1, ergosterol (2), ergocalciferol (3), cholesta-3beta3,5alpha6beta-triol (4), 7-dehydrocholesterol (5) and cholecalciferol (6) were tested. The enzyme activities of MC3T3-E1 cells were increased 3.0-fold by 10 microM 1 and 2.4-fold by 10 microM 4. However, 2, 3, 5 and 6 did not induce MC3T3-E1 cell ALP activity at 0.1-10 microM. These results suggested that the OH groups at C-5 and/or C-6 of 1 and 4 played an important role in their differentiation-inducing activities on MC3T3-E1 cells. Furthermore, 1 suppressed induction of MC3T3-E1 cell apoptosis by serum starvation.

3T3 Cells↗
PubMed2003

Issues of methodology, standardization and metabolite recognition for 25-hydroxyvitamin D when comparing the DiaSorin radioimmunoassay and the Nichols Advantage automated chemiluminescence protein-binding assay in hip fracture cases.

BACKGROUND: Deficiency of vitamin D is commonly associated with hip fracture and treatment with vitamin D reduces hip fracture rates. Consequently, the demand for assays to measure 25-hydroxyvitamin D (25-OHD) has increased. The Nichols Advantage chemiluminescence protein-binding assay (CLPBA) for 25-OHD is a first-generation automated immunoassay with decreased turnaround time, reduced manual handling and non-radioactive label. METHODS: We compared the CLPBA to the DiaSorin radioimmunoassay (RIA) and high-performance liquid chromatography (HPLC) for the measurement of 25-OHD using 161 samples from hip fracture patients and samples before and after institution of ergocalciferol (vitamin D(2)) therapy. RESULTS: A negative bias for the CLPBA at concentrations below 30 nmol/L and a positive bias at 25-OHD values above 30 nmol/L compared with the RIA resulted in diagnostic discordance for one in three samples when using 30 and 50 nmol/L as decision limits. HPLC analysis confirmed the presence of a negative bias for the CLPBA at low values. Both immunoassays under-estimate 25-hydroxyvitamin D(2). CONCLUSIONS: The discordance between 25-OHD values may be due to differences in standardization of each assay relative to HPLC. Our results emphasize the need for assay-specific clinical decision limits.

Automation↗
PubMed2006

Current assays overestimate 25-hydroxyvitamin D3 and underestimate 25-hydroxyvitamin D2 compared with HPLC: need for assay-specific decision limits and metabolite-specific assays.

BACKGROUND: Clinical demand for quick, cheap, precise and accurate 25-hydroxyvitamin D (25(OH)D) results has led to the development of a variety of assay methods. Lack of standardization of these methods has resulted in inter-method disagreement and challenged whether current assays recognize 25(OH)D2 and 25(OH)D3 equally. METHODS: We studied 172 patient samples from hip fracture cases using DiaSorin (DS) and IDS radioimmunoassays and the Nichols Advantage-automated protein binding assay (NA-CLPBA) in comparison to high-performance liquid chromatography (HPLC). 52 patient samples were analysed before and after three months treatment with 1000 IU of daily ergocalciferol (vitamin D2). RESULTS: Linear regression analysis in pre-treatment samples demonstrated a positive Y-intercept for each immunoassay compared with HPLC, and a slope that varied from 0.64 (IDS) to 0.97 (DS, NA-CLPBA). Bland Altman analysis demonstrated that all the three assays had a proportional positive bias relative to HPLC at values from 20 to 50 nmol/L. Regression analysis of post-treatment samples demonstrated a slope that was not significantly different from zero for the IDS and NA-CLPBA and 0.2 for the DS method, with a positive intercept for all assays of between 8 and 22, indicating less than 50% of 25(OH)D2 measured by HPLC was detected. CONCLUSIONS: These results demonstrate the need for assay-specific decision limits for 25(OH)D3 in order to define appropriate thresholds for treatment institution. Treatment with vitamin D2 may not be accurately monitored with any of the three commercial assays studied. Clinicians and biochemists who continue to use 25(OH)D assays need to be urgently informed of these issues.

25-Hydroxyvitamin D 2↗
PubMed2001

Severe nutritional deficiencies in toddlers resulting from health food milk alternatives.

