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Biomedical subjects

T L Clemens

Publications and source records attributed to T L Clemens.

At least 55 records · Page 3Linked to original sources
PubMed1990

Nephrolithiasis and bone involvement in primary hyperparathyroidism.

PURPOSE: The purpose of this study was to compare patients with primary hyperparathyroidism with and without nephrolithiasis with regard to (1) biochemical profile, and (2) presence and extent of bone involvement. PATIENTS AND METHODS: Of 70 unselected patients enrolled in a longitudinal study on the natural history of primary hyperparathyroidism, 62 who underwent complete bone densitometry evaluation were considered. The patients had mild hypercalcemia (2.77 +/- 0.02 mmol/L), as well as elevated parathyroid hormone levels by mid-molecule, N-terminal, and immunoradiometric assays. Bone densitometry was assessed by dual-photon absorptiometry of the lumbar spine and femoral neck, and single-photon absorptiometry of the forearm. RESULTS: Eleven of the 62 patients (18%) had nephrolithiasis. There was no difference in serum parathyroid hormone levels, calcium, phosphorus, serum 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D3 between those with and without kidney stones. Total daily urinary calcium excretion was higher among those who formed stones (8.2 +/- 1.0 mmol versus 6.1 +/- 0.4 mmol, p less than 0.05), but not when expressed per mmol of creatinine (0.72 +/- 0.07 versus 0.69 +/- 0.04). Urinary hydroxyproline was also higher in patients who formed stones (58 +/- 11 mg/24 hours versus 37 +/- 2 mg/24 hours; p less than 0.05). Hypercalciuria occurred in 39% of the entire cohort (n = 24), and in 33% (n = 17) of those without stones. Only 29% (n = 7) of those with hypercalciuria had nephrolithiasis. Calcium excretion correlated positively with serum 1,25-dihydroxyvitamin D3 (r = +0.32, p less than 0.05), and negatively with forearm bone mineral density (all patients: r = -0.34, p less than 0.05; hypercalciuric patients: r = -0.53, p less than 0.05). Circulating 1,25-dihydroxyvitamin D3 levels were elevated in a similar proportion of (1) all patients (31%, n = 19); (2) those with nephrolithiasis (27%); and (3) those without stones (31%). Bone mineral density was less than 80% of normal in 61% of patients, but forearm, femoral neck, and lumbar spine density were indistinguishable among those with and without stones. CONCLUSIONS: Cortical bone demineralization occurs to the same extent and frequency in patients with and without nephrolithiasis, and these two subgroups share similar biochemical and bone densitometric profiles. The pathophysiologic events leading to renal and skeletal involvement in primary hyperparathyroidism may be less selective than previously believed, as evidenced by: (1) increased urinary hydroxyproline in patients with nephrolithiasis, and (2) documentation that urinary calcium excretion reflects not only vitamin D status, but bone resorption was well.

Bone Density↗
PubMed1990

Vitamin D supplementation in elderly nursing home residents increases 25(OH)D but not 1,25(OH)2D.

Vitamin D metabolism in elderly individuals can be compromised by several mechanisms. We previously described reduced concentrations of 1,25-dihydroxyvitamin D [1,25(OH)2D] in 30% of elderly nursing home residents. The present study assesses the effect of vitamin D supplementation on 25-hydroxyvitamin D [25(OH)D] and 1,25(OH)2D. We performed a double-blind study in which 30 elderly nursing home residents were randomly given either 50 micrograms vitamin D or a placebo daily for 6 wk. Vitamin D metabolites, immunometrically assayed parathyroid hormone (IRMA-PTH), ionized calcium, and bone Gla hormone (BGP) were measured in serum at baseline and biweekly for 6 wk. Serum 25(OH)D concentrations increased significantly (P less than 0.0001) over the 6 wk in the treatment group but were unchanged in the placebo group. Serum 1,25(OH)2D, ionized calcium, BGP, and PTH were not significantly altered by the supplement. We conclude that vitamin D supplementation results in an increase in circulating 25(OH)D but not 1,25(OH)2D; however, the long-term effect on bone mineral metabolism remains unclear.

Aged↗
PubMed1990

Suppression of parathyroid hormone secretion with oral calcium in normal subjects and patients with primary hyperparathyroidism.

