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At least 19 recordsLinked to original sources
PubMed1988

Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate.

Calcium supplementation is recommended as a prophylaxis against bone loss. This study was performed to determine the dose dependency of calcium absorption in an attempt to derive an optimum dose schedule. Using the well-described oral calcium load technique, we measured the calcium absorption from three different calcium doses (0.5, 1.0, and 2.0 g) of both calcium carbonate and calcium citrate administered to 21 normal subjects (4 men and 17 women, 22-60 years). Nine subjects underwent two additional loads with 0.2 g of elemental calcium as calcium carbonate and as calcium citrate. The intestinal calcium absorption from calcium carbonate and calcium citrate was estimated from the rise in urinary calcium following oral ingestion of the respective calcium salt. The increment in urinary calcium post-load, reflective of intestinal calcium absorption, rose rapidly from 0 to 0.5 g calcium loads with only slight subsequent increases from the 0.5 g to 2.0 g calcium doses. Thus, results indicate that 0.5 g of calcium is the optimum dose of either calcium salt. Moreover, the increment in urinary calcium post-load was higher from calcium citrate than from calcium carbonate at all four dosage levels. The increment in urinary calcium (during the second 2 hr) following calcium citrate load (0.5 g calcium) was 0.104 +/- 0.096 mg/dl glomerular filtrate (GF), which was higher than that of 0.091 +/- 0.068 mg/dl GF obtained from 2.0 g calcium as calcium carbonate. These results confirm the superior calcium bioavailability from calcium citrate as compared with calcium carbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Acute biochemical variations induced by calcium citrate and calcium carbonate in Type 2 diabetic patients: impaired calcium absorption in Type 2 diabetic patients with prolonged gastric emptying time.

Calcium supplementation is important in the treatment of osteoporosis, a disease that may also occur in diabetic patients. The acute effects of calcium supplementation and their relationship to gastric emptying time, however, have rarely been studied in type 2 diabetic patients. We evaluated the acute biochemical variations induced by the administration of two different calcium preparations, calcium citrate and calcium carbonate, in 16 (male/female: 13/3) Chinese diabetic patients. Serum free calcium, intact parathyroid hormone (i-PTH), and amount of urinary excretion of calcium (uCal/uCr) were evaluated after a single dose of 1200 mg of elemental calcium in each preparation. The free calcium levels did not change significantly in either group. However, significant suppression of i-PTH after calcium citrate administration at 1 h (17.1+/-2.0 pg/ml, P=.023), and after calcium carbonate administration at 2 h (14.2+/-2.5 pg/ml, P=.000), was noted when compared with individual basal level (21.2+/-2.5 and 19.3+/-2.4 pg/ml, respectively). The suppressive effect on i-PTH lasted for 6 h after calcium citrate and 5 h after calcium carbonate preparation of the 6-h study period. After administration of calcium citrate, the uCal/uCr of 2-to-4-h collection was significantly higher than that of the basal and 0-to-2-h collections: 0.25+/-0.04 vs. 0.19+/-0.03, P=.025; and 0.25+/-0.04 vs. 0.19+/-0.02, P=.014, respectively. A similar finding was observed for calcium carbonate: 0.23+/-0.03 vs. 0.18+/-0.02, P=.019; and 0.23+/-0.03 vs. 0.18+/-0.02, P=.011, respectively. We conclude that, in this group of Chinese type 2 diabetic patients in our study, the oral administration of 1200 mg elemental calcium in either calcium citrate or calcium carbonate preparation can induce a significant suppression of i-PTH. This may be helpful in preventing or treating osteoporosis. A prolonged gastric emptying time in these diabetic subjects may contribute to the non-significant alteration in free calcium levels after the administration of either calcium preparation.

Administration, Oral↗
PubMed1999

Meta-analysis of calcium bioavailability: a comparison of calcium citrate with calcium carbonate.

