Antacid hypophosphatemia with

Hypophosphatemia is associated with chronic alcoholism, parenteral nutrition with inadequate phosphate supplementation, chronic ingestion of antacids, diabetic ketoacidosis, and prolonged hyperventilation. 

Milk-alkali syndrome Milk-alkali syndrome, an acute illness with symptoms of headache, nausea, irritability, and weakness, or a chronic illness with alkalosis, hypercalcemia and, possibly, renal impairment, has occurred following the concurrent use of high-dose calcium carbonate and sodium bicarbonate. Hypophosphatemia Prolonged use of aluminum-containing antacids may result in hypophosphatemia in normophosphatemic patients if phosphate intake is not adequate. 

Hypophosphatemia and phosphate depletion may result from inadequate intestinal phosphate absorption. Patients taking aluminum- or magnesium-containing antacids may develop hypophosphatemia, because these antacids bind phosphate in the intestine, rendering it nonabsorbable. The hypophosphatemia observed in patients with malabsorption maybe more closely related to their secondary hyperparathyroidism than to malabsorption of phosphate. Because phosphate is abundant in most foods, dietary deprivation is not usually a cause of phosphate depletion in patients with normal intestinal function and an adequate diet. 

Ion exchange resins (colestipol,colestyramine), which complex with the brie salts and can interfere with the absorption of the oil-soluble vitamins Aluminum antacids can complex with some of the vitamins and, when used chronically, most definitely can cause hypophosphatemia Cystic fibrosis, which can cause fat malabsorption (steatorrhea) attributed to inadequate production of pancreatic lipases... 

Antacids neutralize gastric acid, inactivate pepsin, and bind bile salts. Aluminum-containing antacids also suppress HP and enhance mucosal defense. ° G1 adverse effects are most common with antacids and are dose dependent. Magnesium salts cause an osmotic diarrhea, whereas aluminum salts cause constipation. Diarrhea usually predominates with magnesium/aluminum preparations. Aluminum-containing antacids (except aluminum phosphate) form insoluble salts with dietary phosphorus and interfere with phosphorus absorption. Hypophosphatemia occurs most often in patients with low dietary phosphate intake (e.g., malnutrition or alcoholism). Combined treatment with sucralfate may amplify the hypophosphatemia and the potential for aluminum toxicity (see section on sucralfate). 

The manifestations of hypophosphatemia depend on the chronicity and severity of the phosphate depletion. The major conditions associated with symptomatic hypophosphatemia are chronic alcoholism, intravenous hyperalimentation without adequate phosphate supplementation, and the chronic ingestion of antacids. Severe hypophosphatemia can also be seen during treatment of diabetic ketoacidosis and with prolonged hyperventilation. 

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