It is widely appreciated that health food beverages are not appropriate for infants. Because of continued growth, children beyond infancy remain susceptible to nutritional disorders. We report on 2 cases of severe nutritional deficiency caused by consumption of health food beverages. In both cases, the parents were well-educated, appeared conscientious, and their children received regular medical care. Diagnoses were delayed by a low index of suspicion. In addition, nutritional deficiencies are uncommon in the United States and as a result, US physicians may be unfamiliar with their clinical features. Case 1, a 22-month-old male child, was admitted with severe kwashiorkor. He was breastfed until 13 months of age. Because of a history of chronic eczema and perceived milk intolerance, he was started on a rice beverage after weaning. On average, he consumed 1.5 L of this drink daily. Intake of solid foods was very poor. As this rice beverage, which was fallaciously referred to as rice milk, is extremely low in protein content, the resulting daily protein intake of 0.3 g/kg/day was only 25% of the recommended dietary allowance. In contrast, caloric intake was 72% of the recommended energy intake, so the dietary protein to energy ratio was very low. A photograph of the patient after admission illustrates the typical features of kwashiorkor: generalized edema, hyperpigmented and hypopigmented skin lesions, abdominal distention, irritability, and thin, sparse hair. Because of fluid retention, the weight was on the 10th percentile and he had a rotund sugar baby appearance. Laboratory evaluation was remarkable for a serum albumin of 1.0 g/dL (10 g/L), urea nitrogen <0.5 mg/dL (<0.2 mmol/L), and a normocytic anemia with marked anisocytosis. Evaluation for other causes of hypoalbuminemia was negative. Therapy for kwashiorkor was instituted, including gradual refeeding, initially via a nasogastric tube because of severe anorexia. Supplements of potassium, phosphorus, multivitamins, zinc, and folic acid were provided. The patient responded dramatically to refeeding with a rising serum albumin and total resolution of the edema within 3 weeks. At follow-up 1 year later he continued to do well on a regular diet supplemented with a milk-based pediatric nutritional supplement. The mortality of kwashiorkor remains high, because of complications such as infection (kwashiorkor impairs cellular immune defenses) and electrolyte imbalances with ongoing diarrhea. Children in industrialized countries have developed kwashiorkor resulting from the use of a nondairy creamer as a milk alternative, but we were unable to find previous reports of kwashiorkor caused by a health food milk alternative. We suspect that cases have been overlooked. Case 2, a 17-month-old black male, was diagnosed with rickets. He was full-term at birth and was breastfed until 10 months of age, when he was weaned to a soy health food beverage, which was not fortified with vitamin D or calcium. Intake of solid foods was good, but included no animal products. Total daily caloric intake was 114% of the recommended dietary allowance. Dietary vitamin D intake was essentially absent because of the lack of vitamin D-fortified milk. The patient lived in a sunny, warm climate, but because of parental career demands, he had limited sun exposure. His dark complexion further reduced ultraviolet light-induced endogenous skin synthesis of vitamin D. The patient grew and developed normally until after his 9-month check-up, when he had an almost complete growth arrest of both height and weight. The parents reported regression in gross motor milestones. On admission the patient was unable to crawl or roll over. He could maintain a sitting position precariously when so placed. Conversely, his language, fine motor-adaptive, and personal-social skills were well-preserved. Generalized hypotonia, weakness, and decreased muscle bulk were present. Clinical features of rickets present on examination included: frontal bossing, an obvious rachitic rosary (photographed), genu varus, flaring of the wrists, and lumbar kyphoscoliosis. The serum alkaline phosphatase was markedly elevated (1879 U/L), phosphorus was low (1.7 mg/dL), and calcium was low normal (8.9 mg/dL). The 25-hydroxy-vitamin D level was low (7.7 pg/mL) and the parathyroid hormone level was markedly elevated (114 pg/mL). The published radiographs are diagnostic of advanced rickets, showing diffuse osteopenia, frayed metaphyses, widened epiphyseal plates, and a pathologic fracture of the ulna. The patient was treated with ergocalciferol and calcium supplements. The published growth chart demonstrates the dramatic response to therapy. Gross motor milestones were fully regained within 6 months. The prominent neuromuscular manifestations shown by this patient serve as a reminder that rickets should be considered in the differential diagnosis of motor delay. (ABSTRACT TRUNCATED)

Beverages↗
PubMed2006

Minimizing bone abnormalities in children with renal failure.

