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The varying epidermal melanin content that produces racial pigmentation determines the number of photons that reach the lower (malpighian) cellular layers, where vitamin D3 synthesis takes place. We investigated the effect of racial pigmentation on vitamin D3 formation, stimulating the process with a fixed dose of UVB radiation (wavelengths, 290 to 320 nm). Vitamin D nutritional status was further assessed measuring serum 25-hydroxyvitamin D and the most active serum metabolite, 1,25-dihydroxyvitamin D. Experimental subjects were young (third decade of life) and healthy, representing the white, Oriental (East Asian), Indian (South Asian), and black races. Basal serum vitamin D3 levels were similar among groups, ranging from 2.3 +/- 0.6 nmol/L (mean +/- SEM) for blacks to 3.4 +/- 1.0 nmol/L for Indians. Following whole-body exposure to 27 mJ/cm2 of UVB, there was a significant racial group effect on serum vitamin D3 levels. Post-UVB levels were significantly higher in whites (31.4 +/- 4.4 nmol/L) than in Indians or blacks (12.8 +/- 2.9 and 9.1 +/- 2.1 nmol/L, respectively), while the levels in Orientals (27.8 +/- 4.4 nmol/L) differed significantly from those in blacks and Indians but not in whites. Race had only a marginal effect on serum 25-hydroxyvitamin D, with higher levels in whites than in blacks (69.9 +/- 12.7 vs 29.7 +/- 6.2 nmol/L). Serum 1,25-dihydroxyvitamin D and vitamin D binding protein levels were similar in all groups. We conclude that while racial pigmentation has a photoprotective effect, it does not prevent the generation of normal levels of active vitamin D metabolites.
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PMID:Racial pigmentation and the cutaneous synthesis of vitamin D. 192 73

Abnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH.
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PMID:Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation. 217 4

Fifty patients with liver cirrhosis (36 alcoholic, 1 drug-induced, 7 posthepatitic, and 6 cryptogenic) and normal renal function were investigated to determine whether PTH levels in serum, measured using the common midregion human PTH-(44-68) RIA, are elevated in such patients and whether this is related to impaired liver function rather than to the effect of secondary hyperparathyroidism. Their data were compared with those from 25 control subjects. The median PTH level of 462 +/- 18 ng/L (+/- SEM) was significantly increased (P less than 0.01) in cirrhotics compared with that of 236 +/- 13 ng/L in the control group. Significant correlations were found between PTH levels and parameters of liver function such as prothrombin time (r = -0.40; P less than 0.01), albumin as a percentage of total protein (r = -0.48; P less than 0.01), bilirubin (r = 0.35; P less than 0.05), albumin (r = -0.34; p less than 0.05), and cholesterol (r = -0.32; P less than 0.05), but not for antipyrine clearance, suggesting increasing PTH with decreasing liver function. The median calcium level (2.26 +/- 0.03 mmol/L), corrected for changes in albumin, was near the lower limit of the normal range (2.25-2.60), but corrected calcium and PTH were positively correlated (r = 0.33; P less than 0.05), indicating that the elevation is not reactive to calcium depletion. A negative correlation existed between PTH and 25-hydroxy-cholecalciferol (r = -0.49; P less than 0.05), the main circulating metabolite of vitamin D. Normal values in an immunoradiometric assay that detects the whole sequence of human PTH-(1-84) suggest that fragments rather than the intact hormone are responsible for PTH elevations in cirrhosis. The positive correlation between midregion PTH and corrected calcium is probably an artifact of the correction formula. In conclusion, midregion PTH fragments are increased in patients with liver cirrhosis. The reason for this elevation may well be the impaired liver function rather than secondary hyperparathyroidism.
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PMID:Parathyroid hormone and cirrhosis of the liver. 222 13