OBJECTIVE: To perform a meta-analysis of data from available published trials comparing the bioavailability of calcium carbonate with that of calcium citrate. DATA SOURCES: The whole set was comprised of 15 studies involving 184 subjects who underwent measurement of calcium absorption from calcium carbonate and calcium citrate. Category A excluded four studies for lack of physiological relevance, use of a mixed preparation with low content of calcium carbonate, or wide variability in results. Category B was comprised of five studies (from Category A) involving 71 subjects who took calcium supplements on an empty stomach. Category C was comprised of six studies (from Category A) involving 65 subjects who took calcium preparations with meals. METHOD: The meta-analysis of calcium absorption data from calcium carbonate and calcium citrate, with calculation of effect size and 95% confidence intervals. RESULTS: Calcium absorption from calcium citrate was consistently significantly higher than that from calcium carbonate by 20.0% in the whole set, by 24.0% in Category A, by 27.2% on an empty stomach, and by 21.6% with meals. CONCLUSION: Calcium citrate is better absorbed than calcium carbonate by approximately 22% to 27%, either on an empty stomach or co-administered with meals.

Biological Availability↗
PubMed1990

Superior calcium absorption from calcium citrate than calcium carbonate using external forearm counting.

Calcium absorption from calcium citrate was compared with that obtained from calcium carbonate in 20 normal women. It was measured by external forearm counting technique, where the ratio of forearm radioactivity after an oral dose of labeled calcium salt (containing 500 mg calcium) and after an intravenous injection of trace radiocalcium represented fractional calcium absorption. The fractional calcium absorption from calcium citrate was 39.2 +/- 8.6%, which was significantly higher than the 31.2 +/- 9.4% derived from calcium carbonate (p less than 0.001). Seventeen subjects displayed greater calcium absorption from calcium citrate. The remaining three patients, with a lower calcium absorption from the citrate salt, had high levels of calcium absorption from calcium carbonate. It is concluded that calcium is better absorbed from calcium citrate than calcium carbonate when these salts are taken on an empty stomach in most women. The exception might be those with optimum calcium absorption from calcium carbonate.

Absorption↗
PubMed1996

The lack of influence of long-term potassium citrate and calcium citrate treatment in total body aluminum burden in patients with functioning kidneys.

BACKGROUND: It has been suggested that citrate salts might enhance aluminum (Al) absorption from a normal diet, posing a threat of Al toxicity even in subjects with normal renal function. We have recently reported that in normal subjects and patients with moderate renal failure, short-term treatment with tricalcium dicitrate (Ca3Cit2) does not significantly change urinary and serum Al levels. However, we have not assessed total body Al stores in patients on long-term citrate treatment. OBJECTIVE: The objective of this study was to ascertain body content of Al non-invasively using the increment in serum and urinary Al following the intravenous administration of deferoxamine (DFO) in patients with kidney stones and osteoporotic women undergoing long-term treatment with potassium citrate (K3Cit) or Ca3Cit2, respectively. METHODS: Ten patients with calcium nephrolithiasis and five with osteoporosis who were maintained on potassium citrate (40 mEq/day or more) or calcium citrate 800 mg calcium/day (40 mEq citrate) for 2 to 8 years, respectively, and 16 normal volunteers without a history of regular aluminum-containing antacid use participated in the study. All participants completed the 8 days of study, during which they were maintained on their regular home diet. Urinary Al excretion was measured during a two-day baseline before (Days 5, 6) and for 1 day (Day 7) immediately following a single intravenous dose of DFO (40 mg/kg). Blood for Al was obtained before DFO administration, and at 2, 5 and 24 hours following the start of the infusion. RESULTS: The median 24-hour urinary Al excretion (microgram/day) at baseline versus post-DFO value was 15.9 vs. 44.4 in the normal subjects and 13.3 vs. 35.7 in the patients. These values were all within normal limits and did not change significantly following DFO infusion (p = 0.003 and p = 0.0001, respectively). The median change of 17.1 micrograms/day in urinary Al in the normal subjects was not significantly different from the 18.7 micrograms/day change measured in the patient group (p = 0.30). Similarly, no change in the mean serum Al was detected at any time following the DFO infusion, either in the patient or control group (patients 4.1 to 4.3 ng/ml, controls 7.4 to 4.6 ng/ml). CONCLUSION: The results suggest that abnormal total body retention of Al does not occur during long-term citrate treatment in patients with functioning kidneys.

Adult↗
PubMed1994

Bone repair in calcium-deficient rats: comparison of xylitol+calcium carbonate with calcium carbonate, calcium lactate and calcium citrate on the repletion of calcium.