Exquisite sensitivity of normal parathyroid glands to small changes in ambient calcium concentrations and impaired sensitivity in primary hyperparathyroidism have been shown in vitro. Using an assay for PTH that detects rapid changes in PTH secretion (N-terminal-specific RIA; normal range, less than 3-33 pg/mL), we determined PTH suppressibility in response to a standardized dose of oral calcium in normal subjects and patients with primary hyperparathyroidism. Nine normal subjects were given oral calcium (25 mg/kg), and blood was analyzed half-hourly for 3 h for calcium and N-terminal PTH (N-PTH). Serum calcium rose by 0.34 +/- 0.06 mg/dL (0.085 +/- 0.015 mmol/L), and N-PTH levels declined rapidly from 15.3 +/- 1.4 to 4.2 +/- 1.1 pg/mL (-73 +/- 6%; P less than 0.01). In six subjects N-PTH concentrations became undetectable. Nine patients with primary hyperparathyroidism were tested in the same manner. Serum calcium rose by 0.53 +/- 0.1 mg/dL (0.13 +/- 0.025 mmol/L), and N-PTH levels declined less, from 66 +/- 14 to 52 +/- 12 pg/mL (-21 +/- 4%; P less than 0.05). In none of the patients was the PTH reduced to less than 20 pg/mL. These results illustrate in vivo that the PTH response to oral calcium in primary hyperparathyroidism is markedly different from that in normal subjects.

Administration, Oral↗
PubMed1989

Abnormalities in parathyroid hormone secretion and 1,25-dihydroxyvitamin D3 formation in women with osteoporosis.

We investigated the parathyroid hormone-1,25-dihydroxyvitamin D3 (1,25(OH)2D) axis in osteoporosis by administering phosphate to 8 postmenopausal women with osteoporosis (49 to 78 years old) and to 10 normal women matched for age (50 to 74 years). All subjects responded with a similar increase in the serum phosphorus concentration (women with osteoporosis, 1.15 +/- 0.06 to 1.79 +/- 0.09 mmol per liter; controls, 1.14 +/- 0.05 to 1.73 +/- 0.08 mmol per liter) and a fall in the ionized calcium concentration (women with osteoporosis, 1.12 +/- 0.03 to 1.06 +/- 0.03 mmol per liter; controls, 1.17 +/- 0.01 to 1.11 +/- 0.02 mmol per liter). Parathyroid hormone levels rose 2.5-fold in the control group (15.4 +/- 2.2 to 37.9 +/- 6.1 pg per milliliter) but increased by only 43 percent in the group with osteoporosis (14.8 +/- 2.8 to 21.2 +/- 4.1 pg per milliliter), an increase similar to that previously reported in young normal subjects (53 percent). In healthy older and younger subjects, the levels of 1,25(OH)2D did not change; in the subjects with osteoporosis, however, they decreased significantly (50 percent). We conclude that older women require a greater parathyroid hormone stimulus than younger women to maintain vitamin D homeostasis, because of an age-related decline in the formation of 1,25(OH)2D in response to parathyroid hormone, and that in osteoporosis the age-appropriate parathyroid hormone response to the same hypocalcemic signal is diminished. Our results are consistent with the presence of an abnormality in parathyroid hormone secretory function in osteoporosis in addition to the universal decline in 1,25(OH)2D responsiveness associated with aging.

Aged↗
PubMed1989

Bone mineral density in women with type II diabetes mellitus.

Bone mineral density (BMD) was assessed in 28 women with type II diabetes mellitus and compared to 207 age-matched nondiabetic women. Mean BMD, as measured by dual-photon absorptiometry, 1.12 +/- 0.3 g/cm2 (+/- SEM), was similar to the mean BMD of control subjects, 1.06 +/- 0.1 g/cm2. Only 1 of the 28 diabetic patients had a BMD less than 0.95 g/cm2 ("fracture threshold"), whereas 25% of the control subjects had a BMD below that level. When diabetic and control subjects were matched for weight as well as age, the data continued to show similar BMD among both groups. Moreover, the disparity between the proportion of weight-matched controls (25%) and diabetic subjects (1 of 28) with a BMD below the fracture threshold persisted. Among the group of 17 diabetic subjects receiving insulin, there was a positive relationship between BMD and insulin dose. There was no significant relationship between BMD, duration of diabetes, or hemoglobin Alc. Thus, women with type II diabetes are not at increased risk for diminished BMD and may be protected against bone loss.

Adult↗
PubMed1989

Extracellular calcium modulates vitamin D-dependent calbindin-D28K gene expression in chick kidney cells.

