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PubMed1988

Renal responses to calcium deprivation in young rabbits.

To evaluate the renal adaptations to dietary Ca deprivation, young growing female albino rabbits were fed a Ca-deficient diet for 8 consecutive days while they were housed in metabolism cages. Urinary Ca excretion rates decreased markedly within 24 h of Ca deprivation, reached a nadir by day 5, and remained low thereafter. Concomitantly, urinary P excretion increased. The hypocalciuria during the 8-day study was accounted for by an increased tubular reabsorption of Ca. Urinary cyclic AMP excretion was increased on the first day of Ca deprivation. Plasma immunoreactive parathyroid hormone and calcitriol concentrations were elevated after 8 days of Ca deprivation. Conversely, plasma calcifediol concentrations were decreased. We conclude that there are rapidly induced, appropriate renal homeostatic adaptations to dietary Ca deprivation in the rabbit and suggest that increases in endogenous plasma parathyroid hormone concentration, in part, play a role in mediating these changes.

Animals↗
PubMed1995

Correction of chronic metabolic acidosis in haemodialysed patients by acetate-free biofiltration does not influence parathyroid function.

In eight patients remaining acidotic after more than 1 year of bicarbonate haemodialysis, we studied the effect of correcting the chronic metabolic acidosis using acetate-free biofiltration for 4 months on the course of secondary hyperparathyroidism. An AN69 capillary membrane was employed with a bicarbonate infusion rate initially set at 1.8 l/h in all patients and then adjusted in each one to obtain a predialysis bicarbonate of > or = 23 mmol/l. Standard blood chemistry parameters were determined every 2 weeks. Measurements of PTH, calcifediol and calcitriol, as well as calcium-PTH curves were determined at the beginning and end of the study. While acetate-free biofiltration appears to be an adequate technique for the correction of chronic metabolic acidosis when bicarbonate dialysis fails, this study indicates that it does not influence secondary hyperparathyroidism in haemodialysed patients. The level of intact PTH did not vary significantly and the calcium-PTH curves at 0 and 4 months were superimposable with no significant differences in the set point and the slope of the curves.

Acidosis↗
PubMed1995

Idiopathic juvenile osteoporosis: five-year case follow-up.

Juvenile osteoporosis is a disease of childhood and adolescence exhibiting marked clinical variability in bone change. The disease usually begins in the prepubertal period or even younger. A case of a Chinese boy suffering from back pain and generalized osteoporosis since 9 yr of age who spontaneously recovered at 14 yr of age when entering puberty is reported. The affected patient was clinically normal (as shown by X rays), until he fractured his left humerus. Metabolic studies indicated a negative calcium balance, but serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcifediol, calcitriol, cortisol and sex hormones were normal. X ray showed typical generalized osteoporosis with vertebral collapse. The disease markedly improved within 5 yr. No family history of inherited skeletal disorders or presenile osteoporosis was noted. The diagnosis of idiopathic juvenile osteoporosis was made.

Age of Onset↗
PubMed1995

[Secondary hyperparathyroidism in the elderly. Apropos of 200 assays of intact parathormone].

OBJECTIVES: To evaluate the frequency of high levels of intact parathormone in an elderly population of hospitalized patients and to determine whether there are any correlations with different factors involved in phosphocalcium metabolism, nutritional status and renal function. METHODS: Intact parathormone was assayed in all patients admitted to a geriatric ward (n = 200). Other laboratory tests included serum phosphorus, calcium, total albumin, prealbumin, ionized calcium, creatinine with calculation of the clearance and in 50 patients radioimmunoassay for 25 hydroxyvitamin D. RESULTS: Intact parathormone was abnormally high (> 65 pg/ml) in 40 patients. Mean levels increased significantly with age and reached 70.5 pg/ml in patients 90 years of age and over. No correlation was found between intact parathormone and total serum calcium, corrected serum calcium, albumin or prealbumin. Inversely there was a significant correlation with serum phosphorus and creatinine and creatinine clearance. Serum levels of 25 hydroxyvitamin D were abnormally low in 82% of the patients. There was a constant and significant decrease in intact parathormone level 15 days after calcium and calcifediol substitution therapy in 13 patients. CONCLUSION: The frequency of hyperparathyroidism increases with age to affect nearly 1 out of 2 subjects over 90. It would be useful to determine a threshold level for elderly subjects with a major risk of bone fracture.

Aged↗
PubMed1981

Vitamin D metabolite concentrations in vitamin D deficiency. Are calcitriol levels normal.