Renal osteodystrophy (ROD), a metabolic bone disease accompanying chronic renal failure (CRF), is a major clinical problem in pediatric nephrology. Growing and rapidly remodeling skeletal systems are particularly susceptible to the metabolic and endocrine disturbances in CRF. The pathogenesis of ROD is complex and multifactorial. Hypocalcemia, phosphate retention, and low levels of 1,25 dihydroxyvitamin D(3) related to CRF result in disturbances of bone metabolism and ROD. Delayed diagnosis and treatment of bone lesions might result in severe disability. Based on microscopic findings, renal bone disease is classified into two main categories: high- and low-turnover bone disease. High-turnover bone disease is associated with moderate and severe hyperparathyroidism. Low-turnover bone disease includes osteomalacia and adynamic bone disease. The treatment of ROD involves controlling serum calcium and phosphate levels, and preventing parathyroid gland hyperplasia and extraskeletal calcifications. Serum calcium and phosphorus levels should be kept within the normal range. The calcium-phosphorus product has to be <5 mmol(2)/L(2) (60 mg(2)/dL(2)). Parathyroid hormone (PTH) levels in children with CRF should be within the normal range, but in children with end-stage renal disease PTH levels should be two to three times the upper limit of the normal range. Drug treatment includes intestinal phosphate binding agents and active vitamin D metabolites. Phosphate binders should be administered with each meal. Calcium carbonate is the most widely used intestinal phosphate binder. In children with hypercalcemic episodes, sevelamer, a synthetic phosphate binder, should be introduced. In children with CRF, ergocalciferol (vitamin D(2)), colecalciferol (vitamin D(3)), and calcifediol (25-hydroxyvitamin D(3)) should be used as vitamin D analogs. In children undergoing dialysis, active vitamin D metabolites alfacalcidol (1alpha-hydroxy-vitamin D(3)) and calcitriol (1,25 dihydroxyvitamin D(3)) are applied. In recent years, a number of new drugs have emerged that hold promise for a more effective treatment of bone lesions in CRF. This review describes the current approach to the diagnosis and treament of ROD.

Bone Diseases↗
PubMed1995

25-hydroxycholecalciferol in poultry nutrition.

Vitamin D is a complex of secosteroids that must undergo metabolic alterations to reach optimal biological activity. The parent compounds 1) ergocalciferol (D2) and 2) cholecalciferol (D3) can be synthesized in the leaves of many plants or in the skin of most animals, respectively. Transport of vitamin D steroids after absorption is associated with vitamin D binding proteins (DBP). In general, the relative binding affinities of the vitamin D steroids are: 25-hydroxy vitamin D3 [25-(OH)D3] = 24,25-dihydroxy vitamin D3 [24,25-(OH)2D3] = 25,26-dihydroxy vitamin D3 [25,26-(OH)2D3] > 25-hydroxy vitamin D2 (25-(OH)D2) > 1,25-dihydroxy vitamin D3 [1,25-(OH)2D3] > vitamin D3. The DBP in poultry does not bind D2 forms effectively, and therefore poultry can not use this form of vitamin D adequately. The concentration of 25-(OH)D3 in blood seems to be well correlated with dietary vitamin D intake or exposure to ultraviolet light. The 1 alpha hydroxylase enzyme in the kidney is subject to negative feedback regulation and is critical for formation of the active metabolite 1,25-(OH)2D3. The intracellular vitamin D receptor (VDR) specifically binds 1,25-(OH)2D3 and is necessary for cellular action. Increased levels of two to three orders of magnitude are required for 25-(OH)D3 to compete with 1,25-(OH)2D3 for binding on VDR. Feeding studies with 25-(OH)D3 suggest it has nearly twice the activity of vitamin D3. Hatchability studies have shown that 25-(OH)D3 supports good fertility and hatchability, whereas hens fed only 1,25-(OH)2D3 did not have normal hatchability. Likewise, 1,25-(OH)2D3 seems to reach toxic levels at dietary concentrations only two to three times optimal dietary levels whereas feeding 25-(OH)D3 for extended periods at levels 8 to 10 times requirement seems to have no adverse effects. It seems that 25-(OH)D3 is the most active metabolite of vitamin D3, ultimately capable of supporting both cellular functions and embryonic development in chickens and turkeys when fed as the sole source of vitamin D3.

Animal Nutritional Physiological Phenomena↗
PubMed2004

8: Disorders of bone and mineral other than osteoporosis.