The effect of extracellular calcium ion (Ca2+) concentration on 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3)-induction of vitamin D-dependent calcium-binding protein (calbindin-D28K) and its mRNA levels was examined in primary chick kidney cells in vitro. When exposed to normal medium Ca2+ (1.0 mM), 1,25-(OH)2D3 increased calbindin-D28K mRNA, as measured by Northern analysis, by 4-10 fold over basal levels by 12 to 24 h after addition of hormone. In the presence of 0.5 mM Ca2+, 1,25-(OH)2D3 induced calbindin-D28K mRNA by only 2 fold, whereas, when cells were exposed to 2 mM Ca2+, the induction was 10-15 fold. This calcium modulation of 1,25-(OH)2D3 induction was also observed at the level of calbindin-D28K protein concentrations as measured by radioimmunoassay. The alterations in medium Ca2+ were not associated with any change in the rate of total RNA or protein synthesis. These studies suggest that both Ca2+ and 1,25-(OH)2D3 participate in the regulation of calbindin-D28K gene expression in the kidney.

Animals↗
PubMed1988

Tissue-specific regulation of avian vitamin D-dependent calcium-binding protein 28-kDa mRNA by 1,25-dihydroxyvitamin D3.

We have studied the regulation, by 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), of vitamin D-dependent calcium-binding protein (28-kDa CaBP) mRNA in chick tissues in vivo. Northern analysis of poly(A)+ RNA was carried out using, as hybridization probes, synthetic oligonucleotides complementary to chick 28-kDa CaBP mRNA. In vitamin D-deficient chicks, 28-kDa CaBP mRNA was virtually undetectable in intestine, was clearly detectable in kidney, and present at the highest levels in cerebellum. After a single intravenous dose of 500 ng of 1,25-(OH)2D3, intestinal 28-kDa CaBP mRNA levels were increased 50-fold, kidney levels were increased 4-fold, and cerebellum levels were unchanged. Increased levels of 28-kDa CaBP mRNA were appreciated 2 h after induction and were maximal at 12 h. Pretreatment of vitamin D-deficient chicks with actinomycin D had little effect on the acute phase of the 1,25-(OH)2D3 induction of 28-kDa CaBP mRNA in intestine but blunted the induction in kidney. Pretreatment with cycloheximide caused a delayed response to 1,25-(OH)2D3 in the intestine, although control (noninhibition) levels of 28-kDa CaBP mRNA were present 12 h after hormone administration. By contrast, in the kidney, cycloheximide pretreatment resulted in an increased steady-state (vitamin D-deficient) level of 28-kDa CaBP mRNA, but completely abolished the induction of 1,25-(OH)2D3. Our studies indicate that, whereas 1,25-(OH)2D3 does not regulate 28-kDa CaBP mRNA levels in the brain, the hormone modulates 28-kDa CaBP gene expression in intestine and kidney in a tissue-specific manner, by acting through both transcriptional and post-transcriptional mechanisms.

Animals↗
PubMed1988

Immunocytochemical localization of the 1,25-dihydroxyvitamin D3 receptor in target cells.

We have used a monoclonal antibody (9A7) against the purified avian 1,25-dihydroxyvitamin D3 receptor to develop an immunocytochemical technique for visualization of the protein in fixed tissues and cultured cells. In Bouin's-fixed, chick intestine, 1,25-dihydroxyvitamin D3 receptor-like immunoreactivity was localized mainly in nuclei of epithelial cells and was more abundant in the crypt than in the villar cells. Receptor staining was low or undetectable in liver hepatocytes but was present in nuclei of cells lining the hepatic sinusoids. In rat brain, receptor-like immunoreactivity was abundant and widely distributed, but did not always coincide with the presence of vitamin D-dependent calcium-binding protein; 1,25-dihydroxyvitamin D3 receptor was absent from cerebellar Purkinje cells that contained abundant calcium-binding protein. In disaggregated rat bone cells, receptor immunoreactivity was present in mononuclear cells including osteoblasts and fibroblasts but was absent from osteoclasts. Two separate clones of osteoblast-like, rat osteosarcoma cells, shown in previous studies to be either receptor positive (17/2.8) or negative (24.1), demonstrated nuclear immunoreactivity in exact concordance with receptor levels as determined by ligand binding. The phenomenon of hormone-induced up-regulation of receptor was visualized in receptor-positive 3T6 fibroblasts by demonstration of markedly enhanced nuclear reactivity in cells treated with 10(-7) M 1,25-dihydroxyvitamin D3 for 48 h. Our studies demonstrate the feasibility of the immunocytochemical approach to visualize the 1,25-dihydroxyvitamin D3 receptor in target tissues and show that it is predominantly a nuclear protein in the relatively unoccupied and fully activated states. Moreover, the vitamin D-dependent calcium binding is not a universal marker for 1,25-dihydroxyvitamin D3 action. Rather, our observations suggest that the expression of the 1,25-dihydroxyvitamin D3 receptor may be connected with the state of cellular differentiation.