The levels of vitamin D metabolites were measured in three children with a decreased dietary intake of calcium and vitamin D and sun exposure. All three children had hypocalcemia, hypophosphatemia, and elevated alkaline phosphatase activities. Two children had rickets, aminoaciduria, and elevated immunoreactive parathyroid hormone (iPTH) concentrations. The concentrations of vitamins D2 and D3, 25-hydroxyvitamins D2 and D3 (25-OH-D2 and 25-OH-D3), and 24,25-dihydroxyvitamin D (24,25-[OH]2D) were reduced. Nonetheless, the levels of calcitriol (1,25-[OH]2D) were normal. The combination of hypocalcemia, hypophosphatemia, and increased iPTH concentrations should result in supranormal calcitriol concentrations. Moreover, the ratio of PTH to calcitriol is significantly higher than in normal subjects. Accordingly, in patients with vitamin D deficiency and "normal" calcitriol values, the synthesis of this compound may be reduced. The evaluation of vitamin D deficiency should include the measurement of all metabolites.

24,25-Dihydroxyvitamin D 3↗
PubMed1982

Vitamin D metabolism in hypophosphatemic rickets.

Vitamin D metabolites were measured in 21 patients with hypophosphatemic osteomalacia of juvenile onset. In eight patients who had not received any antirachitic treatment, serum 25-hydroxyvitamin D(25-OH-D) and 1,25-dihydroxyvitamin D (1,25-[OH]2D) values were normal, whereas serum 24,25-dihydroxyvitamin D (24,25-[OH]2D) values were lower than in normal subjects. In 13 patients who were receiving ergocalciferol and oral elemental phosphorus, serum 25-OH-D and 24,25-(OH)2D concentrations were elevated and serum 1,25-(OH)2D values were low. The findings in untreated patients supported the hypothesis that vitamin D metabolism is abnormal in hypophosphatemic rickets/osteomalacia. The reduction of serum 1,25-(OH)2D levels with ergocalciferol and phosphate therapy gives further support to a therapeutic role for 1,25-(OH)2D in this disorder.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Effect of race and diet on human-milk vitamin D and 25-hydroxyvitamin D.

Vitamin D-deficiency rickets continues to be reported in infants fed human milk, and the importance of human milk as a source of vitamin D for infants is controversial. Furthermore, effects of race and of normally consumed maternal vitamin D intake on human-milk vitamin D have not been reported. Milk, serum, and three-day-diet diaries were obtained from 25 mother-infant pairs. Human-milk vitamins D3 and D2 and 25-hydroxyvitamin D3 were lower in blacks vs whites, whereas 25-hydroxyvitamin D2 did not differ. Total-milk vitamin D, but not 25-hydroxyvitamin D, correlated with vitamin D intake. Milk vitamin D2 specifically was correlated with vitamin D intake even after controlling for race. Infant serum 25-hydroxyvitamin D did not correlate with milk vitamin D or 25-hydroxyvitamin D; we speculate that the contribution of vitamin D from human milk in these infants is insignificant relative to the contribution from sunshine exposure.

25-Hydroxyvitamin D 2↗
PubMed1991

How much vitamin D for neonates?

To assess the adequacy of different dosages of neonatal vitamin D, 25-hydroxyvitamin D serum concentrations were longitudinally monitored in 27 low-birth-weight and 25 full-term well infants from birth to 16 weeks after delivery. The infants were randomly assigned to receive either 10 micrograms/d (400 IU/d) or 20 micrograms/d (800 IU/d) of vitamin D or 0.85 or 1.5 micrograms/d of 25-hydroxyvitamin D3. In each infant who received 10 or 20 micrograms/d of vitamin D 25-hydroxyvitamin D, serum concentrations greater than 20 ng/mL were maintained, with some low-birth-weight infants reaching 60-ng/mL concentrations. Similarly, in the low-birth-weight infants receiving 1.5 and 0.85 micrograms/d of 25-hydroxyvitamin D3, serum 25-hydroxyvitamin D levels greater than 12 ng/mL were maintained. In the full-term infants who received 1.5 micrograms/d of 25-hydroxyvitamin D3, serum 25-hydroxyvitamin D concentrations of greater than 12 ng/mL were maintained, but in those who received 0.85 micrograms/d, serum 25-hydroxyvitamin D concentrations of 10 ng/mL could not be maintained. These vitamin D status data document that 10 micrograms (400 IU) of vitamin D represents a sufficient daily intake for both premature and full-term well infants. These data also indicate that while as little as 0.85 micrograms/d of 25-hydroxyvitamin D3 may facilitate vitamin D sufficiency in low-birth-weight neonates, it does not do so in full-term infants.

