The Importance of Phosphate in Regulating Plasma 1,25-(OH)<sub>2</sub>-Vitamin D Levels in Humans: Studies in Healthy Subjects, in Calcium-Stone Formers and in Patients with Primary Hyperparathyroidism*

Gray, Richard W.; Wilz, Donald R.; Caldas, Angela E.; Lemann, Jacob

doi:10.1210/jcem-45-2-299

Cited by 295 publications

(82 citation statements)

References 17 publications

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“…(2) Although calcitriol serum levels should be elevated in the presence of low sPi, (12) normal levels were found in FD patients with low sPi. In addition, serum concentrations of 25(OH)D were lower when sPi was low.…”

Section: Discussionmentioning

confidence: 99%

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Terpstra

Rauch

Plotkin

et al. 2002

Journal of Bone and Mineral Research

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Fibrous dysplasia (FD) of bone can be complicated by renal phosphate wasting. The effect of hypophosphatemia on normal and dysplastic bone of FD patients has not been well characterized. In this study, we compared serum phosphorus (sPi) levels to histomorphometric findings in 27 iliac bone samples from 23 children and adolescents (aged 4.2-16.4 years) with polyostotic FD. The samples were separated into two groups, based on the presence (n ‫؍‬ 10) or absence (n ‫؍‬ 17) of a dysplastic lesion within the specimen. Histomorphometric results were compared with those from 18 age-matched control subjects without metabolic bone disease. In dysplastic lesions, trabeculae were clearly thinner and increased in number. Osteoid indices, osteoblast surface per bone surface, and mineralization lag time were elevated in dysplastic areas, but there was no detectable effect of sPi concentrations on these indices. In nondysplastic bone tissue, low sPi levels were associated with mildly increased osteoid thickness and prolonged mineralization lag time. None of the 13 patients in whom hand X-rays were available at the time of biopsy had radiological signs of rickets. In conclusion, low sPi can cause a mild systemic mineralization defect in FD, but the more severe mineralization defect seen in dysplastic lesions is independent of sPi levels. It is debatable whether the mild systemic mineralization defect warrants treatment with oral phosphorus supplementation if signs of rickets are absent.

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Section: Discussionmentioning

confidence: 99%

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Terpstra

Rauch

Plotkin

et al. 2002

Journal of Bone and Mineral Research

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“…1,25 (OH)2D binds to its receptors in intestinal mucosa to enhance the transport of calcium (3). Renal production of the metabolite is closely regulated by PTH (4, 5), calcium (6), and phosphate (7,8) ( 19,20) and 1,25 (OH)2D (20) and two consecutive 24-h urine samples were obtained for measurement of calcium ( 17) and inorganic phosphate ( 18). Urinary creatinine (21 ) was determined to ensure that urine collections were complete.…”

Section: Introductionmentioning

confidence: 99%

Increased calcium intake does not suppress circulating 1,25-dihydroxyvitamin D in normocalcemic patients with sarcoidosis.

Basile¹,

Liel²,

Shary³

et al. 1993

J. Clin. Invest.

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Ca absorption is regulated by 1,25(OH)2D, and serum values vary inversely with Ca intake. In sarcoidosis, 1,25(OH)2D is produced by alveolar macrophages in response to y-interferon, and patients may develop hypercalcemia after prolonged exposure to sunlight and increased dermal production of vitamin D3. To determine if increased Ca intake suppresses serum 1,25(OH)2D in normocalcemic patients and to identify those at risk, 17 normal subjects and 11 patients were studied on a metabolic ward for two and one-half days while receiving first 400 and then 1,000 mg/d of Ca. On the low Ca intake, serum angiotensin-converting enzyme (ACE), an index of disease activity, was higher in only three of the patients than in the controls, mean serum 1,25(OH)2D was higher in the patients, and mean serum total Ca, serum Ca ", and urinary Ca were not different in the two groups. On the higher Ca intake, mean urinary Ca increased in both groups, but mean serum 1,25(OH)2D was suppressed only in the normal subjects. Thus, 1,25(OH)2D production is abnormally regulated, indicating that (a) normocalcemic patients with sarcoidosis are at risk for developing abnormal Ca metabolism, and (b) a better index of disease activity is provided by the oral Ca suppression test than by serum ACE. (J. Clin. Invest. 1993. 91:1396-1398

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“…In normal humans, severe restriction of dietary phosphorus (< 100 mg/d) induces a large increase in the serum concentration of 1,,25(OH)2D (22)(23)(24)(25)(26), and supplementation of dietary phosphorus (> 3,000 mg/d), a substantial decrease (26). These changes in serum concentration of 1,25(OH)2D are accounted for entirely by changes in its production rate (PR) (26).…”

Section: Introductionmentioning

confidence: 99%

Physiologic regulation of the serum concentration of 1,25-dihydroxyvitamin D by phosphorus in normal men.

Portale¹,

Halloran²,

Morris³

1989

J. Clin. Invest.

259

106

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We asked this question: in normal humans, is either a normal dietary intake or normal serum concentration of phosphorus a determinant of the serum concentration of 1,25(0H-)D? In seven normal men whose dietary phosphorus was decreased from 2,300 to 625 mg/d, each intake for 8-9 d, under strictly controlled, normal metabolic conditions, we measured serum concentrations of 1,25(OH)2D daily, and concentrations of phosphorus hourly throughout a 24-h period, before and after restriction. Decreasing dietary phosphorus induced: (a) a 58% increase in serum levels of 1,25(OH)2D; (b) a 35% decrease in serum levels of phosphorus measured in the afternoon; (c) a 12% decrease in the 24-h mean serum level of phosphorus; but, (d) no decrease in morning fasting levels of phosphorus. Serum concentrations of 1,25(OH)2D varied inversely and significantly with 24-h mean concentrations of phosphorus (r = -0.77, P < 0.001). When these data are combined with those of our prior study in which dietary phosphorus was varied over an extreme range, the relationship between serum levels of 1,25(OH)2D and 24-h mean serum levels of phosphorus is even stronger (r = -0.90, P < 0.001). In the aggregate, the results demonstrate that in normal men, dietary phosphorus throughout a normal range and beyond, can finely regulate the renal production and serum concentration of 1,25(OH)2D, and provide evidence that this regulation is mediated by fine modulation of the serum concentration of phosphorus.

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The Importance of Phosphate in Regulating Plasma 1,25-(OH)₂-Vitamin D Levels in Humans: Studies in Healthy Subjects, in Calcium-Stone Formers and in Patients with Primary Hyperparathyroidism*

Cited by 295 publications

References 17 publications

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Increased calcium intake does not suppress circulating 1,25-dihydroxyvitamin D in normocalcemic patients with sarcoidosis.

Physiologic regulation of the serum concentration of 1,25-dihydroxyvitamin D by phosphorus in normal men.

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The Importance of Phosphate in Regulating Plasma 1,25-(OH)2-Vitamin D Levels in Humans: Studies in Healthy Subjects, in Calcium-Stone Formers and in Patients with Primary Hyperparathyroidism*

Cited by 295 publications

References 17 publications

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Bone Mineralization in Polyostotic Fibrous Dysplasia: Histomorphometric Analysis

Increased calcium intake does not suppress circulating 1,25-dihydroxyvitamin D in normocalcemic patients with sarcoidosis.

Physiologic regulation of the serum concentration of 1,25-dihydroxyvitamin D by phosphorus in normal men.

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Resources

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The Importance of Phosphate in Regulating Plasma 1,25-(OH)₂-Vitamin D Levels in Humans: Studies in Healthy Subjects, in Calcium-Stone Formers and in Patients with Primary Hyperparathyroidism*