Animals↗
PubMed1987

Neoplastic hypercalcemia: physiologic response to intravenous etidronate disodium.

Following a four-day control period during which an elevated serum calcium level either stabilized or continued to rise despite maximally tolerated saline diuresis, 12 patients with neoplastic hypercalcemia were treated with intravenous etidronate disodium (etidronate) 7.5 mg/kg/day for up to seven days. Serum calcium reverted to normal levels in all patients, with the mean pretreatment serum calcium level of 12.5 +/- 0.4 mg/dl dropping to 9.2 +/- 0.2 mg/dl (p less than 0.01) by Day 7. Elevated urinary calcium (1,107 +/- 134 mg/g creatinine) and hydroxyproline levels (154 +/- 16 mg/g creatinine) declined to 245 +/- 52 mg/g creatinine and 75 +/- 14 mg/g creatinine, respectively, suggesting a marked reduction in bone resorption following treatment. Serum phosphorus levels were unchanged, but urinary phosphorus levels dropped rapidly from 1,181 +/- 125 mg/g creatinine before treatment to 723 +/- 94 mg/g creatinine after two days. Serum parathyroid hormone levels (mid-molecule assay) were suppressed before treatment (64 +/- 16 pg/ml), but rose rapidly to 223 +/- 68 pg/ml by Day 7 of treatment. The value of serum 1,25-dihydroxyvitamin D was initially below normal (16 +/- 3 pg/ml), but rose rapidly with treatment to 42 +/- 12 pg/ml by Day 7. Symptoms of hypercalcemia and bone pain improved with treatment, and no serious adverse reactions to treatment were encountered. Intravenous etidronate is apparently an effective and safe treatment for neoplastic hypercalcemia.

Adult↗
PubMed1987

Tumor-induced osteomalacia. Kinetics of calcium, phosphorus, and vitamin D metabolism and characteristics of bone histomorphometry.

A patient with a mesenchymal tumor and hypophosphatemic osteomalacia was studied before and after tumor excision. Initial laboratory values included normal serum calcium, decreased serum phosphorus and tubular reabsorption of phosphate, undetectable 1,25-dihydroxyvitamin D, and normal parathyroid hormone. Histomorphometry of a bone biopsy specimen showed evidence of increased osteoclastic bone resorption. By 16 hours after tumor removal, 1,25-dihydroxyvitamin D level had normalized, but serum phosphorus level was unchanged; at 28 hours, both serum phosphorus value and tubular reabsorption of phosphate were within normal limits. It is concluded that tumor removal is associated with rapid correction both of 1,25-dihydroxyvitamin D production and of renal phosphate wasting. Increased bone resorption suggests the production of an osteoclast activator by the tumor and may explain the typically normal serum calcium value in this disorder.

Adult↗
PubMed1987

Animal model of primary hyperparathyroidism.

An experimental model of hyperparathyroidism was developed in the rat to simulate primary hyperparathyroidism in humans. In this model thyroparathyroidectomized (TPTX) or parathyroidectomized (PTX) animals were infused for 6 days with an amount of bovine synthetic parathyroid hormone (PTH)-(1-34) fragment to restore plasma calcium levels to normal (0.7 U X h-1) or with PTH at twofold (1.4 U X h-1) or threefold (2.1 U X h-1) this basal level. Animals infused with 2.1 U X h-1 of bovine PTH-(1-34) exhibited hypercalcemia, hypophosphatemia, a reduction in theoretical renal threshold for phosphate and an increase in 1,25-dihydroxyvitamin D plasma levels that were approximately threefold the control value. In addition, these animals demonstrated nephrocalcinosis and changes of bone histology that were typical of the findings in patients with primary hyperparathyroidism. In contrast, in animals infused at 1.4 U X h-1, plasma calcium, phosphate, and theoretical renal threshold for phosphate remained within normal limits, but plasma 1,25-dihydroxyvitamin D was increased above control, suggesting that increased activity of 1 alpha-hydroxylase may be the most sensitive index of increased PTH levels. This animal model permits sustained elevation of PTH plasma levels at basal or pathologically elevated levels and should provide an effective means by which to evaluate the consequences of chronic hyperparathyroidism on epithelial function, bone, and other organ systems.