Administration, Oral↗
PubMed1999

In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma.

BACKGROUND: Epidemiologic studies have demonstrated an inverse correlation between dietary calcium and vitamin D intake and the incidence of colorectal carcinoma. Elevated serum levels of 25-hydroxyvitamin D3 (25-OH-D3) are associated with a major reduction in the incidence of this neoplasm. The reduction in tumor size and number induced by calcium supplements in an experimental carcinogenesis model was neutralized by vitamin D3 deficiency. To the authors' knowledge, vitamin D serum levels have never been determined previously in colorectal carcinoma patients. They compared serum 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 25-OH-D3, and parathyroid hormone (PTH) levels of colorectal carcinoma patients with those of healthy controls. METHODS: Serum 1,25(OH)2D3, 25-OH-D3, and PTH levels were determined in 84 colorectal carcinoma patients (10 with Stage I, 29 with Stage II, 25 with Stage III, and 20 with Stage IV) and 30 healthy controls, all of whom were normocalcemic and not taking calcium or vitamin D supplements. RESULTS: 25-OH-D3 serum levels were higher in cancer patients than controls, irrespective of stage. Serum 1,25(OH)2D3 decreased with advancing stage: 73 +/- 18, 48 +/- 16, 39 +/- 12, 34 +/- 13, and 75 +/- 20 pg/mL in Stages I, II, III, IV, and controls, respectively. There was a corresponding increase in serum PTH levels: 58.0 +/- 9.4, 73.7 +/- 14.4, 79.0 +/- 21.3, 100.4 +/- 30.9, and 51.2 +/- 3.9 pg/mL in Stages I, II, III, IV, and controls, respectively. Serum vitamin D metabolite levels did not correlate with gender, age, tumor localization, or histologic grade. CONCLUSIONS: An inverse correlation between serum levels of the active metabolite of vitamin D and colorectal carcinoma stage has been demonstrated for the first time, to the authors' knowledge, in colorectal carcinoma patients. Because 1,25(OH)2D3 has been shown to inhibit proliferation of colonic epithelial cells, decreased serum levels may facilitate the growth of colorectal carcinoma and influence its biologic behavior.

Aged↗
PubMed1998

Titanium surface roughness alters responsiveness of MG63 osteoblast-like cells to 1 alpha,25-(OH)2D3.

Surface roughness has been shown to affect differentiation and local factor production of MG63 osteoblast-like cells. This study examined whether surface roughness alters cellular response to circulating hormones such as 1 alpha,25-(OH)2D3. Unalloyed titanium (Ti) disks were pretreated with HF/HNO3 (PT) and then were machined and acid-etched (MA). Ti disks also were sandblasted (SB), sandblasted and acid etched (CA), or plasma sprayed with Ti particles (PS). The surfaces, from smoothest to roughest, were: PT, MA, CA, SB, and PS. MG63 cells were cultured to confluence on standard tissue culture polystyrene (plastic) or the Ti surfaces and then treated for 24 h with either 10(-8) M or 10(-7) M 1 alpha,25-(OH)2D3 or vehicle (control). Cellular response was measured by assaying cell number, cell layer alkaline phosphatase specific-activity, and the production of osteocalcin, latent (L) TGF beta, and PGE2. Alkaline phosphatase activity was affected by surface roughness; as the surface became rougher, the cells showed a significant increase in alkaline phosphatase activity. Addition of 1 alpha,25-(OH)2D3 to the cultures caused a dose-dependent stimulation of alkaline phosphatase activity that was synergistic with the effect caused by surface roughness alone. 1 alpha,25-(OH)2D3 also caused a synergistic increase in osteocalcin production as well as local factor (LTGF beta and PGE2) production on the rougher CA, SB, and PS surfaces, but it had no effect on the production on smooth surfaces. The inhibitory effect of surface roughness on cell number was not affected by 1 alpha,25-(OH)2D3 except on the SB surface. 1 alpha,25-(OH)2D3 decreased cell number, increased alkaline phosphatase activity and osteocalcin production, and had no effect on LTGF beta or PGE2 production by MG63 cells grown on tissue culture polystyrene. These data suggest that bone cell response to systemic hormones is modified by surface roughness and that surface roughness increases the responsiveness of MG63 cells to 1 alpha,25-(OH)2D3. They also suggest that the endocrine system is actively involved in normal bone healing around implants.