Rickets in children and osteomalacia in adults are caused by undermineralisation of bone, which increases its susceptibility to bending and fracture; treatment is with calcium, vitamin D or phosphate, depending on the specific mineral or vitamin deficiency. In Paget's disease, osteoclasts are overactive and produce woven or "repair" bone, which is mechanically weaker than lamellar bone; treatment is with antiresorptive bisphosphonate drugs. Cancers can produce bone lysis through direct spread within the skeleton or production of endocrine parathyroid hormone-like factors; treatment is with a bisphosphonate, plus appropriate therapy for the cancer. Cancer can also produce hypercalcaemia if the capacity of the kidneys to excrete the calcium dissolved from bone is exceeded; treatment is with saline infusion to increase excretion and a bisphosphonate. Primary hyperparathyroidism is the other common cause of hypercalcaemia and is usually associated with a single parathyroid adenoma; it is best treated with parathyroidectomy. Hypocalcaemia may result from severe decrease in calcium absorbed or lack of parathyroid action; both are treated with calcium and vitamin D (ergocalciferol or calcitriol). These disorders range from nutritional deficiencies to complex genetic and metabolic diseases

Adult↗
PubMed2006

Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: a consensus statement.

Vitamin D deficiency has re-emerged as a significant paediatric health issue, with complications including hypocalcaemic seizures, rickets, limb pain and fracture. A major risk factor for infants is maternal vitamin D deficiency. For older infants and children, risk factors include dark skin colour, cultural practices, prolonged breastfeeding, restricted sun exposure and certain medical conditions. To prevent vitamin D deficiency in infants, pregnant women, especially those who are dark-skinned or veiled, should be screened and treated for vitamin D deficiency, and breastfed infants of dark-skinned or veiled women should be supplemented with vitamin D for the first 12 months of life. Regular sunlight exposure can prevent vitamin D deficiency, but the safe exposure time for children is unknown. To prevent vitamin D deficiency, at-risk children should receive 400 IU vitamin D daily; if compliance is poor, an annual dose of 150,000 IU may be considered. Treatment of vitamin D deficiency involves giving ergocalciferol or cholecalciferol for 3 months (1000 IU/day if < 1 month of age; 3000 IU/day if 1-12 months of age; 5000 IU/day if > 12 months of age). High-dose bolus therapy (300,000-500,000 IU) should be considered for children over 12 months of age if compliance or absorption issues are suspected.

Adolescent↗
PubMed2006

Zoledronic acid prevents bone loss after liver transplantation: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: Clinically important rapid bone loss occurs within 3 to 6 months after liver transplantation and may be associated with osteoporotic fractures. OBJECTIVE: To determine whether bisphosphonate treatment with zoledronic acid reduces transplant-related bone loss more than placebo in adults having liver transplantation for chronic liver disease. DESIGN: 12-month randomized, double-blind, placebo-controlled trial. SETTING: 2 large liver transplantation centers in Australia. PATIENTS: 62 adults having liver transplantation for chronic liver disease. INTERVENTIONS: Infusions of zoledronic acid, 4 mg (n = 32), or saline (n = 30) were given within 7 days of transplantation and again at months 1, 3, 6, and 9 after transplantation. All patients received supplementation with calcium carbonate, 600 mg/d, and ergocalciferol, 1000 U/d. MEASUREMENTS: The primary outcome was bone mineral density (BMD) measured by dual x-ray absorptiometry before transplantation and 3, 6, and 12 months later. Secondary outcomes included bone turnover markers that were measured before transplantation and 1, 3, 6, 9, and 12 months later. RESULTS: There were statistically significant interactions between treatment effects and time for BMD measurements at the lumbar spine (P = 0.002), femoral neck (P = 0.001), and total hip (P < 0.001). Differences in acute bone loss 3 months after transplantation favored zoledronic acid over placebo. Differences between groups in percentage change from baseline adjusted for baseline weight and serum parathyroid hormone (PTH) level were 4.0% (95% CI, 1.1% to 7.0%) for the lumbar spine, 4.7% (CI, 1.9% to 7.6%) for the femoral neck, and 3.8% (CI, 1.7% to 6.0%) for the total hip. At 12 months after transplantation, the difference in percentage change from baseline between the 2 groups adjusted for baseline weight and serum PTH level was 1.1% (CI, -2.1% to 4.4%) for the lumbar spine, 2.7% (CI, 0.0% to 5.4%) for the femoral neck, and 2.4% (CI, 0.1% to 4.7%) for the total hip. Treatment with zoledronic acid induced temporary secondary hyperparathyroidism and postinfusion hypocalcemia statistically significantly more often than did placebo. LIMITATIONS: The trial was not powered to assess fractures, and 10 of 62 (16%) patients were not included in adjusted analyses because of missing weight or serum PTH measurements. CONCLUSION: Treatment with zoledronic acid can prevent bone loss within the first year after liver transplantation.