Acid-Base Equilibrium↗
PubMed1987

1,25-Dihydroxyvitamin D3 induces the synthesis of vitamin D-dependent calcium-binding protein in cultured chick kidney cells.

A 28,000 mol wt vitamin D-dependent calcium-binding protein (CaBP), first isolated from avian intestine, has recently been shown to exist in kidney and other tissues. To study the mechanism regulating the production of renal CaBP, we used primary cultures of chick kidney cells as an in vitro model. Renal cortical tubules isolated from vitamin D-deficient chicks were grown in serum-free, hormone-supplemented medium. Confluent cells were epithelioid and expressed CaBP, as demonstrated by immunocytochemistry and a specific RIA. 1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] increased cellular CaBP content in a dose-dependent manner (10(-10)-10(-7) M) from basal concentrations of 50-240 ng/mg protein to maximal concentrations of 600-1200 ng/mg protein 48 h after dosing. Cycloheximide (2 microM) inhibited 1,25-(OH)2D3 induction of CaBP, indicating that the mechanism requires new protein synthesis. Western blotting of cell extracts confirmed the identity of the inducible protein as the 28,000 mol wt CaBP. 25-Hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 were effective but somewhat less potent inducers of CaBP, whereas vitamin D3 was without significant effect. The activities of 25-hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 are attributed to their rapid conversion by kidney cells to 1 alpha-hydroxylated metabolites. The dose-response profiles for two additional bioresponses in these cells, namely induction of 24-hydroxylase and inhibition of 1 alpha-hydroxylase activity, were comparable to those for CaBP induction. To our knowledge, this is the first description of a cell culture system that exhibits 1,25-(OH)2D3-inducible CaBP in vitro. This model should permit the study of certain aspects of the physiology of 1,25-(OH)2D3 and CaBP in kidney that are not possible in vivo.

Animals↗
PubMed1986

The effect of oral phosphate administration on major indices of skeletal metabolism in normal subjects.

The effect of brief periods of phosphate administration on indices of human skeletal metabolism was investigated. Thirteen subjects (8 women, 5 men; 19-36 years old) received 2 g of oral phosphate daily for 5 days. Serum phosphorus rose 26% (3.8 +/- 0.1 mg/dl to 4.8 +/- 0.1 mg/dl; p less than .01) while total calcium fell (9.3 +/- 0.1 mg/dl to 8.9 +/- 0.1 mg/dl; p less than .01). Parathyroid hormone levels increased by 50% (14.1 +/- 2.0 pg/ml to 21.5 +/- 1.7 pg/ml; p less than .05) although values remained within the normal range. A persistent phosphaturia (0.64 +/- 0.10 g/g Cr to 1.8 +/- 0.4 g/g Cr; p less than .05) and a 69% fall in urinary calcium (80.8 +/- 10.0 mg/g Cr to 24.6 +/- 6.0 mg/g Cr; p less than .001) were observed. 1,25-dihydroxyvitamin D3 and urinary hydroxyproline concentrations did not change significantly but the bone gamma-carboxyglutamic acid protein (BGP) concentration rose 41% by day 2 (9.6 +/- 1.3 mg/ml to 13.5 +/- 2.2 mg/ml; p less than .005) and remained elevated throughout the study period. These results support the possibility that brief periods of phosphate administration may be useful in the therapy of disorders associated with low bone turnover, such as osteoporosis.

Administration, Oral↗
PubMed1986

Bone vitamin D-dependent calcium-binding protein is localized in chondrocytes of growth-plate cartilage.

The cellular distribution of vitamin D-dependent calcium-binding protein (CaBP) was examined in rat and chicken bone by immunocytochemical methods using an antiserum raised against purified chicken intestinal CaBP. In EDTA-decalcified, Vibratome sections of growing rat long bones, specific CaBP immunostaining was observed in cytoplasm of chondrocytes of the growth plate, particularly in regions of calcification. In undecalcified, frozen sections from neonatal rat, positive staining was seen in chondrocytes of tibial growth plate and also in chondrocytes of the long bones of the skull. No specific immunostaining was observed in osteoblasts, osteocytes or osteoclasts in mineralized bone. In frozen sections of tibias from 19-day-old chick embryos specific immunostaining was again confined to dividing chondrocytes of the growth plate and was much less intense in "resting" cartilage. The finding of CaBP in chondrocytes, cells known to possess specific receptors for 1,25-dihydroxyvitamin D3 and to respond to the hormone, suggests a possible functional role for CaBP in chondrocyte maturation, differentiation and/or cartilage calcification.