A procedure is described for measuring the concentration of three major vitamin D metabolites: 25(OH)D, 24,25(OH)2D and 1,25(OH)2D, in 0.5 ml serum. The analytes are extracted using C18, and separated using aminopropyl solid phase extraction cartridges. 25(OH)D is separated completely; less than or equal to 10% overlap is observed between the 24,25(OH)2D and the 1,25(OH)2D fractions, and this overlap did not interfere in subsequent competitive radioligand assay. Coefficient of variation (SEM/mean x 100%) is intra-assay (n = 10) 5.8, 3.1, 5.2%, and inter-assay (n = 5) 10.1, 8.7 and 6.4%, respectively. Recoveries of the three analytes added to a single specimen are 103, 95 and 111%, respectively. One technician can extract and fractionate up to 24 specimens in one day, ready for HPLC or direct estimation.
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PMID:Simultaneous measurement of 25-hydroxy, 24,25-dihydroxy-, and 1,25-dihydroxyvitamin D without use of HPLC. 237 31

Preterm infants (birth weight, 1,089 +/- 91 g; gestational age, 28.9 +/- 0.7 weeks; mean +/- SEM) with mixed medical and surgical indications for parenteral nutrition (PN) were observed to determine the adequacy of infusates with fixed, low-dose vitamin D (25 IU/dl) and two combinations of calcium and phosphorus. The duration of low-dose vitamin D PN ranged from 5 to 52 days, with a median of 27 days. Twelve infants were randomly assigned to low (standard) Ca and P doses (5 mM each; 20 mg/dl of Ca and 15.5 mg/dl of P) and 13 high Ca and P doses (15 mM each; 60 mg/dl of Ca and 46.5 mg/dl of P). The maximum daily vitamin D intake was similar for both groups (31 +/- 1.3 versus 33 +/- 1.2 IU/kg). Vitamin D status in either group, as indicated by serum 25-hydroxyvitamin D (25-OHD) concentrations, was normal. There was no significant difference in observed changes of serial measurements of serum calcium, magnesium, phosphorus, alkaline phosphatase, creatinine (Cr), 25-OHD, and vitamin D-binding protein concentrations or urinary Ca:Cr and Mg:Cr ratios. In the low-dose Ca and P group, the serum P level was consistently less than 4 mg/dl in five infants, serum 1,25-dihydroxyvitamin D concentrations were higher, and tubular reabsorption of phosphorus was consistently greater than 95% and significantly higher than in the high-dose Ca and P groups. Severe bone demineralization apparent on X-ray occurred in two infants, with a fractured distal left ulna in one of the two infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal vitamin D and high calcium and phosphorus needs of preterm infants receiving parenteral nutrition. 249 13

Seventy-one very low birth weight (less than or equal to 1500 gm) infants were studied to determine the sequential changes in serum vitamin D metabolite concentrations between infants with and without radiographically documented rickets, fractures, or both (R/F). Usual intake of vitamin D included 20 IU/kg/day from parenteral nutrition or 400 IU/day supplementation with enteral feeding. Radiographs of both forearms and serum samples were obtained at 3, 6, 9, and 12 months. Twenty-two infants had R/F. At 3 months, significantly lower mean (+/- SEM) serum phosphorus levels (4.5 +/- 0.4 vs 6.1 +/- 0.2 mg/dl), higher 1,25-dihydroxyvitamin D (1,25-[OH]2D) concentrations (96 +/- 5 vs 77 +/- 4 pg/ml), and higher free 1,25-(OH)2D index (1,25-[OH]2D:vitamin D binding protein ratio; 5.2 +/- 0.3 x 10(5) vs 4.0 +/- 0.2 x 10(5] were found in the R/F group. These values returned to normal and were similar between groups on subsequent measurements. Serum calcium, magnesium, and 25-hydroxyvitamin D (25-OHD) concentrations were normal and similar between groups. In both groups, serum vitamin D binding concentrations increased initially but remained stable and normal beyond 6 months. We conclude that in very low birth weight infants with R/F, the vitamin D status (as indicated by serum 25-OHD concentrations) is normal, and that lowered serum phosphorus levels, higher serum 1,25-(OH)2D levels, and a higher free 1,25-(OH)2D index support the thesis that mineral deficiency (especially of phosphorus) may be important in the pathogenesis of R/F in small preterm infants.
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PMID:Serum vitamin D metabolites in very low birth weight infants with and without rickets and fractures. 224 79

