Fractional Intestinal Absorption Research Articles

Ability of 25-hydroxyvitamin D3 therapy to augment serum 1,25- and 24,25-dihydroxyvitamin D in postmenopausal osteoporosis.

Six women (mean age, 62 yr; range, 48--77 yr) who were considered to have postmenopausal osteoporosis, as demonstrated by radiological evidence of vertebral crush fractures, low intestinal calcium (Ca) absorption, and bone biopsies consistent with this diagnosis, received a pharmacological dose of 25-hydroxyvitamin D3 (25OHD3; 20 microgram/day) for 3 months. This treatment increased the serum concentration of 25OHD from 8.7 +/- 4.6 to 30.2 +/- 9.5 (SD) ng/ml (P less than 0.0025), increased the serum concentration of 24,25-dihydroxyvitamin D from 1.2 +/- 1.2 to 7.7 +/- 2.7 ng/ml (P less than 0.025) in three patients, and increased the serum concentration of 1,25-dihydroxyvitamin D from 2.1 +/- 1.7 to 4.3 +/- 1.5 ng/dl (P less than 0.025). Moreover, there were commensurate increases in fractional intestinal Ca absorption from 0.38 +/- 0.03 to 0.49 +/- 0.06 (P less than 0.025) and in urinary Ca from 69 +/- 31 to 127 +/- 67 mg/day (P less than 0.025). There were no significant changes in serum Ca (9.6 +/- 0.5 vs. 9.5 +/- 0.4 mg/dl), serum phosphorus (3.4 +/- 0.2 vs. 3.6 +/- 0.4 mg/dl) or alkaline phosphatase (87 +/- 27 vs. 91 +/- 30 IU/liter) before or after therapy. It is concluded that orally administered 25OHD3 is not only effective in raising the low intestinal Ca absorption observed in postmenopausal osteoporosis but also in increasing the serum concentrations of 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D.

A longitudinal study of bone-mineral content and intestinal calcium absorption in patients with chronic renal failure

In 14 nondialyzed patients with chronic renal failure (CRF) and at the start of treatment a glomerular filtration rate (GFR) of 14–47 ml/min changes in bone mineral mass (BMM), expressed in percentage of the initial value, showed a significant correlation with the mean GFR during an observation period of 16 ± 2 mo. During a predialysis period of 6 mo BMM decreased to 97.8 ± 3.2% of the original value in 9 patients, while after 6, 12, and 16 mo of dialysis treatment, BMM in the same patients fell to 94.5 ± 3.0%, 92.0 ± 3.2% and 91.8 ± 4.6% of the initial value. As after the onset of regular hemodialysis the fractional intestinal absorption of 47Ca does not decrease but even increases in most patients, the importance of the level of intestinal calcium absorption for the development of dialysis bone disease may be questioned.

An Unique Form of Osteomalacia Associated with End Organ Refractoriness to 1,25-Dihydroxyvitamin D and Apparent Defective Synthesis of 25-Hydroxyvitamin D*

A 28-yr-old woman presented with hypocalcemia, hypophosphatemia, secondary hyperparthyroidism, and biopsy-proven osteomalacia despite treatment with vitamin D2, (17.5 mg/day). Three weeks after vitamin D2 treatment was stopped, she was found to have a low normal serum 25-hydroxyvitamin D (25OHD) and high serum 1 alpha, 25-dihydroxyvitamin D [1,25(OH)2D] of 18.6 ng/ml and 21.2 ng/dl, respectively. The fractional intestinal calcium absorption was low at 0.26. Treatment with 25OHD3 (20--50 micrograms/day) corrected the hypocalcemia and secondary hyperparathyroidism, raised intestinal calcium absorption, and reversed the skeletal lesions of osteomalacia. Serum 25OHD concentration rose to 51 ng/ml, while 1,25(OH)2D remained elevated. This case illustrates the probable operation of dual abnormalities in vitamin D metabolism. An impaired end organ responsiveness to 1,25(OH)2D was suggested by a low intestinal calcium absorption in the face of high serum 1,25(OH)2D. Moreover, there may have been a defective vitamin D-25-hydroxylase, since there was a relative refractoriness to treatment with large doses of vitamin D2, an inappropriately low serum 250HD after vitamin D2 therapy, and a responsiveness to treatment with 25OHD3.