Animals↗
PubMed1986

Evidence that calcitonin stimulates 1,25-dihydroxyvitamin D production and intestinal absorption of calcium in vivo.

Although it is well established that parathyroid hormone and phosphate are important regulators of 1,25-dihydroxyvitamin D [1,25(OH)2D] production, it remains unclear whether calcitonin affects vitamin D metabolism in vivo. Experiments were performed in the rat to determine the effect of chronic calcitonin infusion (0.2 U X h-1) on plasma levels of vitamin D metabolites and on calcium metabolism. Thyroparathyroidectomized animals fed a calcium-replete or calcium-free diet were studied for as long as 2 wk before they were killed. In control rats, a calcium-free diet alone for 12 d resulted in an increase in 1,25(OH)2D levels from 24 +/- 5 to 139 +/- 37 pg . ml-1, P = 0.025. The infusion of calcitonin also stimulated 1,25(OH)2D levels compared with controls on a regular diet (80 +/- 17 vs. 38 +/- 6 pg . ml-1, P less than 0.05) and on a calcium-free diet (460 +/- 50 vs. 139 +/- 37 pg . ml-1, P less than 0.001). In addition, calcitonin increased plasma calcium levels in animals on a regular diet by 50%; this effect was most likely due to increased intestinal absorption of calcium, because removal of calcium from the diet markedly blunted this effect. In contrast, calcitonin administration did not significantly affect 25(OH)D plasma levels. Collectively, these data suggest that calcitonin and calcium are independent regulators of 1,25(OH)2D production and that calcitonin stimulates intestinal absorption of calcium, by increasing circulating levels of 1,25(OH)2D.

Animals↗
PubMed1986

Serum vitamin D2 and vitamin D3 metabolite concentrations and absorption of vitamin D2 in elderly subjects.

The serum vitamin D2 and vitamin D3 metabolite concentrations and intestinal absorption of vitamin D2 were determined in healthy ambulatory and chronically institutionalized elderly subjects with normal renal function. The 25-hydroxyvitamin D (25OHD) concentrations were normal in all subjects (range, 8-43 ng/ml), although institutionalized subjects had a significantly lower mean value [19.2 +/- 2 (+/- SEM) ng/ml; P less than 0.01] compared with ambulatory subjects (25.3 +/- 2 ng/ml). All but one ambulatory subject had 25OHD3 as the major circulating form, whereas 25OHD2 was the major circulating metabolite in one third of the institutionalized subjects. The mean 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentration in both groups was normal, but nine subjects had levels at or below the lower limit of normal despite normal 25OHD concentrations. Separate assay of 1,25-(OH)2D2 and 1,25(OH)2D3 revealed proportional distributions similar to those for 25OHD2 and 25OHD3. To study the effect of age on the intestinal absorption of vitamin D, we compared serum vitamin D2 concentrations after oral administration of 50,000 IU vitamin D2 in both healthy vitamin D-sufficient elderly subjects and young adults. We found no evidence of malabsorption of vitamin D in the elderly subjects. In summary, elderly subjects in New York, whether institutionalized or not, have normal serum 25OHD concentrations. However, while most elderly subjects have normal serum 1,25-(OH)2D levels, a significant proportion fail to produce normal concentrations of 1,25-(OH)2D, possibly due to age-related disturbances in renal synthesis of the hormone.

25-Hydroxyvitamin D 2↗
PubMed1985

Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes.

We developed a test procedure for the clinical evaluation of the absorption of vitamin D. Serum vitamin D concentrations were evaluated in seven patients with intestinal fat malabsorption syndromes and in seven healthy, normal subjects, after being given a single oral dose of 50,000 IU (1.25 mg) vitamin D2. In the normal subjects, serum vitamin D concentrations rose from a baseline of less than 5 ng/ml to a peak of over 50 ng/ml by 12 h, gradually falling to baseline levels by 3 days. In five of the seven patients with intestinal fat malabsorption, oral administration of 50,000 IU vitamin D2 did not raise serum vitamin D concentrations above 10 ng/ml. Two patients with severe inflammatory bowel disease had a normal absorption pattern, however. These findings suggest that an oral vitamin D absorption test may be of value for determination of patients at risk for development of vitamin D deficiency. They also raise questions about the efficacy of oral vitamin D preparations in patients with intestinal fat malabsorption.

Adult↗