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Cutaneous vitamin D3 synthesis and release into the circulation is promoted by skin exposure to ultraviolet B radiation (UVB, spectrum 290 to 320 nm). To determine the relation between UVB energy level and cutaneous vitamin D synthetic response, we delivered graded increases of UVB suberythemic radiant energy (3 to 27 millijoules/cm2 [mJ/cm2]) to 32 untanned young white subjects with skin type III (Fitzpatrick-Pathak classification). Serum vitamin D3 was determined 1 hour before (basal value) and 24 hours after a single whole body exposure to UVB in a phototherapy unit. The basal vitamin D3 concentration was similar in all individuals (mean +/- SEM for whole group, 1.6 +/- 0.2 ng/ml). UVB irradiances were followed by proportional rises in serum vitamin D3 (at 27 mJ/cm2, 14.3 +/- 3.7 ng/ml), and the overall correlation between UVB radiation and consequent serum vitamin D3 response (r = 0.81; p less than 0.02) was best described by an exponential function. The minimal UVB radiation level that produced a significant increase in serum vitamin D3 was 18 mJ/cm2, a value similar to the lowest solar broadband UVB irradiance that generates previtamin D3 in vitro from the precursor 7-dehydrocholesterol (20 mJ/cm2). Because in the northern United States winter UVB irradiance does not generally reach this threshold level, we conclude that individuals living at extreme northern (or southern) latitudes may have higher dependence on body stores and dietary supply to meet their vitamin D requirements during winter.
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PMID:In vivo threshold for cutaneous synthesis of vitamin D3. 254 41

Parathyroidectomy (PTx) is indicated in hemodialysis (HD) patients who have severe osteitis fibrosa unresponsive to vitamin D therapy or in whom the latter treatment is contraindicated. Immediately after PTx, plasma immunoreactive parathyroid hormone, calcium and phosphorus concentrations decline abruptly. However, little is known in such patients about the short-term effects of PTx on plasma alkaline phosphatase (AP) activity and plasma aluminum (Al) levels. The present, preliminary study was performed to determine such parameters in 37 HD patients, and to correlate them with data of bone histology. Mean plasma AP activity started to increase after PTx from day 4 onwards. Thus, AP values significantly higher than pre-PTx values were observed at day 7 and 14 (415 +/- 54 vs. 619 +/- 77 and 749 +/- 83 IU/liter, means +/- SEM; N = 37; P less than 0.05 and 0.001, respectively). This increase, in the absence of changes in liver function, was mainly due to the bone-specific iso-AP. Moreover, the degree of increase in plasma AP activity was higher in the subgroup with negative (group I, 21 patients) than in that with positive bone Al staining (group II, 16 patients). However, plasma osteocalcin (BGP) did not change after PTx (N = 8). Basal plasma Al levels were significantly higher in group II both before and two weeks after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Short-term effects of parathyroidectomy on plasma biochemistry in chronic uremia. 257 18

We have studied the effects of diet-induced obesity on thyroidal calcitonin, plasma calcitonin, calcium and phosphorus in rats. Twelve 9-week-old female rats were randomly divided into two groups. One group was fed a low-fat diet while the other was fed a high-fat diet. Both diets had 0.76% Ca, 0.56% P and 2.2 U/g vitamin D; however, the high-fat diet had hydrogenated vegetable oil added at 405 g/kg. All rats were pair-fed and consumed 11 g/day per rat for 27 weeks at which time the rats were fasted overnight and exsanguinated. The rats on the high-fat diet weighted 406 +/- 21 g (mean +/- SEM) versus 292 +/- 13 g for controls and had higher levels of serum calcitonin (104 +/- 12 versus 57 +/- 9 pg/ml). The obese rats also had increased thyroidal calcitonin by radioimmunoassay and increased thyroidal C-cells by immunohistology. The increased calcitonin levels occurred without a concomitant increase in calcium levels. These data indicate that a high-fat diet in rats stimulates C-cell growth and calcitonin secretion.
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PMID:A high-fat diet increases calcitonin secretion in the rat. 278 30


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