Bone Density↗
PubMed1999

[Vitamin D deficiency. Easy to diagnose, often overlooked].

On the basis of five cases the typical clinical picture of patients with severe vitamin D deficiency is presented. The diagnosis can easily be mistaken and it is not uncommon that rheumatic or malignant diseases are suspected instead. By using a simple screening blood test consisting of 25-OH-vitamin D, PTH and alkaline phosphatase most cases will be diagnosed correctly. Important risk factors are reviewed, the most important being: elderly > 70 years, persons with low exposure to direct sunlight, gastrointestinal diseases and persons in anti-convulsive treatment. A treatment regimen consisting of oral supplementation of 1000-1500 mg calcium + 1000 IU vitamin D to patients with an isolated low 25-OH-vitamin D (< 20 nmol/l) is recommended. If the patient also has raised values of PTH or alkaline phosphatase an intramuscular dose of 100,000 IU ergocalciferol pr week for one month is given.

Aged↗
PubMed2002

European best practice guidelines for renal transplantation. Section IV: Long-term management of the transplant recipient. IV.8. Bone disease.

GUIDELINES: A. All kidney-transplanted patients should undergo a systematic evaluation of their skeletal status, including pre-transplant history of renal osteodystrophy, history of fractures and plasma concentrations of calciotropic hormones and other parameters, and if possible measurement of bone mineral density (BMD). B. Glucocorticoid therapy should be given at the lowest possible dosage. As long as patients are receiving steroids, vitamin D treatment (ergocalciferol or 1,25-dihydroxyvitamin D) is highly recommended. C. Optimal prevention of bone disease by vitamin D treatment, sufficient calcium intake, sex hormone substitution and appropriate use of thiazide diuretics should be considered in all transplant patients. D. In established osteopenia, bisphosphonate treatment should be considered despite limited information in transplant recipients. E. Persistent tertiary hyperparathyroidism should be observed for 1 year after transplantation whenever possible to allow for a spontaneous involution. F. In patients with GFR <50 ml/min after transplantation, uraemic osteodystrophy should be prevented.

Bone Diseases↗
PubMed2003

Oral vitamin D3 decreases fracture risk in the elderly.

Vitamin D3 (or its physiologic equivalent, ergocalciferol), administered at a dose of 100,000 IU every 4 months for 5 years, is effective for primary prevention of fractures in the active elderly aged 65 to 85 years. This treatment regimen has no effect on cardiovascular, cancer, or all-cause mortality. Despite a seemingly large dose averaging 800 IU per day, this regimen is a safe, cheap (<$2 per year), and effective therapy for primary prevention of fractures.

Comment↗
PubMed1992

Effect of supplemental calcium on serum and urinary calcium in osteoporotic patients.

A retrospective analysis of osteoporotic patient records was conducted to evaluate the effect of supplemental calcium (Ca) on urinary and serum Ca. Forty-seven patients composed the Ca-supplemented group and 17 patients the nonsupplemented group. Serum Ca values (mean +/- SD) were 9.3 +/- 0.3 and 9.4 +/- 0.4 mg/dl in the nonsupplemented and supplemented groups, respectively. Daily urinary Ca was 137 +/- 88 and 162 +/- 89 mg, respectively. Each group had similar concentrations of serum phosphorus, albumin and creatinine. Data from the Ca-supplemented group were divided into low and high Ca intake. In the low intake group (less than 1000 mg Ca/day), serum and urinary Ca were 9.4 +/- 0.4 and 166 +/- 88. In the high intake group (greater than 1000 mg/day), the values were 9.5 +/- 0.5 and 160 +/- 90, respectively. Seventeen and 36% of nonsupplemented and supplemented patients used estrogen, respectively. No significant effects of estrogen therapy were observed on serum or urinary Ca in either group. More detailed analysis of five patients was undertaken to evaluate the combined effect of supplemental vitamin D (ergocalciferol or calcitriol) and Ca on urinary Ca output. Baseline urinary Ca was 33 +/- 19 mg with an average daily Ca supplement of 1160 mg. After 4-8 weeks of supplemention with Ca and vitamin D, urinary Ca increased to only 68 +/- 33 mg. We conclude that supplemental Ca does not appear to cause a significant increase in urinary Ca and that added vitamin D has little effect on elevating urinary Ca in some older women.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed2006

[Immobilization and hip fracture].