1,25 (OH)2Vitamin D3in Osteoporosis - A Pilot Study

Intestinal calcium absorption may be low in postmenopausal osteoporosis due to a failure of the kidney to produce sufficient quantities of the active vitamin D metabolite 1,25 (OH)2D3. Based on this findings four patients with overt osteoporosis were treated for six months with 0.5 µg 1,25 (OH)2D3/day. Base-line studies under metabolic conditions were repeated after six months of treatment. Bone formation (BF) and bone resorption (BR) were assessed by measuring alkaline serum phosphatase (aPh), urinary hydroxyproline (HyPro), calcium (Ca) accretion (Vo+) and Ca mobilization rate (Vo-) as well as histomorphometric indices of BF and BR in paired bone biopsies. Net effects of treatment were checked by assessing the Ca balance (ΔCa) and the volume density (Vv) of cancellous iliac crest bone. In addition, the serum ionized calcium (SCa2+), the urinary calcium (UCa), and the fractional intestinal Ca absorption (α) were followed at shorter intervals.

Fractional Intestinal Calcium Absorption in Epileptics on Anticonvulsant Therapy.

Fractional intestinal 47Ca calcium absorption (alpha) in 12 epileptic outpatients receiving chronic high-dose anticonvulsant therapy was reduced (p less than 0.05) compared to 12 matched normal controls. Six of the epileptics were treated orally with 0.5 microgram of 1,25-dihydroxycholecalciferol (1,25-DHCC) per day and six with 10 microgram of 25-hydroxycholecalciferol (25-HCC) per day for 10 days. The alpha was determined before and after treatment and compared with the effect of 0.5 microgram of 1,25-DHCC per day given for 10 days to 6 controls. An increase of the same order in alpha was found in all groups (p less than 0.05). No changes were observed in the serum levels of calcium, phosphorus, alkaline phosphatase or iPTH during treatment. Urinary calcium excretion was low in the epileptic patients and rose during treatment. The investigation demonstrates that the sensitivity of the intestine to 1,25-DHCC is normal in epileptic patients on anticonvulsant therapy and that 1,25-DHCC and 25-HCC in the given doses had an equal effect on the reduced intestinal calcium absorption.

Effects of high dialysate calcium concentration on bone remodelling, serum biochemistry, and parathyroid hormone in patients with renal osteodystrophy

The influence of a dialysate calcium concentration of 8.0 mg/100 ml (treatment period 2) vs. 7.0 mg/100 ml (treatment period 1) on plasma calcium, phosphorus, serum immunoreactive parathyroid hormone (iPTH), bone histology, intestinal calcium absorption, and calcium transfer across the dialysis membrane was investigated in six patients with renal osteodystrophy undergoing intermittent hemodialysis. During the periods 1 and 2, the plasma calcium changes before and after dialysis were not significantly different. A significant increase in mean postdialysis plasma calcium level was observed during both periods when compared to mean predialysis level. A significant, inverse relation was found between predialysis plasma calcium and the increase in plasma calcium during hemodialysis runs. Calcium transfer across the dialysis membrane and fractional intestinal absorption of calcium in the postdialysis state were determined in four out of the six patients. During period 2, calcium transfer was higher in all four patients but intestinal calcium absorption was moderately higher only in one and strikingly lower in the remaining three patients when compared to period 1. Although brought up to 8.0 mg/100 ml, this higher dialysate calcium significantly decreased the level of serum iPTH only in one out of the six patients; in this patient, osteoclast count, active resorption surface, and periosteocytic osteolysis decreased. In a second patient, although the level of serum iPTH seemed to decrease markedly osteoclastic and osteocytic resorption did not change. In the remaining four patients, the level of serum iPTH was unchanged and bone resorption parameters were found unchanged or aggravated. It is concluded that providing additional calcium (using a dialysate calcium concentration of 8.0 mg/100 ml), the goal of which was to decrease secondary hyperparathyroidism, proved to be successful only in one patient and failed to do so in the five others. Secondary hyperparathyroidism was even found aggravated in three of them. Thus, the use of a dialysate calcium concentration of 8.0 mg/100 ml did not result in any advantage over that of 7.0 mg/100 ml in five out of six patients studied.

Effects of haemodialysis on fractional intestinal absorption of calcium in uraemia.

