The rationale for the use of antacids in peptic ulcer disease lies in the assumption that buffering of H+ in the stomach permits healing. The use of both low and high doses of antacids is effective in healing peptic ulcers as compared with placebo. Healing rates are comparable with those observed after the use of histamine (H2) blocking agents. The buffering agents in the various antacid preparations consist of combinations of ingredients that include sodium bicarbonate, calcium carbonate, magnesium hydroxide, and aluminum hydroxide. If diarrhea occurs or if there is renal failure, a magnesium-based preparation should be discontinued. The agents are generally safe, but some patients resist because some of the formulations are unpalatable and expensive.

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation; serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications.

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