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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.
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PMID:Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency. 384 Jan 73

Serum osteocalcin (BGP), a vitamin K-dependent gamma-carboxyglutamic acid (GLA) containing bone protein, provides an index of bone turnover in patients with a variety of metabolic bone diseases. BGP increases with increasing age in both sexes, but more so in women. BGP rises above normal when the glomerular filtration rate falls below 30 ml/min. Because of its importance in bone disease, its low mol wt, and the effect of uremia, we measured BGP by RIA in serum and dialysate fluid in patients on hemodialysis (HD) or peritoneal dialysis (PD). In 32 HD patients (22 women and 10 men), serum BGP was not different pre- and postdialysis [67.5 +/- 4.4 (+/- SEM) ng/ml vs. 67.7 +/- 5.2), but was significantly elevated compared to the level in normal subjects (7.3 +/- 0.8 ng/ml). The sex difference previously reported in normal subjects was not found in patients with renal failure. The serum BGP level in 8 PD patients was 49.4 +/- 6.9 ng/ml, with a peritoneal fluid concentration of 27.6 +/- 9.3 ng/ml. The hemodialysate fluid concentration of BGP was 1.7 +/- 0.4 ng/ml, which was significantly lower than the serum BGP levels in the HD patients, the PD patients, and peritoneal fluid (P less than 0.01). A significant correlation existed among BGP, alkaline phosphatase, immunoreactive PTH, creatinine, and blood urea nitrogen. We conclude that BGP is markedly elevated in patients with renal failure, not altered in the serum by HD or PD, but very low in HD dialysate fluid. These findings may reflect a combination of impaired clearance and increased skeletal production. The difference in clearance between the peritoneal and hemodialysis fluid is compatible with the mol wt of BGP. In 15 patients who had successful kidney transplantation, serum BGP was normal despite an elevated serum PTH level.
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PMID:Serum and dialysate osteocalcin levels in hemodialysis and peritoneal dialysis patients and after renal transplantation. 388 31

1,25-dihydroxyvitamin D production in response to two successive infusions of synthetic active 1-34 fragment of human PTH [hPTH-(1-34)] was evaluated in order to develop an understanding of the vitamin D metabolism and the rationale of vitamin D therapy in calcium disorders. Five normal controls, six hypoparathyroid patients, two patients with hypophosphatemic vitamin-D-resistant rickets, one patient with Lowe's synd. and one patient with primary Fanconi's synd. were investigated, and the following results were obtained. All normal controls showed a significant increase in serum 1,25(OH)2D[43 +/- 3.8 (m +/- SEM, n = 5, basal), 53 +/- 4.3 (three hours after the first PTH infusion), 65 +/- 7.7 (six hours) and 66 +/- 4.4 (nine hours) pg/ml]. All patients with PTH-deficient hypoparathyroidism showed a significant increase in serum 1,25(OH)2D, and serum 1,25(OH)2D values were within the normal range after hPTH-(1-34) stimulation. Serum 1,25(OH)2D remained low after hPTH-(1-34) infusions in a patient with pseudohypoparathyroidism type I who showed a significant increase in this value after infusion of dibutyryl cyclic AMP. On the other hand, a patient with normocalcemic pseudohypoparathyroidism type I had a high basal 1,25(OH)2D value, which increased further after hPTH-(1-34) infusions. An almost normal increase in serum 1,25(OH)2D was observed in two patients with hypophosphatemic vitamin-D-resistant rickets, one with Lowe's syndrome and the other with primary Franconi's syndrome. We conclude that these results ae important in obtaining an understanding of calcium and vitamin D metabolism in these disorders and that this PTH stimulation test is a useful method to use in evaluating renal responsiveness in 1,25(OH)2D production to PTH in various calcium disorders.
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PMID:1,25-Dihydroxyvitamin D production after stimulation with synthetic human parathyroid hormone (1-34) in hypoparathyroid and renal tubular disorders. 609 38

An oral calcium tolerance test was administered to 22 hyperparathyroid patients and 162 normal subjects to determine its value in the diagnosis of mild primary hyperparathyroidism. Basal urinary excretion of calcium was higher in patients [0.217 mg/100 ml glomerular filtrate (GF)] than in normal subjects (0.090 mg/100 ml GF), but there was 50% overlap between the two groups. Phosphorus excretion, expressed as the ratio of the maximal tubular reabsorption of phosphorus to the glomerular filtration rate, was lower in patients (2.77) than in normal subjects (3.7), but 38% of the patients fell within the normal range. Urinary excretion of total cAMP also failed to separate hyperparathyroid patients from normal subjects [5.8 +/- 0.32 (+/- SEM) nmol/100 ml GF in patients vs. 3.41 +/- 0.11 in normal subjects]. Determination of nephrogenous cAMP failed to increase the utility of cAMP as a predictor of hyperparathyroidism. In response to oral calcium, the elevation in serum calcium concentration was the same in both groups. The rise in urinary calcium was greater in patients, but showed 77% overlap with that in normal subjects. Conversely, serum immunoreactive PTH, measured with a midregion-specific RIA, was elevated in 90% of the patients. Some normal subjects also had high levels of PTH, but none of these had hypercalcemia. We conclude that the oral calcium tolerance test and measurement of urinary cAMP do not adequately distinguish hyperparathyroid patients from normal subjects. In the absence of renal insufficiency, the combination of hypercalcemia and elevated serum PTH concentration most accurately predicts the diagnosis of primary hyperparathyroidism.
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PMID:Assessment of adenosine 3',5'-monophosphate excretion and an oral calcium tolerance test in the diagnosis of mild primary hyperparathyroidism. 631 54

