Hypochlorhydria from short-term omeprazole treatment does not inhibit intestinal absorption of calcium, phosphorus, magnesium or zinc from food in humans.

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Abstract
Low gastric pH is generally believed to be an important factor in intestinal mineral absorption. Thus, hypochlorhydria could be an important risk factor for mineral malabsorption and the development of marginal mineral status. We studied whether the hypochlorhydria associated with treatment with the anti-ulcer medication omeprazole, a potent gastric proton pump inhibition, would affect intestinal calcium, phosphorus, magnesium, or zinc absorption from food. Thirteen normal, healthy adults were assigned to either a control group (n = 5) receiving no drug treatment or an omeprazole treatment group (n = 8) to produce increased gastric pH. Omeprazole treatment of normal volunteers resulted in a significant change in postprandial gastric pH (pH 6.4 +/− 0.3 vs. 3.6 +/− 0.5 in control subjects, p < 0.01) and baseline fasting pH (pH 5.8 +/− 0.5 vs. pH 1.8 +/− 0.3 in controls, p < 0.01) after an overnight fast. Net mineral absorption from a standard test meal was measured using a whole gut lavage technique. Mineral absorption was measured twice in each subject, once with 120 mL of 0.1 mol/liter hydrochloric acid and a second time with 120 mL of distilled water alone. We found that despite marked changes in gastric pH due to drug treatment or administration of exogenous HCl, no change in the intestinal absorption of calcium, phosphorus, magnesium or zinc from a standard test meal was evident. These findings suggest that changing the gastric pH alone does not modify the net intestinal absorption of several minerals from food. Therefore, it is unlikely that moderate hypochlorhydria resulting from short-term omeprazole treatment substantially increases the risk for developing calcium, phosphorus, magnesium, or zinc deficiencies due to mineral malabsorption.

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