The potential value of xylitol in calcium therapy was evaluated by comparing the effect of dietary xylitol (50 g/kg diet) + calcium carbonate with the effects of calcium carbonate, calcium lactate and calcium citrate on bone repair of young male rats after the rats consumed for 3 wk a calcium-deficient diet (0.2 g Ca/kg diet). After this calcium-depletion period, the rats were fed for 2 wk one of four diets, each containing 5 g Ca/kg diet as one of the four dietary calcium sources. The diet of the control animals was supplemented with CaCO3 (5 g Ca/kg diet) throughout the study. The Ca-deficient rats showed low bone mass, low serum calcium and high serum 1,25-dihydroxycholecalciferol, parathyroid hormone (1-34 fraction) and osteocalcin concentrations. They also excreted magnesium, phosphate and hydroxyproline in the urine in high concentrations, and had high bone alkaline phosphatase and tartrate-resistant acid phosphatase activities. Most of these changes were reversed by the administered of the calcium salts. The highest recoveries of femoral dry weight, calcium, magnesium and phosphate were observed in the groups receiving xylitol+CaCO3 and calcium lactate. Calcium lactate and calcium citrate caused low serum phosphate concentration compared with rats receiving CaCO3 and with the age-matched Ca-replete controls. Xylitol-treated rats excreted more calcium and magnesium in urine than did the other rats, probably due to increased absorption of these minerals from the gut. These results suggest that dietary xylitol improves the bioavailability of calcium salts.

Administration, Oral↗
PubMed1987

Enhanced calcium bioavailability from a solubilized form of calcium citrate.

An improved formulation of calcium citrate with higher aqueous solubility and bioavailability was sought. Mixtures of calcium hydroxide and citric acid, with a calcium to citrate molar ratio ranging from 0.67-1.5, dissolved rapidly in water, creating a metastably supersaturated solution. The presence of an excess of citrate in the mixture delayed the precipitation of calcium citrate and kept calcium in solution longer. Thus, the mixture with a calcium to citrate molar ratio of 1.25, containing 500 mg elemental calcium, dissolved in 300 mL water within 2 min and could be kept in solution for 1 h at a wide pH range between 2 and 7. Intestinal calcium absorption, measured from the increment in urinary calcium during the second 2 h following an oral calcium load (500 mg) in 15 normal subjects was significantly higher from the mixtures (calcium to citrate molar ratios of 1.5 and 1.25) than from tricalcium dicitrate. The fractional calcium absorption, obtained from fecal recovery of radiocalcium after oral administration of 500 mg calcium prelabeled with 47Ca in 11 normal subjects, was also higher for the mixture with a calcium to citrate molar ratio of 1.25. The most efficient calcium absorption was obtained with the mixture of calcium hydroxide and citric acid with a calcium to citrate molar ratio of 1.25. The increment in urinary calcium after an oral load with this mixture was 62.4% greater than that obtained with tricalcium dicitrate [0.138 +/- 0.056 (+/- SD) vs. 0.085 +/- 0.086 mg/dL glomerular filtrate; P less than 0.05]. The fractional calcium absorption was 88.4% higher (0.324 +/- 0.107 vs. 0.172 +/- 0.061; P less than 0.05). This mixture provided the highest concentration of ionic calcium, indicating that calcium (rather than calcium-citrate complex) is the fraction absorbed from the intestinal tract. This study, therefore, suggests that a liquid calcium preparation formulated from the mixture of calcium hydroxide and citric acid is more effective than a solid preparation of tricalcium dicitrate in providing soluble and bioavailable calcium.

Adult↗
PubMed1985

Calcium bioavailability from calcium carbonate and calcium citrate.

Fourteen normal subjects took 1000 mg calcium orally as calcium citrate or calcium carbonate. The amount of calcium absorbed was estimated from the rise in urinary calcium. The urinary calcium following calcium citrate load significantly higher (by 20-66%), whether expressed as the total amount or as the increment above basal (fasting) excretion. Thus, calcium citrate provides a more optimum calcium bioavailability than calcium carbonate.

Administration, Oral↗
PubMed1985

Calcium citrate: reduced propensity for the crystallization of calcium oxalate in urine resulting from induced hypercalciuria of calcium supplementation.