We have assessed the effect of omeprazole (30 mg daily) on gastric acid secretion as well as on basal hormone levels (fasting gastrin; TSH, T3, T4, TBG; insulin, glucagon, C-peptide; prolactin, testosterone, 17-beta-oestradiol, dihydroepiandrosterone, cortisol and PTH) in 8 healthy volunteers before and after a 28 day treatment. On day 29, i. e. one day after the last omeprazole dose, mean stimulated acid output was still reduced from 27.4 +/- 3.5 mmol H+/h (+/- SEM) to 7.8 +/- 1.4 mmol H+/h (72% inhibition). Fasting gastrin levels were raised from 55.5 +/- 6.8 pg/ml to 80.9 +/- 6.7 pg/ml (33% increase). On day 39, stimulated gastric acid secretion and fasting gastrin levels have been returned to pretreatment values. Basal levels of prolactin, testosterone, TSH, T3, T4, TBG, cortisol, PTH, 17-beta-oestradiol, insulin, glucagon, c-peptide, dihydroepiandrosterone remained unchanged by a 28-day omeprazole treatment. Omeprazole is a highly effective antisecretory compound without any effect on the basal hormone levels tested. Even after 28 days its effect on acid secretion and fasting gastrin levels was fully reversible.
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PMID:[4 weeks' administration of omeprazole: effect on acid behavior and basal hormone levels]. 674 Dec

Despite the high circulating levels of immunoreactive PTH in patients with pseudohypoparathyroidism type I (PSPI) the levels of bioactive PTH (bioPTH) have been found to be close to the normal range. To elucidate this dissociation, we have studied the recovery of the biological activity of bovine PTH added to the plasma of patients with either PSPI, or with hypoparathyroidism (PTX), primary hyperparathyroidism (HPT) or of normal subjects. In PSPI (n = 10) the recovery of biological activity was 5.6% +/- 3.6 (mean +/- SEM) whereas in PTX (n = 7), in HPT (n = 4) and in normal subjects (n = 8) it was 79% +/- 5, 75% +/- 9 and 68% +/- 4, respectively. In another PSPI patient, who had undergone total parathyroidectomy, bioPTH was undetectable but the recovery from the plasma of added PTH was 84%. Thus we have found inhibition of PTH bioactivity by plasma of PSPI patients which was absent after parathyroidectomy.
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PMID:Inhibition of cytochemical bioactivity of parathyroid hormone by plasma in pseudohypoparathyroidism type I. 707 1

In 30 normal subjects, the mean (+/- SEM) plasma concentration of PRL was 5.90 +/- 0.40 ng/ml and that of PTH was 0.51 +/- 0.03 ng/ml. There was no significant difference in plasma hormone levels according to age or sex. Ten cases of primary hyperparathyroidism showed PRL concentrations (8.90 +/- 1.80 ng/ml) significantly (P less than 0.01) higher than those of the normal subjects. After adenomectomy, the PRL concentration decreased (5.35 +/- 0.50 ng/ml). However, this decrease was only significant in the 5 of 10 patients who had preoperative plasma PRL levels of 10 ng/ml or more (P less than 0.01). The increase in PRL concentration in 10 cases of secondary hyperparathyroidism with normal glomerular function was also significant (14.25 +/- 3.9 ng/ml; P less than 0.001). Fourteen patients with prolactinoma showed PTH plasma levels (1.25 +/- 0.15 ng/ml) significantly higher than those of normal subjects (P less than 0.001). Eight of the 14 patients received 7.5 mg/24 h of bromocriptine for 3 months; their mean plasma PTH level decreased significantly from 1.60 +/- 0.35 to 0.50 +/- 0.11 ng/ml (P less than 0.01). In 9 cases of secondary hyperprolactinemia, the increase in PTH (0.80 +/- 0.16 ng/ml) was significant compared to the plasma PTH levels in the normal group (P less than 0.05). These results show that an excess of plasma PRL is associated with an excess of plasma PTH and vice versa. The mechanisms of these relationships remain unclear.
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PMID:Comparison between the plasma concentrations of prolactin and parathyroid hormone in normal subjects and in patients with hyperparathyroidism or hyperprolactinemia. 713 Mar 42

