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CALCIUM CARBONATE



Table of Contents
image Oral vitamin D or calcium carbonate in the prevention of renal bone disease?
image Comparison of effects of calcitriol and calcium carbonate on secretion of interleukin-1beta and tumour necrosis factor-alpha by uraemic peripheral blood mononuclear cells
image Effect of dietary calcium on urinary oxalate excretion after oxalate loads
image Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis

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Oral vitamin D or calcium carbonate in the prevention of renalbone disease?

Current Opinion in Nephrology and Hypertension

It is well known that hyperparathyroidism begins early in renalfailure and progresses, probably not linearly, throughout thenatural course of renal diseases and dialysis therapy. Recentprogress in basic medical science has improved our understandingof the mechanisms by which the classically known stimuli for parathyroidhormone synthesis and secretion may act, including hypocalcaemia,hyperphosphataemia and vitamin D3 metabolism disturbances. Inthe treatment of hyperparathyroidism, although some authors stressthe benefit of treating one of these stimuli, it is probably moreeffective to combine the treatment of them all. There is conclusiverecent work showing the efficacy of using both CaCO3 and vitaminD3, either in chronic renal failure or in dialsis patients atevery stage of hyperparathyroidism. Therefore, the treatment ofhyperparathyroidism should start early, long before dialysis,and it should aim to correct any of the causal factors. Both CaCO3and vitamin D3 derivatives may be used in the prevention and treatmentof renal bone disease. The limits of this association are theincreasingly often reported adynamic bone disease, which in ourexperience has not yet given major clinical problems, and hyperphosphataemia.Uncontrolled serum phosphate levels would counterbalance the beneficialeffect of vitamin D3 derivatives on hyperparathyroidism.



Comparison of effects of calcitriol and calcium carbonateon secretion of interleukin-1beta and tumour necrosis factor-alphaby uraemic peripheral blood mononuclear cells

Nephrology Dialysis Transplantation (United Kingdom), 1996, 11/SUPPL.3 (15-21)

We studied 26 non-dialysed patients with chronic renal failure(creatinine clearance (CCr) 32.6 plus or minus 12.7 ml/min). Theywere divided into three groups according to their CCr and serumintact parathyroid hormone (PTH) and were given 0.5 microg/dayoral calcitriol (calcitriol group, n = 8), 3 g/day calcium carbonate(CaCO3 group, n = 10), or neither (control uraemic group, n =8). Serum intact PTH decreased from 154 plus or minus 75 to 90plus or minus 43 pg/ml in the calcitriol group (P < 0.01) andfrom 162 plus or minus 97 to 77 plus or minus 62 pg/ml in theCaCO3 group (P < 0.001). Calcium carbonate was also effectivein suppressing serum tartrate-resistant acid phosphatase,alkaline phosphatase and intact osteocalcin levels, while calcitrioldid not suppress serum osteocalcin. Secretion of interleukin-1beta(IL-1beta) and tumour necrosis factor-alpha (TNF-alpha)by phytohaemagglutinin A (PHA)-activated peripheral bloodmononuclear cells (PBMC) was greater in uraemic patients thanin age-matched healthy controls (n = 8). Calcitriol was effectivein suppressing secretion of both cytokines, while calcium carbonatewas capable of suppressing only TNF-alpha secretion. CCrdecreased from 37.4 plus or minus 15.4 to 33.0 plus or minus 11.8ml/min (P < 0.05) in the CaCO3 group, while it did not decreasein either the calcitriol group or the control uraemic group duringa 6 month period. These results suggest that supplementation withcalcitriol is necessary to maintain bone formation and normalizeIL-1beta and TNF-alpha secretion by activated PBMC inuraemic patients.



Effect of dietary calcium on urinary oxalate excretion afteroxalate loads

American Journal of Clinical Nutrition (USA), 1997, 65/5 (1453-1459)

An experimental model that allowed differentiation between endogenouslyand exogenously derived urinary oxalate was used to assess theeffect of different forms and doses of ingested calcium on oxalateabsorption and excretion. In replication 1 (R-1), subjectsparticipated in three oxalate load (OL) tests: baseline (OL alone),calcium carbonate (OL with concomitant calcium carbonate ingestion),and calcium citrate malate (CCM) (OL with concomitant CCM ingestion).The calcium salts each provided 300 mg elemental Ca. OLs consistedof 180 mg unlabeled and 18 mg 1,2(13C2)oxalic acid. In R-2,subjects participated in four OL tests: baseline (OL alone) andOLs administered concomitantly with 100, 200, or 300 mg Ca. Timedurine samples after the OL were collected at 2-h intervalsfor the initial 6 h and samples were pooled into 9-h aliquotsfor the remaining 18 h of the 24 h period. In R-1, 24-hmean exogenous oxalate decreased (P < 0.05) after the OL from36.2 mg (baseline) to 16.1 mg (after calcium carbonate) and to14.3 mg (after CCM) whereas endogenous oxalate remained relativelyconstant. Mean 24-h oxalate absorption decreased significantlyfrom that at the time of the baseline treatment (18.3%) afterboth calcium carbonate (8.1%) and CCM (7.2%) treatments. In R-2,mean 24-h oxalate absorption was significantly lower after200 (5.9%) and 300 (7.6%) mg Ca than after 100 mg Ca (9.1%) andthe OL alone (11.3%). Concomitant meal ingestion significantlydecreased oxalate absorption in the absence of dietary calciumbut not in association with the 300-mg Ca treatment. Theoverall data provide definitive evidence that dietary calciumcan reduce oxalate absorption and excretion. Calcium carbonateand CCM were equally effective in this regard and a minimum of200 mg elemental Ca maximized this effect in conjunction withan oxalic acid intake of 198 mg.



Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis

Calcified Tissue International (USA), 1996, 58/4 (226-230)

A randomized, prospective, double-blind lest was curriedout to compare the effects of heated oyster shell-seaweedcalcium (AAA Ca), calcium carbonate, and placebo in 58 elderly,hospitalized women with the mean age of 80 divided into threegroups. Group A received 900 mg/day Ca as AAA Ca. Group B 900mg/day Ca as CaCO3, and Group C placebo besides regular hospitaldiet containing approximately 600 mg Ca/day for 24 months. Fromthe 25th to the 30th month, all groups were given AAA Ca. Lumbarspine and radial bone mineral density (BMD) were measured at 3-monthintervals. Urinary Ca/Cr and serum alkaline phosphatase, intactand midportion serum parathyroid hormone (PTH), and calcitoninwere also measured at intervals. From the 6th to the 24th monthof the study, the ratio of lumbar spine BMD (L2-L4 by DPX,Lunar) to the basal pretest value was consistently mid significantlyhigher in Group A than Group C but not higher in Group B thanin Group C. PTH, measured 12 months after the beginning of thestudy, was lower in Group A than in Group C, but no significantdifference was found between Groups B and C. At 3 months afterthe placebo was switched to AAA Ca in Group C. serum PTH was significantlydecreased from the level during placebo supplement. Morning urineCa/Cr decreased in Groups A after 18 months and in B after 12months, but not in C. Serum alkaline phosphatase decreased inGroup A significantly compared with Group C, but not in GroupB. AAA Ca appears to be effective for increasing BMD in elderlysubjects.

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