Fractional intestinal absorption of calcium was measured in 41 haemodialysed patients 4 hours after an oral dose of 47 Ca. Fractional intestinal calcium absorption was 40.3 +/- 1.9% (SEM) when measured 10 to 12 hours after a haemodialysis session (dialysate calcium concentration: 1.75 mmol/litre). This value was significantly lower (p less than 0.001) than that in 26 healthy controls (56.8 +/- 1.8%) and higher (p less than 0.05) than that of 35 patients with chronic renal failure treated conservatively (34.5 +/- 2.1%). In 17 patients, fractional intestinal calcium absorption was measured just before and just after a dialysis session. Pre-dialysis fractional intestinal calcium absorption (33.7 +/- 3.0%) was not significantly different from fractional intestinal calcium absorption in uraemic patients treated conservatively, while after dialysis fractional intestinal calcium absorption had increased significantly to 42.0 +/- 2.6% (p less than 0.001). It is suggested that the transient increase in fractional intestinal calcium absorption observed after dialysis could be related to dialysis induced volume depletion rather than to a vitamin D-dependent mechanism.

Fractional Intestinal Absorption and Retention of Calcium Measured by Whole-Body Counting. Application of a Power Function Model

Fractional Intestinal Absorption and Retention of Calcium Measured by Whole-Body Counting. Application of a Power Function Model

Fractional Intestinal Absorption and Retention of Calcium Measured by Whole-Body Counting. Application of a Power Function Model

By application of a power function model, fractional intestinal calcium absorption was investigated with a new technique involving whole-body counting after successive oral and intravenous administration of standard doses of 47Ca. The fractional calcium retention 7 days after the oral load of 47Ca was also measured. Fractional calcium retention averaged 30.3% in normal subjects and 11.5% in 11 patients with intestinal malabsorption. In the same groups fractional calcium absorption averaged 46.6% and 16.4%, respectively. Fractional calcium retention and intestinal calcium absorption were significantly correlated to body surface area, and there was a well-defined relation between fractional retention and absorption of calcium...

Fractional intestinal calcium absorption in azotemic rats in vivo.

The fractional intestinal calcium absorption was estimated from whole body retention data after intragastric and intraperitoneal application of47Ca. Calcium absorption was the same in partially nephrectomised and sham operated rats. The results point towards compensation by distal gut segments for well-known impaired proximal calcium absorption.

Nurse-training scheme for ex-tuberculosis patients.

<h3>Background</h3> Reducing intestinal phosphorus absorption is a cornerstone in CKD-MBD management. Yet, knowledge gaps include how CKD pathophysiology affects intestinal phosphorus absorption. <i>In vivo</i> rodent studies suggest that intestinal phosphorus absorption remains inappropriately normal in early-moderate CKD, despite declining 1,25-dihydroxyvitamin D (1,25D). We measured intestinal phosphorus absorption in patients with moderate CKD versus healthy adults using a direct radiotracer method. <h3>Methods</h3> Patients with CKD and healthy adults matched for age, sex, and race were enrolled in this 8-day controlled diet study: the first 6 days outpatient and the final 2 days inpatient. Oral and intravenous doses of ³³P and serial blood and urine sampling determined intestinal phosphorus absorption during the final 2 days. Secondary outcomes included fasting biochemistries and 24-hour urine phosphorus (uP). <h3>Results</h3> In total, <i>n</i>=8 patients with CKD (eGFR=29–55 ml/min per 1.73 m²) and <i>n</i>=8 matched healthy controls completed the study. On a controlled diet, no difference in fractional intestinal phosphorus absorption was detected between patients with CKD and healthy adults (0.69 versus 0.62, respectively; <i>P</i>=0.52), and this was similar for 24-hour uP (884 versus 935 mg/d, respectively; <i>P</i>=0.70). Fractional intestinal phosphorus absorption was not significantly related to 24-hour uP. Patients with CKD had higher serum intact PTH and intact FGF23 and lower 1,25D. The relationship between 1,25D and fractional intestinal phosphorus absorption was not statistically significant. <h3>Conclusions</h3> Intestinal phosphorus absorption with typical dietary intake did not differ in patients with moderate CKD compared with controls, despite lower serum 1,25D levels. In this setting, a relationship between 24-hour uP and fractional or absolute intestinal absorption was not evident. Further investigation is needed to determine what factors influence intestinal phosphorus absorption in CKD and the apparent lack of compensation by the intestine to limit phosphorus absorption in the face of declining kidney function and reduced 1,25D. Whether this is evident across a range of dietary phosphorus intakes, as well as CKD severity, also needs to be determined. <h3>Clinical Trial registry name and registration number:</h3> Phosphorus Absorption in Healthy Adults and in Patients with Moderate Chronic Kidney Disease, NCT03108222