The effect of calcium citrate (800 mg calcium/day in 4 divided doses) on urinary biochemistry and crystallization of calcium salts was examined in 18 normal subjects. During treatment, urinary calcium increased significantly (from 150 +/- 65 (SD) to 248 +/- 77 mg/day). Urinary citrate rose from 611 +/- 208 to 730 +/- 225 mg/day, owing largely to the alkali load. The urinary saturation of calcium oxalate rose by only 41% during calcium citrate treatment, due mainly to citrate complexation of calcium (rather than by 62% without such complexation). Moreover, the formation product of calcium oxalate rose during treatment, indicating that the enhanced citrate excretion augmented the inhibitor activity against calcium oxalate crystallization. Thus, calcium citrate may not be attendant with the risk for stone formation usually associated with calcium supplementation.

Adult↗
PubMed1994

Effect of calcium citrate supplementation on urinary calcium oxalate saturation in female stone formers: implications for prevention of osteoporosis.

In 14 women aged 37-68 y with a history of renal calcium calculi, bone densities were 12.0% below those of age-matched control subjects at the L2-4 lumbar spine (P = 0.007) and 6.4% less at the femoral neck (P = 0.095). A low-oxalate diet was supplemented with 1 g Ca/d as citrate. In 6 mo, plasma 1,25(OH)2D concentrations fell from 53.2 +/- 18.8 to 41.9 +/- 15.2 ng/L (P = 0.02) and parathyroid hormone from 39.1 +/- 17.0 to 30.8 +/- 12.5 ng/L (P = 0.02). Calcium oxalate saturation was 2.15 +/- 1.38 at baseline, 2.27 +/- 1.00 at 1 mo, and 2.06 +/- 1.57 at 6 mo. The increase in urinary calcium at 1 mo from 4.411 +/- 1.87 to 6.514 +/- 2.82 mmol/24 h (P = 0.01) was offset by a parallel increase in citrate excretion from 2.909 +/- 1.45 to 3.455 +/- 1.34 mmol/24 h (P = 0.03). Calcium citrate supplementation did not increase the lithogenicity of the women in this protocol.

Adult↗
PubMed1994

Limited risk of kidney stone formation during long-term calcium citrate supplementation in nonstone forming subjects.

The physiological and physicochemical effects of long-term calcium citrate supplementation (25 mmol. calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 +/- 0.42 mmol. per day (standard deviation) before treatment to 5.16 +/- 0.75 mmol. per day after 1-month of treatment (p < 0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 +/- 0.67 mmol. per day (p < 0.0125) but remained higher than the pretreatment value (p < 0.0125). Fractional intestinal calcium absorption and serum 1,25-dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 +/- 0.092 to 0.374 +/- 0.035 (p < 0.05) and from 103 +/- 7 to 77 +/- 14 pmol./l. (p < 0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 +/- 0.061 (p < 0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 +/- 14 pmol./l. Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 +/- 3.3 to 15.0 +/- 2.5 mmol. per day (p < 0.0125) and 14.0 +/- 2.5 mmol. per day (p < 0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20% and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment. In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.

Adult↗
PubMed1990

Fluoride bioavailability from slow-release sodium fluoride given with calcium citrate.

Clinical pharmacology of slow-release sodium fluoride given with calcium citrate was examined in acute and long-term studies. Following a single oral administration of 50 mg slow-release sodium fluoride, a peak serum fluoride concentration (Cmax) of 184 ng/ml was reached in 2 h; thereafter, serum fluoride concentration declined with a T1/2 of 5.9 h. The concurrent administration of calcium citrate (400 mg calcium) gave an equivalent Tmax (time required to attain Cmax) and T1/2, but a lower Cmax of 135 ng/ml. The coadministration of a meal with fluoride also reduced Cmax but increased Tmax. The area under the serum concentration curve of slow-release sodium fluoride was reduced 17-27% by a meal or calcium citrate. Thus, calcium citrate reduced fluoride absorption and peak fluoride concentration in serum of slow-release sodium fluoride but did not affect the time required to reach peak concentration or the rate of subsequent decline. The effect of a meal was similar, except for a longer period required to reach peak serum concentration. During long-term administration of 25 mg slow-release sodium fluoride coadministered with 400 mg calcium as calcium citrate on a twice daily schedule, the trough level of serum fluoride could be kept between 95 and 190 ng/ml, believed to be the therapeutic window.