Alkaline Phosphatase↗
PubMed1999

Diastereoselective synthesis, binding affinity for vitamin D receptor, and chiral stationary phase chromatography of hydroxy analogs of 1,25-dihydroxycholecalciferol and 25-hydroxycholecalciferol.

A series of analogs of 1,25-dihydroxycholecalciferol and 25-hydroxycholecalciferol were obtained with an additional hydroxyl in the aliphatic side chain at carbon atom C-24. These analogs were synthesized by direct and diastereo-selective alpha-hydroxylation of enolates derived from respective vitamin D esters using Davies chiral oxaziridines. The use of (+)-(2R,8aS)-(8, 8-dichlorocamphoryl)sulfonyl oxaziridine resulted in (R) stereochemistry of the new asymmetric center for both series of analogs. Similarly, (-)-(2S,8aR) oxaziridine gave (S) analogs. The diastereomeric purity of hydroxy analogs was determined by high-performance liquid chromatography on a chiral stationary phase. High diastereopurity of hydroxylation of vitamin D esters was obtained without the use of any chiral auxiliary. The binding affinity of (24R)-1,24,25-trihydroxycholecalciferol for the calf thymus intracellular vitamin D receptor was one order of magnitude higher than that of the respective (24S)-diastereomer.

Animals↗
PubMed1987

Hypercalcemia and osteoclast proliferation in adult T-cell leukemia.

Eighteen autopsy cases of adult T-cell leukemia (ATL) were investigated clinicopathologically. Thirteen of the patients had hypercalcemia during their clinical course. Nine of the thirteen had a high level of serum calcium at the terminal stage, even after extensive chemotherapy. Microscopic examination of the bone revealed proliferation of osteoclasts and bone resorption in eight patients. No osteoclast proliferation or bone resorption was found in the other nine normocalcemic patients. The infiltration of ATL cells was observed in only two patients--one was hypercalcemic and the other, normocalcemic. The factors affecting the serum calcium level were examined in two hypercalcemic patients. Hypercalcemia could not be accounted for by parathyroid hormone or prostaglandins E levels, which were in the normal range, or by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, which were low. Our findings are consistent with the mechanism proposed by several investigators, that the malignant T-lymphocytes produced an osteoclast-activating-factor-like substance that caused osteoclast proliferation and hypercalcemia.

Adult↗
PubMed2001

Baculovirus-expressed vitamin D-binding protein-macrophage activating factor (DBP-maf) activates osteoclasts and binding of 25-hydroxyvitamin D(3) does not influence this activity.

Vitamin D-binding protein (DBP) is a multi-functional serum protein that is converted to vitamin D-binding protein-macrophage activating factor (DBP-maf) by post-translational modification. DBP-maf is a new cytokine that mediates bone resorption by activating osteoclasts, which are responsible for resorption of bone. Defective osteoclast activation leads to disorders like osteopetrosis, characterized by excessive accumulation of bone mass. Previous studies demonstrated that two nonallelic mutations in the rat with osteopetrosis have independent defects in the cascade involved in the conversion of DBP to DBP-maf. The skeletal defects associated with osteopetrosis are corrected in these mutants with in vivo DBP-maf treatment. This study evaluates the effects of various forms of DBP-maf (native, recombinant, and 25-hydroxyvitamin D(3) bound) on osteoclast function in vitro in order to determine some of the structural requirements of this protein that relate to bone resorbing activities. Osteoclast activity was determined by evaluating pit formation using osteoclasts, isolated from the long bones of newborn rats, incubated on calcium phosphate coated, thin film, Ostologic MultiTest Slides. Incubation of osteoclasts with ex vivo generated native DBP-maf resulted in a dose dependent, statistically significant, activation of the osteoclasts. The activation was similar whether or not the vitamin D binding site of the DBP-maf was occupied. The level of activity in response to DBP-maf was greater than that elicited by optimal doses of other known stimulators (PTH and 1,25(OH(2)D(3)) of osteoclast function. Furthermore, another potent macrophage activating factor, interferon--gamma, had no effect on osteoclast activity. The activated form of a full length recombinant DBP, expressed in E. coli showed no activity in the in vitro assay. Contrary to this finding, baculovirus-expressed recombinant DBP-maf demonstrated significant osteoclast activating activity. The normal conversion of DBP to DBP-maf requires the selective removal of galactose and sialic acid from the third domain of the protein. Hence, the differential effects of the two recombinant forms of DBP-maf is most likely related to glycosylation; E. coli expressed recombinant DBP is non-glycosylated, whereas the baculovirus expressed form is glycosylated. These data support the essential role of glycosylation for the osteoclast activating property of DBP-maf.