On the basis of recent findings that adult black women had similar calcium absorption but higher levels of 1,25-dihydroxyvitamin D [1,25-(OH)2D] than white women, we hypothesized that blacks have a gut resistance to the action of calcitriol. To test this, we studied 11 black [age, 32.4 +/- 5.7 (+/- SD) yr] and 12 white women (28.4 +/- 5.5 yr). The women were maintained on a constant 500-mg calcium diet for 4 weeks, and each received calcitriol (0.25 microgram) four times daily for the last 2 weeks. After 2 and 4 weeks, each subject had measurements of fractional 45Ca absorption index and blood and urine tests. At 2 weeks, the black women had similar calcium absorption indexes [18.7 +/- 1.9% (+/- SEM)/L vs. 20.0 +/- 1.8%/L; age adjusted], borderline higher 1,25-(OH)2D levels [95.7 +/- 6.4 (+/- SEM) vs. 78.2 +/- 6.2 pmol/L; P = 0.071; age adjusted], higher serum PTH levels, and lower urinary calcium excretion. Calcitriol therapy induced similar increments in plasma 1,25-(OH)2D levels in the two groups, but a smaller increment in calcium absorption in the black women (18.4 +/- 8.6% vs. 44.6 +/- 7.8%; P = 0.043; means adjusted for age and initial absorption index). These findings support the hypothesis that, compared with whites, healthy premenopausal black women have gut resistance to the action of calcitriol.
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PMID:Calcium absorption responses to calcitriol in black and white premenopausal women. 755 98

PTH has been postulated to play a role in both nocturnal and age-related increases in bone resorption. We tested this hypothesis directly in 10 young (ages 24-35 yr) and 10 elderly (ages 71-78 yr) normal women by measuring the cross-linked N-telopeptide of type I collagen (NTx), a marker for bone collagen breakdown, in 4-h urine collections before and during suppression of PTH secretion by a 24-h iv infusion of calcium. Serum ionized calcium and PTH levels were also measured every 2 h before and during the infusion. In both groups of women, serum PTH levels and urinary NTx excretion followed a circadian pattern before calcium infusion (analysis of variance, P = 0.0001) with peaks in the afternoon and at night for PTH and at night for urinary NTx. During the calcium infusion, the nocturnal urinary NTx excretion peak persisted (P = 0.0001), despite elimination of both PTH peaks. Urinary 24-h NTx excretion (nanomoles per millimoles of creatinine) at baseline was higher in the elderly women (mean +/- SEM, 25.7 +/- 2.1) than in the young women (19.3 +/- 1.7) (P < 0.01), and the decrease during calcium infusion was greater (7.5 +/- 1.9 vs. 4.1 +/- 1.5, P < 0.05). Therefore, the increase in serum PTH levels with age is one of the major factors responsible for the age-related increase in bone resorption. PTH does not mediate the circadian pattern of bone resorption but does play a role in setting the absolute level of bone resorption at which this pattern occurs.
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PMID:Role of parathyroid hormone in mediating nocturnal and age-related increases in bone resorption. 759 43

Phenytoin therapy is a well recognized cause of gingival hyperplasia, a condition characterized by increased gingival collagen synthesis, and may also cause acromegalic-like facial features. Based on these clinical findings suggestive of anabolic actions, we sought to test the hypothesis that phenytoin acts on normal bone cells to induce osteogenic effects. To test the direct actions of phenytoin on human bone cells, we measured the dose responses to phenytoin for [3H]thymidine incorporation, cell number, alkaline phosphatase specific activity, and collagen synthesis in human hip bone-derived cells. Phenytoin significantly and reproducibly increased [3H]thymidine incorporation, cell number, alkaline phosphatase specific activity, and collagen synthesis in a biphasic manner with optimal stimulatory doses between 5-10 mumol/L. Thus, micromolar concentrations of phenytoin can act directly on human bone cells to stimulate osteoblast proliferation and differentiation. We next sought to test the hypothesis that phenytoin stimulates bone formation in humans in vivo. Accordingly, three serum biochemical markers of bone formation, i.e. osteocalcin, skeletal alkaline phosphatase, and procollagen C-terminal extension peptide, were measured in 39 male epileptic patients, 20-60 yr of age, with an average duration of phenytoin therapy of 10.5 +/- 1.62 yr (mean +/- SEM). In this group of patients, the mean serum phenytoin level was 9.56 +/- 0.90 mg/L (mean +/- SEM; equivalent to 34.9 +/- 3.3 mumol/L). Thirty apparently healthy male subjects of similar age and taking no medication were included as controls. Serum calcium, 25-hydroxyvitamin D3, and PTH levels in the phenytoin-treated patients were not significantly different from those in the age-matched controls and were within the clinical laboratory normal range of our hospitals, indicating that the patients did not develop hypocalcemia, vitamin D deficiency, or secondary hyperparathyroidism. Serum levels of osteocalcin, skeletal alkaline phosphatase, and procollagen peptide in the phenytoin-treated patients were significantly increased compared to those in the age-matched subjects; in each case these biochemical markers were significantly correlated with the serum phenytoin level, but not with the dose or duration of phenytoin treatment. These findings are consistent with the interpretation that phenytoin increases the bone formation rate in humans in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Phenytoin increases markers of osteogenesis for the human species in vitro and in vivo. 762 28


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