Adult↗
PubMed1994

Aluminum and lead absorption from dietary sources in women ingesting calcium citrate.

Animal models suggest that citrate-containing compounds augment absorption of aluminum from food and tap water, causing aluminum accumulation in bone and brain despite normal renal function. Citrate also enhances lead absorption in animals. We questioned whether use of calcium citrate by women as a calcium supplement causes an increase in aluminum or lead absorption from dietary sources. Changes in 24-hour urine aluminum and lead excretion, plasma aluminum level, and whole blood lead level were assessed in 30 healthy women before and during treatment with calcium citrate (800 mg of elemental calcium per day). During calcium citrate therapy, urinary aluminum excretion and plasma aluminum level increased significantly. In contrast, there were no changes in urine or whole blood lead levels. We conclude that treatment with calcium citrate significantly increases absorption of aluminum from dietary sources. Additional studies are needed to determine whether long-term use of calcium citrate leads to aluminum accumulation and toxicity.

Adult↗
PubMed1988

Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF.

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, greater than 9 mg/dl; serum phosphorus, less than 5.5 mg/dl; and total CO2 content, greater than 22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 +/- 1.2 mg/dl (mean +/- SD) versus 8.9 +/- 0.8 mg/dl (P less than 0.001); phosphorus 5.5 +/- 1.9 mg/dl versus 7.0 +/- 2.3 mg/dl (P less than 0.005); and calcium-phosphate product, 52 +/- 18 versus 61 +/- 21 (P less than 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 were then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (greater than 10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.

Adult↗
PubMed1991

Calcium citrate markedly enhances aluminum absorption from aluminum hydroxide.

The effect of calcium citrate on intestinal aluminum absorption, assessed by the increment in urinary aluminum excretion, was evaluated in eight normal men. Baseline urinary aluminum excretion was determined for 2 days; thereafter, subjects ingested aluminum hydroxide for 3 days. In a cross-over study, subjects were given either calcium citrate, 950 mg four times a day, or placebo during the 3 days of aluminum hydroxide ingestion (2.4 g/d). Plasma aluminum levels were measured on the second control day and the third day of aluminum hydroxide ingestion. Baseline urinary aluminum excretion was 0.02 +/- 0.004 (6.5 +/- 1.1 micrograms/g creatinine) and 0.03 +/- 0.005 mumol/mmol creatinine (7.4 +/- 1.3 micrograms/g creatinine). These values increased during aluminum hydroxide therapy, but values were much greater when calcium citrate was ingested with aluminum hydroxide. On 3 consecutive days, urinary aluminum excretion levels were 11.1 +/- 3.23, 8.8 +/- 2.9, and 5.3 +/- 0.7 times greater during the administration of calcium citrate with aluminum hydroxide than with aluminum hydroxide alone. Plasma aluminum levels did not differ in the two treatment groups. Thus, calcium citrate markedly enhances the absorption of aluminum from aluminum hydroxide and the two must not be prescribed together in patients with renal failure.

Adult↗
PubMed1998

Citrate, calcium, phosphate and magnesium in sows' milk at initiation of lactation.

Colostrum and milk were collected from ten sows at frequent intervals from before farrowing until 9 d after farrowing. Ionized calcium, pH, and total concentrations of citrate, calcium, phosphate and magnesium were measured in whole milk. The diffusible fraction of the mammary secretion was separated by ultrafiltration and was used for the measurement of diffusible citrate, calcium, phosphate and magnesium. The pH before farrowing was 5.7, and increased to 6.5 on day 4 as total calcium and phosphate also increased. Before farrowing, total and diffusible citrate were 7.8 and 7.3 mM respectively, while diffusible phosphate was 11.9 mM, and these concentrations all decreased during the study period. Total magnesium ranged between 3.3 and 4.1 mM, while diffusible magnesium ranged between 2.0 and 3.1 mM. While these concentrations and patterns of change of diffusible calcium and citrate are quite different from those of women's milk during the first week after birth, theoretical physicochemical relationships between diffusible calcium and citrate, and ionized calcium and HPO4(2-) were corroborated by these results. We conclude that diffusible citrate plays an important role in the determination of the concentration of diffusible calcium. However, while citrate may be the major determinant of the total concentration of calcium in women's milk, this is not the case in sows' milk.

Animals↗