Amino Acid Sequence↗
PubMed1999

Serum vitamin D levels and incident changes of radiographic hip osteoarthritis: a longitudinal study. Study of Osteoporotic Fractures Research Group.

OBJECTIVE: The purpose of this study was to determine the relationship of serum levels of 25-vitamin D and 1,25-vitamin D to incident changes of radiographic hip osteoarthritis (OA) among elderly white women. METHODS: Baseline and followup hip radiographs of 237 subjects were obtained an average of 8 years apart. Hips were scored for individual radiographic features (IRF) and assigned a summary grade based on the number and type of IRF present. Serum 25- and 1,25-vitamin D levels from baseline samples were analyzed by radioimmunoassay. Logistic and linear regression were used to examine the association of 25- and 1,25-vitamin D levels with radiographic changes, adjusting for age, health status, physical activity, weight, vitamin D supplement use, and calcaneal bone mineral density. RESULTS: The risk of incident hip OA defined as the development of definite joint space narrowing was increased for subjects who were in the middle (odds ratio [OR] 3.21, 95% confidence interval [95% CI] 1.06, 9.68) and lowest (OR 3.34, 95% CI 1.13, 9.86) tertiles for 25-vitamin D compared with subjects in the highest tertile. Vitamin D levels were not associated with incident hip OA defined as the development of definite osteophytes or new disease according to the summary grade. No association between serum 1,25-vitamin D and changes in radiographic hip OA was found. CONCLUSION: Low serum levels of 25-vitamin D may be associated with incident changes of radiographic hip OA characterized by joint space narrowing.

Aged↗
PubMed1980

Vitamin D metabolism in patients treated with phenytoin and phenobarbitone.

There are many reports of abnormalities in calcium metabolism and even of frank osteomalacia in patients taking anticonvulsant drugs. Although enzyme induction has been suggested to be the cause of increased requirements for vitamin D leading to these changes, this has still to be proved. We have studied the metabolism of [3H]cholecalciferol and 25-hydroxycholecalciferol in subjects taking anticonvulsant drugs. The rate of removal of cholecalciferol from the plasma was no different from that in control subjects and no abnormality was detected in the production of disappearance of 25-hydroxycholecalciferol. However, plasma concentrations of 25-hydroxycholecalciferol fell more rapidly during the winter in epileptic subjects than in control subjects. Our results do not confirm that these changes are due to enzyme induction.

Calcifediol↗
PubMed2005

Hypoparathyroidism-retardation-dysmorphism (HRD) syndrome in triplets.

We report female triplets with the clinical and biochemical manifestations of hypoparatyroidism-retardation-dysmorphism (HRD) syndrome also known as Sanjad-Sakati syndrome. They were born at 35 weeks gestation after assisted pregnancy (in vitro fertilization). The parents are first degree cousins from Saudi Arabia.

Abnormalities, Multiple↗
PubMed1982

Decreased serum 24,25-dihydroxyvitamin D concentration during long-term anticonvulsant therapy in adult epileptics.

Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 1 alpha, 25-dihydroxyvitamin D [1, 25-(OH)2D] were measured in 30 ambulatory adult epileptic patients during long-term anticonvulsant treatment with phenytoin, phenobarbital, or carbamazepine. For the entire group, serum 24,25-(OH)2D was decreased (p less than 0.0005) as compared to normal subjects to a mean value of 0.7 +/- 0.1 (SEM) ng/ml. However, serum 1, 25-(OH)2D was increased at 50 +/- 7 pg/ml (p less than 0.025). Serum 25-OHD declined insignificantly to 19 +/- 3 ng/ml. All three drugs caused a significant reduction of serum 24,25-(OH)2D concentrations. A significant decrease in serum 25-OHD was observed only for the phenobarbital-treated patients. Serum 1, 25-(OH)2D was high in patients receiving phenytoin or carbamazepine but not in those taking phenobarbital. The findings suggest that while various anticonvulsant drugs appear to exert different effects on vitamin D metabolism, a universal finding is diminished serum 24,25-(OH)2D. The results support the notion that 24,25-(OH)2D deficiency may play an important role in the pathogenesis of anticonvulsant-induced osteomalacia.

Adolescent↗