Factors affecting calcium precipitation during neutralisation in a simulated intestinal environment.

Maintaining soluble calcium in the gastrointestinal tract after administration of a calcium supplement is essential for intestinal absorption. Due to the low solubility of calcium carbonate, calcium may precipitate as the carbonate salt during intestinal neutralisation with bicarbonate. The influence of neutralising solution, calcium salt and the presence of amino acids and bile components were determined in an in vitro system. After dissolution of calcium citrate or chloride salt in 0.1 N HCl, the mixture was neutralised to pH 7 with either HCO3(-) or OH(-). For further investigation, amino acids or bile components were added to the initial solution to simulate the effect of digested protein and bile, respectively. The pH and PCO2 were monitored, and samples were analysed for calcium during neutralisation. Precipitation of calcium occurred with the citrate salt, while the chloride salt only precipitated at a high secretion rate of HCO3(-), where no calcium remained in solution at pH 7 and PCO2 was at saturation. There was a buffering effect by amino acids, and bile components maintained calcium in solution. The total soluble calcium under the different physiological conditions in vitro may be used to further understand calcium solubility in vivo, a contributing factor of calcium absorption.

Exploration of intestinal calcium precipitation as a barrier to absorption at high calcium doses.

PURPOSE: To investigate the hypothesis that intestinal bicarbonate secretions precipitate calcium as the carbonate salt, thereby resulting in poor absorption (20-40%) from calcium supplements. METHODS: The in vitro effect of calcium dose and bicarbonate secretion rate on soluble calcium was determined by neutralizing elemental Ca(2+)(250, 475, and 630 mg) in 0.1 N HCl to pH 7 with a bicarbonate secretion rate of 0.12 or 1.2 mEq/min. P (CO2) and pH of the solutions were monitored. Soluble calcium was analyzed using atomic absorption spectrometry. Additionally, the transport of calcium across Caco-2 cell monolayers was determined. RESULTS: Calcium from a 250 mg dose remained soluble during bicarbonate secretion, regardless of rate. Once the dose increased, the calcium remaining in solution decreased during neutralization with bicarbonate. The Ca(2+)/CaHCO(3) (+) ratio had no effect on calcium permeation across Caco-2 cell monolayers. CONCLUSIONS: The physicochemical mechanism of intestinal calcium precipitation supports published clinical data by suggesting that once the solubility product of calcium carbonate is reached, increasing the calcium dose results in significant precipitation at intestinal pH values.