HYPOCHLORHYDRIA FROM SHORT-TERM OMEPRAZOLE TREATMENT DOES NOT INHIBITINTESTINAL-ABSORPTION OF CALCIUM, PHOSPHORUS, MAGNESIUM OR ZINC FROM FOOD IN HUMANS

Objective: Low gastric pH is generally believed to be an important fac tor in intestinal mineral absorption. Thus, hypochlorhydria could be a n important risk factor for mineral malabsorption and the development of marginal mineral status. We studied whether the hypochlorhydria ass ociated with treatment with the anti-ulcer medication omeprazole, a po tent gastric proton pump inhibitor, would affect intestinal calcium, p hosphorus, magnesium, or zinc absorption from food. Methods: 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 volunte ers 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) a fter an overnight fast. Net mineral absorption from a standard test me al 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 al one. Results: We found that despite marked changes in gastric pH due t o 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. Conclusions: These findings suggest t hat changing the gastric pH alone does not modify the net intestinal a bsorption of several minerals from food. Therefore, it is unlikely tha t moderate hypochlorhydria resulting from short-term omeprazole treatm ent substantially increases the risk for developing calcium, phosphoru s, magnesium, or zinc deficiencies due to mineral malabsorption.