Hip fracture is among the most common causes of acute immobilization in elderly patients, and elderly patients with hip fracture are at high risk for a subsequent hip fracture. At baseline, both groups had high serum concentrations of ionized calcium, high urinary deoxypyridinoline (DPD) concentrations, suggesting immobilization-induced hypercalcemia. We previously showed deficiency of vitamins D and K(1) causes reduced bone mineral density (BMD) in female Alzheimer's disease (AD) patients. In a random and prospective study of AD patients, 100 patients received 45 mg menatetrenone, 1,000 IU ergocalciferol and 600 mg calcium daily for 2 years, and the remaining 100 (untreated group) did not. Treatment with MK-4 and vitamin D(2) with calcium supplements increases the BMD in elderly female patients with AD and leads to the prevention of nonvertebral fractures. The risk of hip fracture after stroke is 2 to 4 times as high as that in age-matched healthy controls. Hyperhomocysteinemia is a risk factor for both ischemic stroke and osteoporotic fractures in elderly persons. Randomized, controlled, double-blinded study of 628 consecutive elderly hemiplegic patients at least 1 year following first ischemic stroke. Patients were assigned to daily oral treatment with 5 mg of folate and 1,500 microg of mecobalamin or double placebos, and 559 completed the 2 year follow up. Plasma homocysteine levels in the decreased by 38% in the treatment group and increased by 31% in the placebo group. The number of the hip fractures per 1,000 patient-years was 10 and 43 for the treatment and placebo groups, respectively (p<0.001). In this Japanese population with a high baseline fracture risk, combined treatment with folate and vitamin B(12) is safe and effective in reducing the risk of a hip fracture in elderly stroke patients. Because of limited study power, the relative risk reduction may only be around 0.5.

Aged↗
PubMedDate not supplied

Liquid chromatographic methods for vitamins A and D in multivitamin-mineral formulations.

Liquid chromatographic screening procedures have been developed for the estimation of vitamins A and D in multivitamin-mineral tablet, capsule, gelatin capsule, and syrup formulations. The procedure can be used for measuring vitamin A present as either retinyl acetate or retinyl palmitate, and also for measuring the contribution to total vitamin A activity from 13-cis retinyl esters. The retinyl esters and their isomers are resolved from each other and their oxidation products. Ergocalciferol and cholecalciferol are not resolved from each other but they are resolved from other vitamin D isomers and from vitamins A, E, and K and their degradation products. Both assays use a 3 microns amino column, with a mobile phase of hexane for vitamin A and 1% isopropanol in hexane for vitamin D. The precision of replicate injections for vitamins A and D is better than 1% and the recovery from spiked syrups is better than 98%. The coefficient of variation for both assay methods is about 5%. Twenty formulations were analyzed for vitamin A and 24 were analyzed for vitamin D.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Determination of ergosterol in cereals, mixed feed components, and mixed feeds by liquid chromatography.

A sensitive, rapid, reproducible, and reliable liquid chromatographic (LC) method is described for determination of ergosterol in feedstuffs. The sample is saponified directly and the saponified mixture is extracted with n-hexane. Ergosterol is determined without further purification or cleanup steps by using a liquid chromatograph with a 250 X 4.6 mm column packed with LiChrosorb Si 60, 5 microns, and a high pressure column prefilter. The ultraviolet detector is set at 282 nm. The limit of detection was 0.1 ppm; recovery ranged between 96.7 and 102.2%. Diode array technology is used for identification and peak purity control. Under strong UV irradiation (254 nm) and oxygen or nitrogen atmosphere ergosterol was converted almost quantitatively to ergocalciferol. Under the described conditions of the method, ergosterol proved to be stable. Ergosterol was determined in cereals, mixed feeds (e.g., for swine and poultry), and their components of plant and animal origin. It was not found in carcass meal, meat-and-bone meal, citrus pulps, or molasses; only traces were detected in fish meal.

Animal Feed↗